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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Reduced intestinal inflammation induced by dextran sodium sulfate in interleukin-6-deficient mice.

Interleukin-6 (IL-6) is a multifunctional cytokine secreted by various cells, and is involved in the acute phase response and the immune response through T and B cell activation. To further define the role of IL-6 in intestinal inflammation, we studied the effects of dextran sulfate sodium (DSS) administration in mice with targeted deletions of the IL-6 gene. Acute colitis was induced in female IL-6-/- and IL-6+/+ mice by giving 4.5% DSS orally in drinking water for 8 days. The colonic mucosal injury and inflammation was evaluated based on survival rate, body-weight changes, total colon length and histological findings. Colonic mRNA expression for tumor necrosis factor (TNF)-alpha, IL-6, IL-10 and inducible nitric oxide synthase (iNOS) was measured by RT-PCR. Colonic IL-6 mRNA levels of wild-type mice continued to increase throughout the study period. At each assessment, colonic injury was significantly attenuated in DSS-treated IL-6-/- mice compared with DSS-treated IL-6+/+ mice. Histological study also showed a reduced infiltration of inflammatory cells, especially neutrophils, and mucosal cell disruption in DSS-treated IL-6-/- mice compared with DSS-treated IL-6+/+ mice. In the colons of DSS-treated IL-6-/- mice, the expression of both TNF-alpha mRNA and iNOS mRNA was reduced on day 5. In contrast, IL-10 mRNA expression was enhanced compared with DSS-treated IL-6+/+ mice. In conclusion, DSS-induced inflammation appears to be significantly inhibited in IL-6-/- mice compared to wild-type mice. These data suggest that persistent and marked blockade of IL-6 bioactivity provides some beneficial effects on intestinal inflammation.[1]

References

  1. Reduced intestinal inflammation induced by dextran sodium sulfate in interleukin-6-deficient mice. Naito, Y., Takagi, T., Uchiyama, K., Kuroda, M., Kokura, S., Ichikawa, H., Yanagisawa, R., Inoue, K., Takano, H., Satoh, M., Yoshida, N., Okanoue, T., Yoshikawa, T. Int. J. Mol. Med. (2004) [Pubmed]
 
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