In Situ Expression of Interleukin-10 in Noninflamed Human Gut and in Inflammatory Bowel Disease

• Published in: The American journal of pathology Vol. 153; no. 1; pp. 121 - 130
• Main Authors: Autschbach, Frank, Braunstein, Jutta, Helmke, Burkhard, Zuna, Ivan, Schürmann, Guido, Niemir, Zofia I., Wallich, Reinhard, Otto, Herwart F., Meuer, Stefan C.
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Elsevier Inc 01-07-1998; ASIP; American Society for Investigative Pathology
• Subjects: Adult; Aged; Biological and medical sciences; Female; Gastroenterology. Liver. Pancreas. Abdomen; Humans; Immunoenzyme Techniques; In Situ Hybridization; Inflammatory Bowel Diseases - immunology; Interleukin-1 - metabolism; Interleukin-10 - metabolism; Intestinal Diseases - immunology; Intestines - immunology; Leukocytes, Mononuclear - metabolism; Male; Medical sciences; Middle Aged; Other diseases. Semiology; Regular; RNA, Messenger - analysis; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus; Human; Immunohistochemistry; Pathogenesis; In situ; Interleukin; Cytokine; Lamina propria; Hybridization; Gene expression; Inflammatory disease; Pathology; Crohn disease; Mononuclear cell; Messenger RNA; Interleukin 10; Digestive diseases; Intestinal disease; Molecular biology; Comparative study; Macrophage; Ulcerative colitis
• ISSN: 0002-9440; 1525-2191
• DOI: 10.1016/S0002-9440(10)65552-6

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.