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Expression of IL-12-related molecules in human intestinal microvascular endothelial cells is regulated by TLR3
Department of Medicine B University of Münster, Münster, Germany.
Department of Medicine B University of Münster, Münster, Germany.
Department of Medicine B University of Münster, Münster, Germany.
Department of Medicine B University of Münster, Münster, Germany.
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2007 (English)In: American Journal of Physiology - Gastrointestinal and Liver Physiology, ISSN 0193-1857, E-ISSN 1522-1547, Am J Physiol Gastrointest Liver Physiol, Vol. 293, no 6, G1315-G1324 p.Article in journal (Refereed) Published
Abstract [en]

Members of the interleukin (IL)-12 family constitute subunits of IL-12, -23, and -27. These ILs represent pivotal mediators in the regulation of cell-mediated immune responses and in animal models of human inflammatory bowel disease. Recent work has suggested that intestinal endothelial cells might serve as a second line of defense in bacterial sensing of invading pathogens. The purpose of this study was to examine the production of IL-12 family members in intestinal endothelial cells (HIMEC). HIMEC were stimulated with proinflammatory agents (TNF-alpha, IFN-gamma, IL-1beta) and microbial antigens [LPS, lipoteichoic acid, peptidoglycan, CpG-DNA, flagellin, poly(I:C)]. Expression of IL-12 family members and of Toll-like receptor (TLR)3 in HIMEC was assessed by real-time RT-PCR, immunostaining, flow cytometry, and immunoblot analysis. HIMEC display an induction of Epstein-Barr virus-induced gene 3 (EBI3), IL-12p35, and IL-23p19, whereas no expression of IL-12p40 and IL-27p28 was detectable. The strongest induction was induced by proinflammatory factors known to utilize the NF-kappaB pathway, and expression of EBI3 and IL-23p19 was diminished by an NF-kappaB inhibitor. HIMEC display regulated expression of TLR3. Adhesion and transmigration assays showed proinflammatory responses after HIMEC stimulation. HIMEC are capable of producing IL-12 family members as a response to microbial stimuli. The TLR3 agonist, poly(I:C), was shown to enhance leukocyte adhesion in vitro in HIMEC. Our data suggest that the intestinal microvasculature is responsive to ligands of TLR3 expressed on intestinal endothelial cells, thereby adding to the regulation of adaptive immunity and leukocyte recruitment.

Place, publisher, year, edition, pages
Bethesda, United States: American Physiological Society , 2007. Vol. 293, no 6, G1315-G1324 p.
Keyword [en]
Epstein-Barr virus-induced gene 3; inflammatory bowel disease; Tolllike receptor 3
National Category
Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:liu:diva-141653DOI: 10.1152/ajpgi.00142.2007ISI: 000251510500024PubMedID: 17947455Scopus ID: 2-s2.0-37149049108ISBN: 0193-1857 (Print) 0193-1857 (Linking) OAI: oai:DiVA.org:liu-141653DiVA: diva2:1149717
Note

Heidemann, Jan Ruther, Christoph Kebschull, Moritz Domschke, Wolfram Bruwer, Matthias Koch, Stefan Kucharzik, Torsten Maaser, Christian eng Research Support, Non-U.S. Gov't 2007/10/20 09:00 Am J Physiol Gastrointest Liver Physiol. 2007 Dec;293(6):G1315-24. Epub 2007 Oct 18.

Available from: 2017-10-16 Created: 2017-10-16 Last updated: 2017-10-26Bibliographically approved

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