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Development of intestinal inflammation in double IL‐10‐ and leptin‐deficient mice
Author(s) -
Siegmund Britta,
Sennello Joseph A.,
Lehr Hans A.,
Batra Arvind,
Fedke Inka,
Zeitz Martin,
Fantuzzi Giamila
Publication year - 2004
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0404239
Subject(s) - leptin , inflammation , endocrinology , medicine , autoimmunity , colitis , biology , lamina propria , splenocyte , knockout mouse , immune system , immunology , obesity , epithelium , receptor , genetics
Leptin‐deficient ( ob/ob ) mice are resistant in different models of autoimmunity and inflammation, suggesting that leptin regulates immunity and inflammation. To investigate whether leptin deficiency modulates the spontaneous intestinal inflammation observed in interleukin (IL)‐10‐deficient mice, double IL‐10‐ and leptin‐deficient [IL‐10 knockout (KO) ob/ob ] mice were generated and compared with single IL‐10 KO mice for colitis severity. Body weight in IL‐10 KO ob/ob mice was significantly reduced compared with that of ob/ob mice. However, when compared with wild‐type or IL‐10 KO mice, IL‐10 KO ob/ob mice were still markedly obese. IL‐10 KO and IL‐10 KO ob/ob mice developed colitis with a comparable time‐course and severity in terms of macroscopic and histologic scores. Likewise, production of inter feron‐γ, IL‐6, and IL‐13 from colon cultures and splenocytes did not differ among these two groups. Conversely, rates of apoptosis were higher in lamina propria lymphocytes obtained from the colon of IL‐10 KO ob/ob compared with IL‐10 KO mice. In conclusion, although leptin deficiency has been associated with resistance in models of autoimmunity and inflammation induced by exogenous stimuli, leptin appears not to play a significant role in the spontaneous colitis of IL‐10 KO mice, although it modulates survival of intestinal lymphocytes.