PMID- 7814646 OWN - NLM STAT- MEDLINE DCOM- 19950209 LR - 20220318 IS - 0021-9738 (Print) IS - 0021-9738 (Linking) VI - 95 IP - 1 DP - 1995 Jan TI - A distinct array of proinflammatory cytokines is expressed in human colon epithelial cells in response to bacterial invasion. PG - 55-65 AB - Pathogenic bacteria that penetrate the intestinal epithelial barrier stimulate an inflammatory response in the adjacent intestinal mucosa. The present studies asked whether colon epithelial cells can provide signals that are important for the initiation and amplification of an acute mucosal inflammatory response. Infection of monolayers of human colon epithelial cell lines (T84, HT29, Caco-2) with invasive strains of bacteria (Salmonella dublin, Shigella dysenteriae, Yersinia enterocolitica, Listeria monocytogenes, enteroinvasive Escherichia coli) resulted in the coordinate expression and upregulation of a specific array of four proinflammatory cytokines, IL-8, monocyte chemotactic protein-1, GM-CSF, and TNF alpha, as assessed by mRNA levels and cytokine secretion. Expression of the same cytokines was upregulated after TNF alpha or IL-1 stimulation of these cells. In contrast, cytokine gene expression was not altered after infection of colon epithelial cells with noninvasive bacteria or the noninvasive protozoan parasite, G. lamblia. Notably, none of the cell lines expressed mRNA for IL-2, IL-4, IL-5, IL-6, IL-12p40, IFN-gamma, or significant levels of IL-1 or IL-10 in response to the identical stimuli. The coordinate expression of IL-8, MCP-1, GM-CSF and TNF alpha appears to be a general property of human colon epithelial cells since an identical array of cytokines, as well as IL-6, also was expressed by freshly isolated human colon epithelial cells. Since the cytokines expressed in response to bacterial invasion or other proinflammatory agonists have a well documented role in chemotaxis and activation of inflammatory cells, colon epithelial cells appear to be programmed to provide a set of signals for the activation of the mucosal inflammatory response in the earliest phases after microbial invasion. FAU - Jung, H C AU - Jung HC AD - Department of Medicine, University of California, San Diego, La Jolla 92093-0623. FAU - Eckmann, L AU - Eckmann L FAU - Yang, S K AU - Yang SK FAU - Panja, A AU - Panja A FAU - Fierer, J AU - Fierer J FAU - Morzycka-Wroblewska, E AU - Morzycka-Wroblewska E FAU - Kagnoff, M F AU - Kagnoff MF LA - eng GR - DK-35108/DK/NIDDK NIH HHS/United States GR - DK-40582/DK/NIDDK NIH HHS/United States GR - DK-47739/DK/NIDDK NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, Non-P.H.S. PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - J Clin Invest JT - The Journal of clinical investigation JID - 7802877 RN - 0 (Chemokine CCL2) RN - 0 (Chemotactic Factors) RN - 0 (Cytokines) RN - 0 (Interleukin-8) RN - 0 (RNA, Messenger) RN - 0 (Tumor Necrosis Factor-alpha) RN - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor) SB - IM CIN - J Clin Invest. 2001 Jan;107(1):27-30. PMID: 11134175 MH - Animals MH - Bacterial Infections/*immunology MH - Base Sequence MH - Cell Line MH - Chemokine CCL2 MH - Chemotactic Factors/biosynthesis MH - Colonic Diseases/*immunology MH - Cytokines/*biosynthesis/genetics MH - Epithelial Cells MH - Epithelium/metabolism MH - Gene Expression Regulation/drug effects MH - Giardia lamblia MH - Giardiasis/metabolism MH - Granulocyte-Macrophage Colony-Stimulating Factor/biosynthesis MH - Humans MH - Inflammation/*metabolism MH - Interleukin-8/biosynthesis MH - Molecular Sequence Data MH - RNA, Messenger/analysis MH - Tumor Necrosis Factor-alpha/biosynthesis/pharmacology PMC - PMC295369 EDAT- 1995/01/01 00:00 MHDA- 1995/01/01 00:01 PMCR- 1995/01/01 CRDT- 1995/01/01 00:00 PHST- 1995/01/01 00:00 [pubmed] PHST- 1995/01/01 00:01 [medline] PHST- 1995/01/01 00:00 [entrez] PHST- 1995/01/01 00:00 [pmc-release] AID - 10.1172/JCI117676 [doi] PST - ppublish SO - J Clin Invest. 1995 Jan;95(1):55-65. doi: 10.1172/JCI117676.