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NEUROREGULATION AND MOTILITY

Transcriptional regulation of inflammatory mediators secreted by human colonic circular smooth muscle cells

Division of Gastroenterology, Departments of ¹Internal Medicine and ²Neuroscience and Cell Biology, Enteric Neuromuscular Disorders and Visceral Pain Center, The University of Texas Medical Branch at Galveston, Galveston, Texas

Submitted 12 November 2004 ; accepted in final form 10 March 2005

We investigated the transcriptional regulation of secretion of pro- and anti-inflammatory mediators by human colonic circular smooth muscle cells (HCCSMC) in response to tumor necrosis factor (TNF)-. Gene chip array analysis indicated that HCCSMC express a specific panel of 11 cytokines, chemokines, and cell adhesion molecules in a time-dependent manner in response to TNF-. The chip array data were supported by quantitative analysis of mRNA and protein expressions of interleukin (IL)-6, IL-8, intercellular adhesion molecule (ICAM)-1 and IL-11. The proinflammatory mediators were expressed early, whereas the anti-inflammatory cytokine IL-11 was expressed late after TNF- treatment. The expression of ICAM-1 on HCCSMC increased lymphocyte adhesion to these cells, which was blocked by pretreatment with antibody to ICAM-1. TNF- acted on both R₁ and R₂ receptors to induce the expression of ICAM-1. Pretreatment of HCCSMC with antisense oligonucleotides to p65 nuclear factor-B (NF-B) blocked the expression of ICAM-1, whereas pretreatment with antisense oligonucleotides to p50 NF-B had little effect. The overexpression of p65 NF-B enhanced the constitutive expression of ICAM-1, and TNF- treatment had no further effect. The delayed expression of endogenous IL-11 limited the expression of ICAM-1, and pretreatment of HCCSMC with antisense oligonucleotides to IL-11 enhanced it. We conclude that TNF- induces gene expression in HCCSMC for programmed synthesis and release of pro- and anti-inflammatory mediators.

nuclear factor- B; myo-immune interactions; motility; cytokines

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