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Mouse genetic background influences severity of immune responses following trauma-hemorrhage

Studies have shown that following bacterial infection or endotoxin administration, immune functions are regulated differently in mice of different genetic background. Since the susceptibility to sepsis following trauma-hemorrhage is dependant on the severity of injury, it is important to determine w...

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Published in:Cytokine (Philadelphia, Pa.) Pa.), 2005-05, Vol.30 (4), p.168-176
Main Authors: Matsutani, Takeshi, Anantha Samy, T.S., Kang, Shih-Ching, Bland, Kirby I., Chaudry, Irshad H.
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container_start_page 168
container_title Cytokine (Philadelphia, Pa.)
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creator Matsutani, Takeshi
Anantha Samy, T.S.
Kang, Shih-Ching
Bland, Kirby I.
Chaudry, Irshad H.
description Studies have shown that following bacterial infection or endotoxin administration, immune functions are regulated differently in mice of different genetic background. Since the susceptibility to sepsis following trauma-hemorrhage is dependant on the severity of injury, it is important to determine whether genetic background of the animal influence immune functions after trauma-hemorrhage. The aim of our studies, therefore, was to assess differences in the immune functions in genetically different strains of age-matched C3H/HeN and C57BL/6 male mice following trauma-hemorrhage. The analysis for immune functions included: proliferation of splenocyte and bone-marrow cells, IL-2 and IFN-γ release by splenocytes, and TNF-α and IL-10 release by splenic, peritoneal, liver (Kupffer cell), and bone-marrow macrophages. The results show significant differences in splenocyte and bone-marrow functions, and in the release of the mediators of immune function by immune competent cells: (a) between the two genetic strains, and (b) in each mouse strain following trauma-hemorrhage. Thus, genetic background appears to significantly influence the severity of immune responses in males following trauma-hemorrhage.
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subjects Animals
Bone Marrow Cells
Bone-marrow proliferation
Cell Proliferation
Cytokine release
Genetic Predisposition to Disease
Hemorrhage - genetics
Hemorrhage - immunology
Immunity, Cellular - genetics
Interferon-gamma - metabolism
Interleukin-10 - metabolism
Interleukin-2 - metabolism
Macrophages - metabolism
Mice
Mice, Inbred C3H
Mice, Inbred C57BL
Spleen - cytology
Spleen - immunology
Spleen - metabolism
Splenocytes
Tumor Necrosis Factor-alpha - metabolism
Wounds and Injuries - genetics
Wounds and Injuries - immunology
title Mouse genetic background influences severity of immune responses following trauma-hemorrhage
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