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Autor     Heinz Fehrenbach
Titel    Alveolar epithelial type II cell: defender of the alveolus revisit
Zeitschrift    Respiratory Research
Ausgabe    2
Datum    15. January 2001
Nummer    1
Seiten    33-46
ISSN    1465-9921
URL    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC59567/pdf/RR-2-1-033.pdf

Literaturverz.   

yes
Fußnoten    yes
Fragmente    11


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The alveolar epithelium can be classified as a continuously renewing tissue since it comprises a population of alveolar type II epithelial cells that are characterized by almost unlimited potential to proliferate. It is still a matter of debate whether all AECII or only a small population act as the alveolar epithelial stem cell population (Uhal, 1997). The concept of AECII as stem cells of the adult alveolar epithelium was proposed by Kapanci and colleagues, and is widely accepted today (Kapanci et al., 1969). During ontogenesis, the AECII may derive from precursor cell common to AECII and Clara cells (Wuenschell et al., 1996). Furthermore AECII proliferate and differentiate to AECI to repair the damaged alveolar epithelium after lung injury or during fetal lung development, thus contributing to epithelial repair, whereas AECI are terminally differentiated, lack mitotic activity, and are easily injured. The programmed cell death or apoptosis is an important mechanism of cell removal or renewing of tissue. AECII are known to express the membrane receptor Fas (CD95, APO-1), the ligation of which may initiate the apoptotic cascade (Fine et al., 1997). This can be achieved by binding of Fas-ligand or the Fas-stimulating antibodies. There is some evidence that apoptosis of AECII is an integral mechanism of alveolar septal modelling in lung morphogenesis (Scavo et al., 1998; Schittny et al., 1998). Notably, apoptotic AECII appeared to be removed not only by alveolar macrophages but also by AECII cell neighbours (Fehrenbach et al., 2001).

Fehrenbach H. Alveolar epithelial type II cell: defender of the alveolus revisited. Respir Res. 2001; 2 (1): 33-46. Epub 2001 Jan 15. Review.

Fine A, Anderson NL, Rothstein TL, Williams MC, Gochuico BR. Fas expression in pulmonary alveolar type II cells. Am J Physiol. 1997 Jul; 273 (1Pt1): L64-71.

Kapanci Y, Weibel ER, Kaplan HP, Robinson FR. Pathogenesis and reversibility of the pulmonary lesions of oxygen toxicity in monkeys. II. Ultrastructural and morphometric studies. Lab Invest. 1969 Jan; 20 (1): 101-18.

Scavo LM, Ertsey R, Chapin CJ, Allen L, Kitterman JA. Apoptosis in the development of rat and human fetal lungs.Am J Respir Cell Mol Biol. 1998 Jan; 18 (1): 21-31.

Schittny JC, Djonov V, Fine A, Burri PH. Programmed cell death contributes to postnatal lung development. Am J Respir Cell Mol Biol. 1998 Jun; 18 (6): 786-93.

Uhal BD. Cell cycle kinetics in the alveolar epithelium. Am J Physiol. 1997 Jun; 272 (6Pt1): L1031-45. Review.

Wuenschell CW, Sunday ME, Singh G, Minoo P, Slavkin HC, Warburton D. Embryonic mouse lung epithelial progenitor cells co-express immunohistochemical markers of diverse mature cell lineages. J Histochem Cytochem. 1996 Feb; 44 (2): 113-23.

[page 33, Abstract]

AE2 cells proliferate, differentiate into AE1 cells, and remove apoptotic AE2 cells by phagocytosis, thus contributing to epithelial repair.

[page 38]

The alveolar epithelium can be classified as a continuously renewing tissue since it comprises a population of cells

[page 39]

(AE2) that are characterised by the almost unlimited potential to proliferate. [...] It is still a matter of debate whether all AE2 cells or only a subpopulation act as the alveolar epithelial stem cell population (for review, see [103]).

[...]

The concept of the AE2 cell as a stem cell of the adult alveolar epithelium was proposed by Kapanci and coworkers [108], and is widely accepted today (for review, see [103]). During ontogenesis, the AE2 cell may derive from a precursor cell common to AE2 and Clara cells [109].

[page 40]

One important mechanism of cell removal that was recognised almost a century ago [129] is programmed cell death or apoptosis [130]. [...] AE2 cells are known to express the membrane receptor Fas (CD95, APO-1), ligation of which may initiate the apoptotic cascade [134]. This can be achieved by binding of Fasligand or the Fas-stimulating antibodies. There is some evidence that apoptosis of AE2 cells is an integral mechanism of alveolar septal modelling in lung morphogenesis [135,136].

[...]

Notably, apoptotic AE2 cells (Fig. 6) appeared to be removed not only by alveolar macrophages but also by AE2 cell neighbours [138].


103. Uhal BD: Cell cycle kinetics in the alveolar epithelium. Am J Physiol 1997, 272:L1031–1045.

108. Kapanci Y, Weibel ER, Kaplan HP, Robinson FR: Pathogenesis and reversibility of the pulmonary lesions of oxygen toxicity in monkeys. II. Ultrastructural and morphometric studies. Lab Invest 1969, 20:101–117.

109. Wuenschell CW, Sunday ME, Singh G, Minoo P, Slavkin HC, Warburton D: Embryonic mouse lung epithelial progenitor cells coexpress immunohistochemical markers of diverse mature cell lineages. J Histochem Cytochem 1996, 44:113–123.

129. Gräper L: A new point of view regarding the physiological elimination of cells [in German]. Arch Zellforsch 1914, 12:373–394.

130. Rich T, Watson CJ, Wyllie A: Apoptosis: the germs of death. Nat Cell Biol 1999, 1:E69–71.

134. Fine A, Anderson NL, Rothstein TL, Williams MC, Gochuico BR: Fas expression in pulmonary alveolar type II cells. Am J Physiol 1997, 273:L64–71.

135. Scavo LM, Ertsey R, Chapin CJ, Allen L, Kitterman JA: Apoptosis in the development of rat and human fetal lungs. Am J Respir Cell Mol Biol 1998, 18:21–31.

136. Schittny JC, Djonov V, Fine A, Burri PH: Programmed cell death contributes to postnatal lung development. Am J Respir Cell Mol Biol 1998, 18:786–793.

138. Fehrenbach H, Kasper M, Koslowski R, Tan P, Schuh D, Müller M, Mason RJ: Alveolar epithelial type II cell apoptosis in vivo during resolution of keratinocyte growth factor-induced hyperplasia in the rat. Histochem Cell Biol 2000, 114:49–61.

Anmerkungen

On the last line the author gives "Fehrenbach et al., 2001" for the statement "Notably, apoptotic AECII appeared to be removed not only by alveolar macrophages but also by AECII cell neighbours". The author might either mean Fehrenbach et al. (2000), which is the reference for this statement in the source, or he means Fehrenbach (2001), which is the only publication with Fehrenbach as first author listed in the bibliography. In either case, it does not become clear to the reader that the whole passage is adapted from the source.

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(Hindemith), WiseWoman

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The best example for a cell-cell interaction between AECII and resident cells is the direct contact with AECI and during proliferation with AECII neighbours as well. These lateral cell-cell contacts within the alveolar epithelium are maintained by cell junction complex that includes gap junctions (Kasper et al, 1996). Additionally, AECII [have direct contact to fibroblasts at the basal membrane or with capillary endothelial cells (Marin et al., 1982).]

Kasper M, Traub O, Reimann T, Bjermer L, Grossmann H, Muller M, Wenzel KW Upregulation of gap junction protein connexin43 in alveolar epithelial cells of rats with radiation-induced pulmonary fibrosis. Histochem Cell Biol. 1996 Oct; 106 (4): 419-24.

Marin L, Dameron F, Relier JP. Changes in the cellular environment of differentiating type II pneumocytes. Quantitative study in the perinatal rat lung. Biol Neonate. 1982; 41 (3-4): 172-82.

Interaction with resident cells

First of all, the AE2 cell is in direct contact with AE1 cells and during proliferation with AE2 cell neighbours as well. These lateral cell-cell contacts within the alveolar epithelium are maintained by a cell junction complex that includes gap junctions [142]. The basal cell membrane is in close proximity to fibroblasts, in particular during the canalicular phase of lung morphogenesis, while modelling of the alveolar septum results in an increase in the spatial relationship of the AE2 cells with capillary endothelial cells of the adult lung [143].


142. Kasper M, Traub O, Reimann T, Bjermer L, Grossmann H, Müller M, Wenzel KW: Upregulation of gap junction protein connexin43 in alveolar epithelial cells of rats with radiationinduced pulmonary fibrosis. Histochem Cell Biol 1996, 106: 419–424.

143. Marin L, Dameron F, Relier JP: Changes in the cellular environment of differentiating type II pneumocytes. Quantitative study in the perinatal rat lung. Biol Neonate 1982, 41:172–182.

Anmerkungen

Following one reference to Fehrenbach for having termed type II epithelial cells "as integrative units of the alveolus", the author adopts over pp. 13-16 an uninterrupted review of some 30 articles from Fehrenbach without indicating this source.

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[Additionally, AECII9] have direct contact to fibroblasts at the basal membrane or with capillary endothelial cells (Marin et al., 1982).

A strong evidence for a direct interaction of AECI and AECII was presented by Ashino and colleagues (Ashino et al., 2000). Mechanical stimulation of AECI is thought to result in Ca2+-oscillations, which were transmitted via intraepithelial gap junctions to AECII and modulate exocytosis rate of lamellar bodies. Direct inhibitory interactions between AECI and AECII have been postulated to suppress AECII proliferation. Loss of AECI during injury might then trigger the release of AECII from growth inhibition (Mason and McCormack, 1994). E-cadherin as a further candidate to mediate contact inhibition, has been localized to the basolateral membrane of AECII (Kasper et al., 1995; St. Croix et al., 1998).

But even an indirect cell-cell interaction for AECII to other AECII is possible by the negative feedback loop by which surfactant protein A (SP-A) upon release into the alveolar space inhibits surfactant exocytosis in vitro (Dobbs et al., 1987). Although AECII are equipped with membrane receptors for SP-A (Strayer et al., 1996), the in vivo relevance of this autocrine mechanism by which AECII may regulate their own action remains elusive, because mice that are deficient in SP-A did not show any defect in surfactant secretion nor any respiratory deficiency (Ikegami et al., 1998). Thus, some alternative mechanism must compensate the negative SP-A feedback loop. Another potential feedback mechanism that has been postulated is the inhibition of AECII proliferation via AECII derived transforming growth factor (TGF)-β in bleomycin-induced experimental lung fibrosis (Khali et al., 1994). A number of growth factors are released by AECII, which might act in an autocrine way via the corresponding receptors expressed by AECII.

As mentioned before, fibroblasts are in contact to AECII. This reciprocal cell-cell interaction is relevant to the modelling of alveolus during lung morphogenesis as well as during remodelling associated with alveolar repair following lung injury (Kasper et al., 1996; O´Reilly et al., 1997; Shannon, et al., 1997). Both direct and indirect cell-cell interactions have been reported.


Dobbs LG, Wright JR, Hawgood S, Gonzalez R, Venstrom K, Nellenbogen J. Pulmonary surfactant and its components inhibit secretion of phosphatidylcholine from cultured rat alveolar type II cells. Proc Natl Acad Sci U S A. 1987 Feb; 84 (4): 1010-4.

Ikegami M, Korfhagen TR, Whitsett JA, Bruno MD, Wert SE, Wada K, Jobe AH. Characteristics of surfactant from SP-A-deficient mice. Am J Physiol. 1998 Aug; 275 (2Pt1): L247-54.

Kasper M, Traub O, Reimann T, Bjermer L, Grossmann H, Muller M, Wenzel KW Upregulation of gap junction protein connexin43 in alveolar epithelial cells of rats with radiation-induced pulmonary fibrosis. Histochem Cell Biol. 1996 Oct; 106 (4): 419-24.

Kasper M, Huber O, Grossmann H, Rudolph B, Trankner C, Muller M. Immunocytochemical distribution of E-cadherin in normal and injured lung tissue of the rat. Histochem Cell Biol. 1995 Nov; 104 (5): 383-90.

Khalil N, O'Connor RN, Flanders KC, Shing W, Whitman CI. Regulation of type II alveolar epithelial cell proliferation by TGF-beta during bleomycin-induced lung injury in rats. Am J Physiol. 1994 Nov; 267 (5Pt1): L498-507.

Marin L, Dameron F, Relier JP. Changes in the cellular environment of differentiating type II pneumocytes. Quantitative study in the perinatal rat lung. Biol Neonate. 1982; 41 (3-4): 172-82.

Mason RJ, McCormack FX. Alveolar type II cell reactions in pathogenic states. In Lung surfactant:Basic research in the pathogenesis of lung disorders. Edited by Müller B, von WichertP. Basel; Karger, 1994: 194-204.

O'Reilly MA, Stripp BR, Pryhuber GS. Epithelial-mesenchymal interactions in the alteration of gene expression and morphology following lung injury. Microsc Res Tech. 1997 Sep 1; 38 (5): 473-9. Review.

Shannon JM, Deterding RR Epithelial-mesenchymal interactions in lung development. In Lung growth and development. Edited by Mc Donald JA. New York; Marcel Dekker, Inc., 1997: 81-118.

St Croix B, Sheehan C, Rak JW, Florenes VA, Slingerland JM, Kerbel RS. E-Cadherin-dependent growth suppression is mediated by the cyclin-dependent kinase inhibitor p27(KIP1). J Cell Biol. 1998 Jul 27; 142 (2): 557-71.

Strayer DS, Pinder R, Chander A. Receptor-mediated regulation of pulmonary surfactant secretion. Exp Cell Res. 1996 Jul 10; 226 (1): 90-7.

The basal cell membrane is in close proximity to fibroblasts, in particular during the canalicular phase of lung morphogenesis, while modelling of the alveolar septum results in an increase in the spatial relationship of the AE2 cells with capillary endothelial cells of the adult lung [143].

The in situ study of Ashino and co-workers [64] presented strong evidence of a direct interaction of AE1 and AE2 cells. Mechanical stimulation of AE1 cells is thought to result in [Ca2+]i-oscillations (see above), which are transmitted via interepithelial gap junctions to AE2 cells and modulate exocytosis rate of lamellar bodies [64]. Direct inhibitory interactions between AE1 and AE2 cells have been postulated to suppress AE2 cell proliferation [144].

Loss of AE1 cells during lung injury might then be the trigger to release AE2 cells from growth inhibition. Although E-cadherin, a candidate mediator of contact inhibition [145], has been localised to the basolateral membrane of adult human AE2 cells [146], experimental evidence for contact inhibition of AE2 cell proliferation by AE1 cells still remains to be presented.

The most intensely studied example of an indirect AE2–AE2 cell interaction is probably the negative feedback loop by which SP-A, released into the alveolar space, inhibits surfactant exocytosis in vitro [69]. Although AE2 cells are equipped with membrane receptors for SPA [70], the in vivo relevance of this autocrine mechanism by which AE2 cells may regulate their own action is still not convincing (as pointed out recently [52]). Since mice that are deficient for SP-A did not show any defect in surfactant secretion nor any respiratory deficiency [147], there must be some alternative mechanism compensating for the loss of a SP-A feedback loop, if present at all.

Another potential feedback mechanism that has been postulated is the inhibition of AE2 cell proliferation via AE2-cell-derived transforming growth factor (TGF)-b in bleomycin-induced experimental lung fibrosis [148]. A number of growth factors are released by AE2 cells, which might act in an autocrine way via the corresponding receptors expressed by AE2 cells (see Supplementary Table 2).

Fibroblasts

The interaction of AE2 cells with fibroblasts is probably the best studied reciprocal cell-cell relationship which is relevant to the modelling of alveoles during lung morphogenesis (for review see, eg, [149]) as well as during remodelling associated with alveolar repair following lung injury (for review see, eg, [123,150]). Both direct and indirect cell-cell interactions have been reported, in most instances from studies of cells grown in culture.


143. Marin L, Dameron F, Relier JP: Changes in the cellular environment of differentiating type II pneumocytes. Quantitative study in the perinatal rat lung. Biol Neonate 1982, 41:172–182.

64. Ashino Y, Ying X, Dobbs LG, Bhattacharya J: [Ca2+]i oscillations regulate type II cell exocytosis in the pulmonary alveolus. Am J Physiol Lung Cell Mol Physiol 2000, 279:L5–13.

144. Mason RJ, McCormack FX: Alveolar type II cell reactions in pathologic states. In Lung surfactant: Basic research in the pathogenesis of lung disorders. Edited by Müller B, von Wichert P. Basel; Karger, 1994:194–204.

145. St. Croix B, Sheehan C, Rak JW, Florenes VA, Slingerland JM, Kerbel RS: E-Cadherin-dependent growth suppression is mediated by the cyclin-dependent kinase inhibitor p27(KIP1). J Cell Biol 1998, 142:557–571.

146. Kasper M, Behrens J, Schuh D, Müller M: Distribution of E-cadherin and Ep-CAM in the human lung during development and after injury. Histochem Cell Biol 1995, 103:281–286.

69. Dobbs LG, Wright JR, Hawgood S, Gonzalez R, Venstrom K, Nellenbogen J: Pulmonary surfactant and its components inhibit secretion of phosphatidylcholine from cultured rat alveolar type II cells. Proc Natl Acad Sci U S A 1987, 84:1010–1014.

70. Strayer DS, Pinder R, Chander A: Receptor-mediated regulation of pulmonary surfactant secretion. Exp Cell Res 1996, 226:90–97.

52. Rooney SA: Regulation of surfactant secretion. In Lung surfactant: cellular and molecular processing. Edited by Rooney SA. Austin, Texas; RG Landes Company, 1998:139–163.

123. Kasper M, Haroske G: Alterations in the alveolar epithelium after injury leading to pulmonary fibrosis. Histol Histopathol 1996, 11:463–483.

150. O’Reilly MA, Stripp BR, Pryhuber GS: Epithelial-mesenchymal interactions in the alteration of gene expression and morphology following lung injury. Microsc Res Tech 1997, 38:473–479.

147. Ikegami M, Korfhagen TR, Whitsett JA, Bruno MD, Wert SE, Wada K, Jobe AH: Characteristics of surfactant from SP-Adeficient mice. Am J Physiol 1998, 275:L247–254.

148. Khalil N, O’Connor RN, Flanders KC, Shing W, Whitman CI: Regulation of type II alveolar epithelial cell proliferation by TGFbeta during bleomycin-induced lung injury in rats. Am J Physiol 1994, 267:L498–507.

149. Shannon JM, Deterding RR: Epithelial-mesenchymal interactions in lung development. In Lung growth and development. Edited by McDonald JA. New York; Marcel Dekker, Inc., 1997: 81–118.

Anmerkungen

In pp. 13-16, the author adopts an uninterrupted review of some 30 articles from Fehrenbach without indicating this source.

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Hindemith

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The interaction of alveolar epithelial and capillary endothelial cells is well examined. It was reported that from pulmonary endothelial cells conditioned medium stimulate fetal lung epithelial cell growth (Smith et al., 1986) and that endothelin-1 increases AECII surfactant secretion in vitro via a protein kinase C and Ca2+-mediated pathway (Sen et al., 1994). As a source of endothelin-1, endothelial cells are therefore principally competent to act in a paracrine manner on AECII, which were reported to express the endothelin receptor A (Markewitz et al., 1995). Furthermore, alveolar type II epithelial cells themselves may synthesize endothelin-1 and stimulate endogenous prostaglandin E2 synthesis in an autocrine fashion (Markewitz et al., 1995).

Recently, a very special mechanism of indirect intercellular communication between AECII and endothelial cells has been suggested. Stimulation of alveolar epithelial cells with tumour necrosis (TNF)-α was reported to increase epithelial Ca2+ influx and to activate epithelial cytoplasmic phospholipase A2, and results in basolateral release of arachidonic acid. Free arachidonic acid is thought to increase endothelial Ca2+ influx and expression of P-selectin (Kuebler et al., 2000), which is known to be crucial for initiation of leukocyte adherence. Thus, AECII could act as transducers of an inflammatory signal from the alveolus to the capillary bed to recruit granulocytes to the site of inflammation.

Alveolar macrophages are one of the mobile cell types that interact with AECII. Among the multitude of secretory products synthesized and released by alveolar macrophages (Kasper et al., 1996; Lohmann-Matthes et al., 1994) there are some factors that act as mitogens for AECII, such as hepatocyte growth factor (Mason et al., 1994) and heparin-binding epidermal growth factor (Leslie et al., 1997). Conversely, AECII were shown to express the chemokines RANTES and MCP-1, which chemotactically attract macrophages (O´Brien et al., 1998), as well as GM-CSF (Blau et al., 1994; Christensen et al., 1995), which in turn may stimulate macrophage growth (Worgall et al., 1999). Furthermore, SP-A released from AECII modulate macrophage functions such as oxygen radical release (Weissbach et al. 1994) and nitric oxide production (Stamme et al., 2000).

Interactions of AECII with leukocytes have just recently come into focus. AECII synthesize some cytokines affecting leukocytes, such as interleukin (IL)-6 or IL-8.

Little is known about the interaction of alveolar epithelial and capillary endothelial cells. Pulmonary endothelial cell conditioned medium was reported to stimulate foetal lung epithelial cell growth [156]. [...]

Endothelin-1 was observed to increase AE2 cell surfactant secretion in vitro via a protein kinase C and Ca2+-mediated pathway [158]. As a source of endothelin-1, endothelial cells are therefore principally competent to act in a paracrine manner on AE2 epithelial cells, which were reported to express the endothelin receptor A [159]. One has to take into account that AE2 cells themselves may synthesise endothelin-1 and stimulate endogenous prostaglandin E2 synthesis in an autocrine fashion [159].

Recently, a very special mechanism of indirect intercellular communication between AE2 cells and endothelial cells has been suggested based on in situ fluorescence imaging studies in alveoli of isolated perfused lungs [160]. Stimulation of alveolar epithelial cells with tumour necrosis factor (TNF)-a was reported to increase epithelial [Ca2+]; and to activate epithelial cytoplasmic phospholipase A2, and results in basolateral release of arachidonic acid. Free arachidonic acid is thought to increase endothelial [Ca2+]; and expression of P-selectin [160], which is known to be crucial for initiation of leukocyte adherence. Thus, AE2 cells may act as transducers of an inflammatory signal from the alveolus to the capillary bed to recruit granulocytes to the site of inflammation.

Interaction with mobile cells

Alveolar macrophages

Among the multitude of secretory products synthesised and released by alveolar macrophages (for reviews, see [123,161]) there are some factors that act as mitogens for AE2 cells, such as hepatocyte growth factor [162] and heparin-binding epidermal growth factor-like protein [163]. Conversely, AE2 cells were shown to express the chemokines RANTES and MCP-1, which chemotactically attract macrophages [164], as well as GM-CSF [165,166], which in turn may stimulate macrophage growth [167]. Furthermore, SP-A released from AE2 cells may modulate macrophage functions such as, oxygen radical release [168], and nitric oxide production [169]. One has to take into account, however, that there may be species-specific differences [162,163].

Leukocytes

Interactions of AE2 cells with leukocytes have just come into focus. AE2 cells may synthesise some cytokines affecting leukocytes, such as interleukin (IL)-6 or IL-8 (see Supplementary Table 2).


156. Smith SK, Giannopoulos G: Influence of pulmonary endothelial cells on fetal lung development. Pediatr Pulmonol 1985, 1: S53–S59.

158. Sen N, Grunstein MM, Chander A: Stimulation of lung surfactant secretion by endothelin-1 from rat alveolar type II cells. Am J Physiol 1994, 266:L255–262.

159. Markewitz BA, Kohan DE, Michael JR: Endothelin-1 synthesis, receptors, and signal transduction in alveolar epithelium: evidence for an autocrine role. Am J Physiol 1995, 268:L192–200.

160. Kuebler WM, Parthasarathi K, Wang PM, Bhattacharya J: A novel signalling mechanism between gas and blood compartments of the lung. J Clin Invest 2000, 105:905–913.

123. Kasper M, Haroske G: Alterations in the alveolar epithelium after injury leading to pulmonary fibrosis. Histol Histopathol 1996, 11:463–483.

161. Lohmann-Matthes ML, Steinmuller C, Franke-Ullmann G: Pulmonary macrophages. Eur Respir J 1994, 7:1678–1689.

162. Mason RJ, Leslie CC, McCormick-Shannon K, Deterding RR, Nakamura T, Rubin JS, Shannon JM: Hepatocyte growth factor is a growth factor for rat alveolar type II cells. Am J Respir Cell Mol Biol 1994, 11:561–567.

163. Leslie CC, McCormick-Shannon K, Shannon JM, Garrick B, Damm D, Abraham JA, Mason RJ: Heparin-binding EGF-like growth factor is a mitogen for rat alveolar type II cells. Am J Respir Cell Mol Biol 1997, 16:379–387.

164. O’Brien AD, Standiford TJ, Christensen PJ, Wilcoxen SE, Paine R, 3rd: Chemotaxis of alveolar macrophages in response to signals derived from alveolar epithelial cells. J Lab Clin Med 1998, 131:417–424.

165. Blau H, Riklis S, Kravtsov V, Kalina M: Secretion of cytokines by rat alveolar epithelial cells: possible regulatory role for SP-A. Am J Physiol 1994, 266:L148–155.

166. Christensen PJ, Armstrong LR, Fak JJ, Chen GH, McDonald RA, Toews GB, Paine R III: Regulation of rat pulmonary dendritic cell immunostimulatory activity by alveolar epithelial cellderived granulocyte macrophage colony- stimulating factor. Am J Respir Cell Mol Biol 1995, 13:426–433.

167. Worgall S, Singh R, Leopold PL, Kaner RJ, Hackett NR, Topf N, Moore MA, Crystal RG: Selective expansion of alveolar macrophages in vivo by adenovirus-mediated transfer of the murine granulocyte-macrophage colony-stimulating factor cDNA. Blood 1999, 93:655–666.

168. Weissbach S, Neuendank A, Pettersson M, Schaberg T, Pison U: Surfactant protein A modulates release of reactive oxygen species from alveolar macrophages. Am J Physiol 1994, 267: L660–666.

169. Stamme C, Walsh E, Wright JR: Surfactant protein A differentially regulates IFN-g- and LPS-induced nitrite production by rat alveolar macrophages. Am J Respir Cell Mol Biol 2000, 23: 772–779.

Anmerkungen

The author adopts on pp. 13-16 an uninterrupted review of some 30 articles from Fehrenbach without indicating this source. Continued from Fragment_014_01.

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Schumann

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[Via] these cytokines, AECII might be involved in the induction of differentiation of basophil, eosinphil, and neutrophil granulocytes and maintenance of inflammatory reactions. Recent data support the idea that AECII have an accessory function in T lymphocyte activation (Zissel et al., 2000). This has been suggested on the basis of the findings that the cells bear MHC class-II molecules (Schneeberger et al., 1986). Via these cytokines, AE2 cells might be involved in the induction of differentiation of basophil, eosinophil, and neutrophil granulocytes and maintenance of inflammatory reactions. Recent data support the idea that AE2 cells have an accessory function in T-lymphocyte activation [170]. This has been suggested on the basis of the finding that the cells bear receptors of MHC class II [171].

170. Zissel G, Ernst M, Rabe K, Papadopoulos T, Magnussen H, Schlaak M, Müller-Quernheim J: Human alveolar epithelial cells type II are capable of regulating T-cell activity. J Investig Med 2000, 48:66–75.

171. Schneeberger EE, DeFerrari M, Skoskiewicz MJ, Russell PS, Colvin RB: Induction of MHC-determined antigens in the lung by interferon-gamma. Lab Invest 1986, 55:138–144.

Anmerkungen

The author adopts on pp. 13-16 an uninterrupted review of some 30 articles from Fehrenbach without indicating this source. This is the final part.

After a short interruption, in which the author expands on Zissel and introduces a post-Fehrenbach (2005) article, the author continues to adopt two smaller text passages from Fehrenbach without indicating this source, ending on p. 17 line 7.

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Additionally, AECII were reported to inhibit lymphocyte proliferation in vitro without altering their activation state (Paine et al., 1991). Moreover, AECII derived TGF-β (Zissel et al., 2000) could indirectly inhibit T cell proliferation via blockade of activating factors, such as IL-2. In contrast, granulocyte macrophage-colony stimulating factor (GM-CSF) released at the basolateral surface of AECII could increase the potential of dendritic cells to induce T-cell proliferation (Christensen et al., 1995).

Christensen PJ, Armstrong LR, Fak JJ, Chen GH, McDonald RA, Toews GB, Paine R 3rd. Regulation of rat pulmonary dendritic cell immunostimulatory activity by alveolar epithelial cell-derived granulocyte macrophage colony-stimulating factor. Am J Respir Cell Mol Biol. 1995 Oct; 13 (4): 426-33.

Paine R 3rd, Mody CH, Chavis A, Spahr MA, Turka LA, Toews GB. Alveolar epithelial cells block lymphocyte proliferation in vitro without inhibiting activation. Am J Respir Cell Mol Biol. 1991 Sep; 5 (3): 221-9.

Zissel G, Ernst M, Rabe K, Papadopoulos T, Magnussen H, Schlaak M, Muller-Quernheim J. Human alveolar epithelial cells type II are capable of regulating T-cell activity. J Investig Med. 2000 Jan; 48 (1): 66-75.

AE2 cells were reported to inhibit lymphocyte proliferation in vitro without altering their activation state [172]. AE2-cell-derived TGF-β [170] may indirectly inhibit T-cell proliferation via blockade of activating factors, such as IL-2. In contrast, GM-CSF released at the basolateral surface of AE2 cells may increase the potential of dendritic cells to induce T-cell proliferation [166].

166. Christensen PJ, Armstrong LR, Fak JJ, Chen GH, McDonald RA, Toews GB, Paine R III: Regulation of rat pulmonary dendritic cell immunostimulatory activity by alveolar epithelial cellderived granulocyte macrophage colony- stimulating factor. Am J Respir Cell Mol Biol 1995, 13:426–433.

170. Zissel G, Ernst M, Rabe K, Papadopoulos T, Magnussen H, Schlaak M, Müller-Quernheim J: Human alveolar epithelial cells type II are capable of regulating T-cell activity. J Investig Med 2000, 48:66–75.

172. Paine R III, Mody CH, Chavis A, Spahr MA, Turka LA, Toews GB: Alveolar epithelial cells block lymphocyte proliferation in vitro without inhibiting activation. Am J Respir Cell Mol Biol 1991, 5:221–229.

Anmerkungen

The source is not mentioned here.

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[7.] Mag/Fragment 016 27 - Diskussion
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The surface-active agent was characterized in numerous biochemical studies of BAL material and is now known to be composed of ∼90% lipids (with ∼80-90% phospholipids) and of ∼10% proteins (Griese, 1999). Unlike most other lipid-rich components of cells and organs, the surfactant lipids are characterized by an [unusually high level of satured [sic] fatty acid chains, such as the predominant dipalmitoylphosphatidylcholines, which contribute substantially to the unique properties of pulmonary surfactant (van Golde et al., 1994).]

Griese M. Pulmonary surfactant in health and human lung diseases: state of the art. Eur Respir J. 1999 Jun; 13 (6): 1455-76. Review.

van Golde LMG, BatenburgJJ, Robertson B The pulmonary surfactant system. News in Physiol Sciences 1994, 9:13-20.

This surface-active agent, termed surfactant, was characterised in numerous biochemical studies of bronchoalveolar lavage (BAL) material and is now known to be composed of ≈90% (mass) lipids (with ≈80-90% phospholipids) and of ≈10% proteins. Its composition may deviate greatly in pathologic states (for review, see eg [7]). Unlike most other lipid-rich components of cells and organs, the surfactant lipids are characterised by an unusually high level of saturated fatty acid chains, such as the predominant dipalmitoylphosphatidylcholines, which contribute substantially to the unique properties of pulmonary surfactant (for review, see eg [8]).

7. Griese M: Pulmonary surfactant in health and human lung diseases: state of the art. Eur Respir J 1999, 13:1455–1476.

8. Van Golde LMG, Batenburg JJ, Robertson B: The pulmonary surfactant system. News in Physiol Sciences 1994, 9:13–20.

Anmerkungen

The source is not given. To be continued on the next page: Mag/Fragment_017_01

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[8.] Mag/Fragment 017 01 - Diskussion
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[Unlike most other lipid-rich components of cells and organs, the surfactant lipids are characterized by an] unusually high level of satured [sic] fatty acid chains, such as the predominant dipalmitoylphosphatidylcholines, which contribute substantially to the unique properties of pulmonary surfactant (van Golde et al., 1994). The protein fraction comprises a highly variable amount of serum proteins (Griese; 1999) and four apoproteins that are associated with surfactant and contribute to its specific function (Weaver and Whitsett, 1991).

Griese M. Pulmonary surfactant in health and human lung diseases: state of the art. Eur Respir J. 1999 Jun; 13 (6): 1455-76. Review.

van Golde LMG, BatenburgJJ, Robertson B The pulmonary surfactant system. Newsin Physiol Sciences 1994, 9:13-20.

Weaver TE, Whitsett JA. Function and regulation of expression of pulmonary surfactant-associated proteins. Biochem J. 1991 Jan 15; 273 (Pt2): 249-64. Review.

Unlike most other lipid-rich components of cells and organs, the surfactant lipids are characterised by an unusually high level of saturated fatty acid chains, such as the predominant dipalmitoylphosphatidylcholines, which contribute substantially to the unique properties of pulmonary surfactant (for review, see eg [8]). The protein fraction comprises a highly variable amount of serum proteins (50–90% of protein) [7] and four apoproteins that are associated with surfactant and contribute to its specific functions [9].

7. Griese M: Pulmonary surfactant in health and human lung diseases: state of the art. Eur Respir J 1999, 13:1455–1476.

8. Van Golde LMG, Batenburg JJ, Robertson B: The pulmonary surfactant system. News in Physiol Sciences 1994, 9:13–20.

9. Weaver TE, Whitsett JA: Function and regulation of pulmonary surfactant-associated proteins. Biochem J 1991, 273:249–264.

Anmerkungen

The source is not given.

The copied passage starts on the previous page: Mag/Fragment_016_27

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[9.] Mag/Fragment 017 18 - Diskussion
Zuletzt bearbeitet: 2014-03-16 20:53:46 WiseWoman
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The other function of alveolar surfactant relies on the nature of SP-A and SP-D as collectins. Both proteins are able to bind to the surface of various pathogens, thus acting as opsonins to facilitate their elimination by alveolar macrophages. Therefore, alveolar surfactant is also responsible for host defence (Crouch, 2000; Pison et al., 1994; Wright, 1998).

Surfactant is synthesized by alveolar type II epithelial cells and released upon appropriate stimuli by exocytosis from special intracellular storage organelles termed lamellar bodies. Once released into the alveolar space, freshly secreted lamellar body material undergoes several steps of transformation that are necessary to establish the surface-active lining layer. Cyclic compression and expansion during ventilation result in a fraction of spent surfactant that will largely be recycled by AECII. Thus, single constituents of surfactant run through several cycles before being removed by alveolar macrophages and replaced by de novo synthesis (Fehrenbach, 2001).

Although the bronchiolar Clara cells and submucosal cells also synthesize and release the mature proteins SP-A, SP-B and SP-D (Kalina et al., 1992; Voorhout et al., 1992) the alveolar type II epithelial cell is the only type of pulmonary cell that [produces all surfactant components including phospholipids as well as all four surfactant proteins. The mature 3.5 -3.7kDa small SP-C is thought to be exclusively released by AECII cells (Beers et al., 1994; Phelps and Floros et al., 1991).]


Beers MF, Kim CY, Dodia C, Fisher AB. Localization, synthesis, and processing of surfactant protein SP-C in rat lung analyzed by epitope-specific antipeptide antibodies. J Biol Chem. 1994 Aug 12; 269 (32): 20318-28.

Crouch EC. Surfactant protein-D and pulmonary host defense. Respir Res. 2000; 1 (2): 93-108. Epub 2000 Aug 25. Review.

Fehrenbach H. Alveolar epithelial type II cell: defender of the alveolus revisited. Respir Res. 2001; 2 (1): 33-46. Epub 2001 Jan 15. Review.

Kalina M, Mason RJ, Shannon JM. Surfactant protein C is expressed in alveolar type II cells but not in Clara cells of rat lung. Am J Respir Cell Mol Biol. 1992 Jun; 6 (6): 594-600.

Phelps DS, Floros J. Localization of pulmonary surfactant proteins using immunohistochemistry and tissue in situ hybridization. Exp Lung Res. 1991 Nov-Dec; 17 (6): 985-95.

Pison U, Max M, Neuendank A, Weissbach S, Pietschmann S. Host defence capacities of pulmonary surfactant: evidence for 'non-surfactant' functions of the surfactant system. Eur J Clin Invest. 1994 Sep; 24 (9): 586-99. Review.

Voorhout WF, Veenendaal T, Kuroki Y, Ogasawara Y, van Golde LM, Geuze HJ. Immunocytochemical localization of surfactant protein D (SP-D) in type II cells, Clara cells, and alveolar macrophages of rat lung. J Histochem Cytochem. 1992 Oct; 40 (10): 1589-97.

Wright JR. Host defense functions of surfactant In Lung surfactant:cellular and molecular processing. Edited by Ronney SA. Austin, Texas; R. G. Landes Company, 1998: 191-214.

Another function of alveolar surfactant postulated by Macklin [1], host defence, has attracted major scientific interest in recent years (for reviews, see [32,33]). This function of surfactant relies on the nature of SP-A and SPD as collectins. Both proteins are able to bind to the surface of various pathogens, thus acting as opsonins to facilitate their elimination by alveolar macrophages [32–34]. [...]

[...] It is synthesised by the AE2 cells and released upon appropriate stimuli by exocytosis from special intracellular storage organelles termed lamellar bodies. Once released into the alveolar space, freshly secreted lamellar body material undergoes several steps of transformation that are necessary to establish the surface-active lining layer. Cyclic compression and expansion during ventilation result in a fraction of spent surfactant that will largely be recycled by the AE2 cells. Thus, single constituents of surfactant may run through several cycles before being removed by alveolar macrophages and replaced by de novo synthesis (for comprehensive review, see [11]).

Synthesis

Although the bronchiolar Clara cells synthesise and release the mature proteins SP-A, SP-B, and SP-D (Fig. 2a) [37,38], the AE2 cell is the only type of pulmonary cell that produces all the surfactant components (phospholipids [Fig. 3] as well as all four surfactant proteins). The mature 3.5–3.7 kDa small SP-C (Fig. 2b) is thought to be released by AE2 cells only [39,40].


1. Macklin CC: The pulmonary alveolar mucoid film and the pneumonocytes. Lancet 1954, 29:1099–1104.

11. Rooney SA: Lung surfactant: cellular and molecular processing. Austin, Texas, RG Landes Company, 1998.

32. Pison U, Max M, Neuendank A, Weissbach S, Pietschmann S: Host defence capacities of pulmonary surfactant: evidence for ‘non- surfactant’ functions of the surfactant system. Eur J Clin Invest 1994, 24:586–599.

33. Wright JR: Host defense functions of surfactant. In Lung surfactant: cellular and molecular processing. Edited by Rooney SA. Austin, Texas; R. G. Landes Company, 1998:191–214.

34. Crouch EC: Surfactant protein-D and pulmonary host defense. Respir Res 2000, 1:93–108.

37. Kalina M, Mason RJ, Shannon JM: Surfactant protein C is expressed in alveolar type II cells but not in Clara cells of rat lung. Am J Respir Cell Mol Biol 1992, 6:594–600.

38. Voorhout WF, Veenendaal T, Kuroki Y, Ogasawara Y, van Golde LM, Geuze HJ: Immunocytochemical localization of surfactant protein D (SP-D) in type II cells, Clara cells, and alveolar macrophages of rat lung. J Histochem Cytochem 1992, 40: 1589–1597.

39. Phelps DS, Floros J: Localization of pulmonary surfactant proteins using immunohistochemistry and tissue in situ hybridization. Exp Lung Res 1991, 17:985–995.

40. Beers MF, Kim CY, Dodia C, Fisher AB: Localization, synthesis, and processing of surfactant protein SP-C in rat lung analyzed by epitope-specific antipeptide antibodies. J Biol Chem 1994, 269:20318–20328.

Anmerkungen

The source is mentioned on the last line of the second paragraph. It is not clear to the reader that the preceding two as well as the following two paragraphs are taken from the source almost literally, together with several references to the literature.

To be continued on the next page: Mag/Fragment_018_01

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[10.] Mag/Fragment 018 01 - Diskussion
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[Although the bronchiolar Clara cells and submucosal cells also synthesize and release the mature proteins SP-A, SP-B and SP-D (Kalina et al., 1992; Voorhout et al., 1992) the alveolar type II epithelial cell is the only type of pulmonary cell that] produces all surfactant components including phospholipids as well as all four surfactant proteins. The mature 3.5-3.7 kDa small SP-C is thought to be exclusively released by AECII cells (Beers et al., 1994; Phelps and Floros et al., 1991).

About 85% of the secreted surfactant is taken up again, metabolised and re-secreted by AECII. Re-uptake and recycling have been demonstrated for all surfactant lipids and for all four surfactant proteins. The degradation of surfactant is accomplished by alveolar macrophages with only minimal contribution (Herbein et al., 2000; Nicholas, 1996; Young et al., 1993).


Beers MF, Kim CY, Dodia C, Fisher AB. Localization, synthesis, and processing of surfactant protein SP-C in rat lung analyzed by epitope-specific antipeptide antibodies. J Biol Chem. 1994 Aug 12; 269 (32): 20318-28.

Herbein JF, Savov J, Wright JR. Binding and uptake of surfactant protein D by freshly isolated rat alveolar type II cells. Am J Physiol Lung Cell Mol Physiol. 2000 Apr; 278 (4): L830-9.

Kalina M, Mason RJ, Shannon JM. Surfactant protein C is expressed in alveolar type II cells but not in Clara cells of rat lung. Am J Respir Cell Mol Biol. 1992 Jun; 6 (6): 594-600.

Nicholas TE. Pulmonary surfactant: no mere paint on the alveolar wall. Respirology. 1996 Dec; 1 (4): 247-57. Review.

Phelps DS, Floros J. Localization of pulmonary surfactant proteins using immunohistochemistry and tissue in situ hybridization. Exp Lung Res. 1991 Nov-Dec; 17 (6): 985-95.

Voorhout WF, Veenendaal T, Kuroki Y, Ogasawara Y, van Golde LM, Geuze HJ. Immunocytochemical localization of surfactant protein D (SP-D) in type II cells, Clara cells, and alveolar macrophages of rat lung. J Histochem Cytochem. 1992 Oct; 40 (10): 1589-97.

Young SL, Fram EK, Larson E, Wright JR. Recycling of surfactant lipid and apoprotein-A studied by electron microscopic autoradiography. Am J Physiol. 1993 Jul; 265 (1Pt1): L19-26.

[page 35]

Synthesis

Although the bronchiolar Clara cells synthesise and release the mature proteins SP-A, SP-B, and SP-D (Fig. 2a) [37,38], the AE2 cell is the only type of pulmonary cell that produces all the surfactant components (phospholipids [Fig. 3] as well as all four surfactant proteins). The mature 3.5-3.7 kDa small SP-C (Fig. 2b) is thought to be released by AE2 cells only [39,40].

[page 38]

Today it is established that most of the secreted surfactant — estimated at about 85% [24] — is taken up again, metabolised and re-secreted by the AE2 cells. Re-uptake and recycling have been demonstrated for surfactant lipids [58] and all four surfactant proteins [51,58,96,97]. [...]

The degradation of surfactant is accomplished by the alveolar macrophages with only minimal contribution, if any, from AE2 cells.


24. Nicholas TE: Pulmonary surfactant: no mere paint on the alveolar wall. Respirology 1996, 1:247–257.

37. Kalina M, Mason RJ, Shannon JM: Surfactant protein C is expressed in alveolar type II cells but not in Clara cells of rat lung. Am J Respir Cell Mol Biol 1992, 6:594–600.

38. Voorhout WF, Veenendaal T, Kuroki Y, Ogasawara Y, van Golde LM, Geuze HJ: Immunocytochemical localization of surfactant protein D (SP-D) in type II cells, Clara cells, and alveolar macrophages of rat lung. J Histochem Cytochem 1992, 40: 1589–1597.

39. Phelps DS, Floros J: Localization of pulmonary surfactant proteins using immunohistochemistry and tissue in situ hybridization. Exp Lung Res 1991, 17:985–995.

40. Beers MF, Kim CY, Dodia C, Fisher AB: Localization, synthesis, and processing of surfactant protein SP-C in rat lung analyzed by epitope-specific antipeptide antibodies. J Biol Chem 1994, 269:20318–20328.

51. Herbein JF, Savov J, Wright JR: Binding and uptake of surfactant protein D by freshly isolated rat alveolar type II cells. Am J Physiol 2000, 278:L830–839.

58. Young SL, Fram EK, Larson E, Wright JR: Recycling of surfactant lipid and apoprotein-A studied by electron microscopic autoradiography. Am J Physiol 1993, 265:L19–L26.

96. Breslin JS, Weaver TE: Binding, uptake, and localization of surfactant protein B in isolated rat alveolar type II cells. Am J Physiol 1992, 262:L699–707.

97. Pinto RA, Wright JR, Lesikar D, Benson BJ, Clements JA: Uptake of pulmonary surfactant protein C into adult rat lung lamellar bodies. J Appl Physiol 1993, 74:1005–1011.

Anmerkungen

The source is mentioned further up on the previous page, but without any indication that the here documented passage might have been taken from it. See Mag/Fragment_017_18.

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[11.] Mag/Fragment 055 13 - Diskussion
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Already 1977 Mason and Williams developed the concept of the alveolar type II epithelial cell (AECII) as a defender of the alveolus (Mason and Williams, 1977). AECII may act as immunoregulatory cells and can interact with resident and mobile cells, either directly by membrane contact or indirectly via cytokines/growth factors and their receptors. Thus alveolar type II epithelial cells represent an integrative unit of immune responses within the alveolus.

Mason RJ, Williams MC. Type II alveolar cell. Defender of the alveolus. Am Rev Respir Dis. 1977 Jun; 115 (6Pt2): 81-91.

In 1977, Mason and Williams developed the concept of the alveolar epithelial type II (AE2) cell as a defender of the alveolus. [...] AE2 cells may act as immunoregulatory cells. AE2 cells interact with resident and mobile cells, either directly by membrane contact or indirectly via cytokines/growth factors and their receptors, thus representing an integrative unit within the alveolus.
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