In situ expression of interleukin-10 in noninflamed human gut and in inflammatory bowel disease

F Autschbach, J Braunstein, B Helmke, I Zuna… - The American journal of …, 1998 - Elsevier
F Autschbach, J Braunstein, B Helmke, I Zuna, G Schürmann, ZI Niemir, R Wallich, HF Otto…
The American journal of pathology, 1998Elsevier
A dysregulated secretion of contra-inflammatory cytokines such as interleukin-10 (IL-10)
could play a role in the pathogenesis of inflammatory bowel disease (IBD). We have
investigated the expression of IL-10 in gut tissues from patients with Crohn's disease (CD),
ulcerative colitis (UC) and controls by mRNA in situhybridization and immunohistochemistry.
Intestinal epithelial cells were found to express IL-10 mRNA and IL-10 protein in all of the
tissues investigated without any major differences in the expression patterns. However …
A dysregulated secretion of contra-inflammatory cytokines such as interleukin-10 (IL-10) could play a role in the pathogenesis of inflammatory bowel disease (IBD). We have investigated the expression of IL-10 in gut tissues from patients with Crohn's disease (CD), ulcerative colitis (UC) and controls by mRNA in situhybridization and immunohistochemistry. Intestinal epithelial cells were found to express IL-10 mRNA and IL-10 protein in all of the tissues investigated without any major differences in the expression patterns. However, compared with noninflamed gut, significantly increased numbers of mononuclear cells (MNCs) producing IL-10 were present in inflamed gut, both in CD and UC. This cytokine was expressed most prominently by inflammatory infiltrates enriched in macrophages, although T cells seem to contribute to its production as well. Elevated IL-10 expression in IBD was mainly detected in the submucosa, whereas IL-10 production by lamina propria cells remained comparably low. In contrast, the expression of IL-1β mRNA was preferentially increased in the lamina propria. Our data argue against a general deficiency in IL-10 production in IBD. The results suggest rather that the local production of IL-10 by mucosal MNCs in IBD is insufficient to down-regulate pro-inflammatory cytokines such as IL-1β in the lamina propria compartment.
Elsevier