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Angaben zur Quelle [Bearbeiten]

Autor     Federico Moriconi, Hans Christiansen, Dirk Raddatz, Joszef Dudas, Robert Michael Hermann, Margret Rave-Fränk, Nadeem Sheikh, Bernhard Saile, Clemens Friedrich Hess, Giuliano Ramadori
Titel    Effect of Radiation on Gene Expression of Rat Liver Chemokines: In vivo and in vitro Studies
Zeitschrift    Radiation Research
Datum    Februar 2008
Nummer    2
Seiten    162-169
URL    http://www.jstor.org/stable/30130593

Literaturverz.   

yes
Fußnoten    yes
Fragmente    4


Fragmente der Quelle:
[1.] Iam/Fragment 004 03 - Diskussion
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The interest of gastroenterologists, radiation oncologists and pathologists in radiation-induced liver disease has been generated by clinical observations of the deterioration of liver function occurring after abdominal irradiation with at least 30 Gy in patients with chronic liver diseases or even in patients with a healthy liver. This toxicity limits the use of radioimmunotherapy for malignant lymphomas, radio-chemotherapy for biliopancreatic carcinomas, and radiotherapy for liver malignancies (Greco et al. 2004;Wang et al. 1995). The molecular pathogenesis of hepatocellular damage after irradiation and the development of radiation-induced liver disease is still unknown.

Greco C, Catalano G, Di GA, Orecchia R (2004) Radiotherapy of liver malignancies. From whole liver irradiation to stereotactic hypofractionated radiotherapy. Tumori 90:73-79

Wang S, Quadri SM, Tang XZ, Stephens LC, Lollo CP, Bartholomew RM, Vriesendorp HM (1995) Liver toxicity induced by combined external-beam irradiation and radioimmunoglobulin therapy. Radiat Res 141:294-302

Introduction

The interest of gastroenterologists, radiation oncologists and pathologists in radiation-induced liver disease has been generated by clinical observations of the deterioration of liver function occurring after abdominal irradiation with at least 30 Gy in patients with chronic liver diseases or even in patients with a healthy liver. This toxicity limits the use of radioimmunotherapy for malignant lymphomas, radio-chemotherapy for biliopancreatic carcinomas, and radiotherapy for liver malignancies (1-3).

[...] The molecular pathogenesis of hepatocellular damage after irradiation and the development of radiation-induced liver disease is still unknown.


1. S. Wang, S. M. Quadri, X. Z. Tang, L. C. Stephens, C. T. Lollo, R. M. Bartholomew and H. M. Vriesendorp, Liver toxicity induced by combined external-beam irradiation and radioimmunoglobulin therapy. Radiat. Res. 141, 294–302 (1995).

2. C. Sempoux, Y. Horsmans, A. Geubel, J. Fraikin, B. E. Van Beers, J. F. Gigot, J. Lerut and J. Rahier, Severe radiation-induced liver disease following localized radiation therapy for biliopancreatic carcinoma: activation of hepatic stellate cells as an early event. Hepatology 26, 128–134 (1997).

3. C. Greco, G. Catalano, A. Di Grazia and R. Orecchia, Radiotherapy of liver malignancies. From whole liver irradiation to stereotactic hypofractionated radiotherapy. Tumori 90, 73–79 (2004).

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The CXC (or α) chemokines, such as Interleukin-8(IL-8)/CXCL8, CXCL9/MIG, CXCL10/IP10, CXCL11/ITAC and CXCL12/SDF1 have the potential to activate and attract neutrophils and T lymphocytes (Harris et al. 1996) while the C-C (or β) chemokines, such as MCP1/CCL2, MIP-1α/CCL3, MIP-1β/CCL4, MIP-3α/CCL20 and MIP-3β/CCL19, are predominantly chemoattractants for multiple leukocyte subtypes, including monocytes, eosinophils, basophils, T lymphocytes, dendritic cells, natural killer (NK) cells and, to a lesser extent, neutrophils (Ajuebor et al. 1998).

Ajuebor MN, Flower RJ, Hannon R, Christie M, Bowers K, Verity A, Perretti M (1998) Endogenous monocyte chemoattractant protein-1 recruits monocytes in the zymosan peritonitis model. J Leukoc Biol 63:108-116

Harris JG, Flower RJ, Watanabe K, Tsurufuji S, Wolitzky BA, Perretti M (1996) Relative contribution of the selectins in the neutrophil recruitment caused by the chemokine cytokine-induced neutrophil chemoattractant (CINC). Biochem Biophys Res Commun 221:692-696

[Page 162]

The C-X-C (or α) chemokines, such as CINC1, IP10, MIG, ITAC and SDF1, have the potential to activate and attract neutrophils and T lymphocytes (18), while the C-C (or β) chemokines, such as

[Page 163]

MCP1, MIP1α, MIP1β, MIP3α and MIP3β, are predominantly chemoattractants for multiple leukocyte subtypes, including monocytes, eosinophils, basophils, T lymphocytes, dendritic cells, natural killer (NK) cells and, to a lesser extent, neutrophils (19).


18. J. G. Harris, R. J. Flower, K. Watanabe, S. Tsurufuji, B. A. Wolitzky and M. Perretti, Relative contribution of the selectins in the neutrophil recruitment caused by the chemokine cytokine-induced neutrophil chemoattractant (CINC). Biochem. Biophys. Res. Commun. 221, 692–696 (1996).

19. M. N. Ajuebor, R. J. Flower, R. Hannon, M. Christie, K. Bowers, A. Verity and M. Perretti, Endogenous monocyte chemoattractant protein-1 recruits monocytes in the zymosan peritonitis model. J. Leukoc. Biol. 63, 108–116 (1998).

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The response of hepatocytes to radiation is heterogeneous and is dependent on oxygen concentration. However, in general, hepatocytes are considered more radioresistant than other cells (Alati et al. 1989b;Alati et al. 1989a). In contrast, the liver is a radiosensitive organ. The threshold dose for injury after whole-liver irradiation has been reported to be between 20 and 30 Gy (Anscher et al. 1990). In animal studies, liver irradiation above a threshold dose is not followed by a recovery phase and a complete return to normal. Instead, progressive liver fibrosis and cirrhosis may occur (Geraci et al. 1993).

Alati T, Eckl P, Jirtle RL (1989a) An in vitro micronucleus assay for determining the radiosensitivity of hepatocytes. Radiat Res 119:562-568

Alati T, Van CM, Jirtle RL (1989b) Radiosensitivity of parenchymal hepatocytes as a function of oxygen concentration. Radiat Res 118:488-501

Anscher MS, Crocker IR, Jirtle RL (1990) Transforming growth factor-beta 1 expression in irradiated liver. Radiat Res 122:77-85

Geraci JP, Mariano MS (1993) Radiation hepatology of the rat: parenchymal and nonparenchymal cell injury. Radiat Res 136:205-213

Geraci JP, Mariano MS, Jackson KL (1993) Radiation hepatology of the rat: time-dependent recovery. Radiat Res 136:214-221

The response of hepatocytes to radiation is heterogeneous and is dependent on oxygen concentration (4). However, in general, hepatocytes are considered more radioresistant than other cells (5–10). In contrast, the liver is a radiosensitive organ. The threshold dose for injury after whole-liver irradiation has been reported to be between 20 and 30 Gy (11). In animal studies, liver irradiation above a threshold dose is not followed by a recovery phase and a complete return to normal. Instead, progressive liver fibrosis and cirrhosis may occur (12).

4. T. Alati, M. Van Cleeff and R. L. Jirtle, Radiosensitivity of parenchymal hepatocytes as a function of oxygen concentration. Radiat. Res. 118, 488–501 (1989).

5. T. Alati, P. Eckl and R. L. Jirtle, An in vitro micronucleus assay for determining the radiosensitivity of hepatocytes. Radiat. Res. 119, 562–568 (1989).

6. T. Alati, M. Van Cleeff, S. C. Strom and R. L. Jirtle, Radiation sensitivity of adult human parenchymal hepatocytes. Radiat. Res. 115, 152–160 (1988).

7. R. L. Jirtle, G. Michalopoulos, J. R. McLain and J. Crowley, Transplantation system for determining the clonogenic survival of parenchymal hepatocytes exposed to ionizing radiation. Cancer Res. 41, 3512–3518 (1981).

8. R. L. Jirtle, J. R. McLain, S. C. Strom and G. Michalopoulos, Repair of radiation damage in noncycling parenchymal hepatocytes. Br. J. Radiol. 55, 847–851 (1982).

9. R. L. Jirtle, G. Michalopoulos, S. C. Strom, P. M. DeLuca and M. N. Gould, The survival of parenchymal hepatocytes irradiated with low and high LET radiation. Br. J. Cancer 6, 197–201 (1984).

10. R. L. Jirtle, P. M. DeLuca, W. M. Hinshaw and M. N. Gould, Survival of parenchymal hepatocytes irradiated with 14.3 MeV neutrons. Int. J. Radiat. Oncol. Biol. Phys. 10, 895–899 (1984).

11. R. L. Jirtle, M. S. Anscher and T. Alati, Radiation sensitivity of the liver. Adv. Radiat. Biol. 14, 269–311 (1990).

12. J. P. Geraci, M. S. Mariano and K. L. Jackson, Radiation hepatology of the rat: Time-dependent recovery. Radiat. Res. 136, 214–221 (1993).

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[4.] Iam/Fragment 081 18 - Diskussion
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This mechanism could be true in our case as leucopoenia has also been observed in current model (Moriconi et al. 2008). Another possible explanation could be considered: radiation-induced chemokines and cytokines expression may influence leukocyte production in the bone marrow. It may modify the expression of adhesion molecule genes in blood leukocytes in a way that is different from that necessary for adhesion and transmigration of inflammatory cells. This question is now under investigation.

Moriconi F, Christiansen H, Raddatz D, Dudas J, Hermann RM, Rave-Frank M, Sheikh N, Saile B, Hess CF, Ramadori G (2008) Effect of radiation on gene expression of rat liver chemokines: in vivo and in vitro studies. Radiat Res 169:162-169

Radiation-induced cytokine expression may influence leukocyte production in the bone marrow. Another reason for the lack of leukocyte infiltration may be that radiation modifies the expression of adhesion molecule genes in both liver cells and blood leukocytes in a way that is different from that necessary for adhesion and transmigration of inflammatory cells. This question is now under investigation.
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