Journal
INFLAMMATORY BOWEL DISEASES
Volume 6, Issue 4, Pages 290-302Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1002/ibd.3780060407
Keywords
mice; interleukin 10; colitis; pathology; genetics
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Funding
- NCI NIH HHS [CA-34196] Funding Source: Medline
- NIDDK NIH HHS [DK44240] Funding Source: Medline
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Severity of inflammatory bowel disease in IL-IO gene-targeted mice is in part determined by genetic background. In the current study, a targeted IL-10 gene was transferred into the C3H/HeJBir substrain, known to exhibit high T-cell and B-cell responses to enteric flora, and to be highly sensitive to colitigenic stress. IL-10-deficient C3H/HeJBir mice developed early onset colitis in contrast to IL-10-deficient C57BL/6J congenic mice. Histopathologic analysis of disease in C3H/HeJBir.Il10(-/-) and C57BL/6J.Il10(-/-) mice showed significant differences at all ages studied. Hybrids of these congenic strains (F1.Il10(-/-)) were produced to study the mode of inheritance as well as subphenotypes that correlated with histopathology. Lesions in F1 mice were intermediate between parental strains. C3H-contributed subphenotypes that correlated best with histopathology were peripheral blood granulocyte percentage, serum amyloid A concentration, spleen weight/body weight ratio, and mesenteric lymph node weight/body weight ratio. Neither enhanced humoral immunity (secretory IgA, anti-Escherichia coli cellular membrane Ig) characteristic of C3H/HeJBir, nor T-cell percentages in peripheral blood correlated as well. This study represents a necessary step in elucidating murine genetic modifiers controlling colitis sensitivity.
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