Modulation of pathogen-induced CCL20 secretion from HT-29 human intestinal epithelial cells by commensal bacteria.
Authors
Sibartie, ShomikO'Hara, Ann M
Ryan, Jude
Fanning, Aine
O'Mahony, Jim
O'Neill, Shaun
Sheil, Barbara
O'Mahony, Liam
Shanahan, Fergus
Affiliation
Alimentary Pharmabiotic Centre, University College Cork, National University of Ireland, Cork, Ireland. shomiksibartie@gmail.comIssue Date
2009MeSH
BacteriaBacterial Infections
Chemokine CCL20
Enzyme-Linked Immunosorbent Assay
Flagellin
Gene Expression Regulation
HT29 Cells
Host-Pathogen Interactions
Humans
Immunity, Mucosal
Immunomodulation
Interleukin-8
Intestinal Mucosa
NF-kappa B
Transcriptional Activation
Metadata
Show full item recordCitation
Modulation of pathogen-induced CCL20 secretion from HT-29 human intestinal epithelial cells by commensal bacteria. 2009, 10:54 BMC Immunol.Journal
BMC immunologyDOI
10.1186/1471-2172-10-54PubMed ID
19814810Abstract
BACKGROUND: Human intestinal epithelial cells (IECs) secrete the chemokine CCL20 in response to infection by various enteropathogenic bacteria or exposure to bacterial flagellin. CCL20 recruits immature dendritic cells and lymphocytes to target sites. Here we investigated IEC responses to various pathogenic and commensal bacteria as well as the modulatory effects of commensal bacteria on pathogen-induced CCL20 secretion. HT-29 human IECs were incubated with commensal bacteria (Bifidobacterium infantis or Lactobacillus salivarius), or with Salmonella typhimurium, its flagellin, Clostridium difficile, Mycobacterium paratuberculosis, or Mycobacterium smegmatis for varying times. In some studies, HT-29 cells were pre-treated with a commensal strain for 2 hr prior to infection or flagellin stimulation. CCL20 and interleukin (IL)-8 secretion and nuclear factor (NF)-kappaB activation were measured using enzyme-linked immunosorbent assays. RESULTS: Compared to untreated cells, S. typhimurium, C. difficile, M. paratuberculosis, and flagellin activated NF-kappaB and stimulated significant secretion of CCL20 and IL-8 by HT-29 cells. Conversely, B. infantis, L. salivarius or M. smegmatis did not activate NF-kappaB or augment CCL20 or IL-8 production. Treatment with B. infantis, but not L. salivarius, dose-dependently inhibited the baseline secretion of CCL20. In cells pre-treated with B. infantis, C. difficile-, S. typhimurium-, and flagellin-induced CCL20 were significantly attenuated. B. infantis did not limit M. Paratuberculosis-induced CCL20 secretion. CONCLUSION: This study is the first to demonstrate that a commensal strain can attenuate CCL20 secretion in HT-29 IECs. Collectively, the data indicate that M. paratuberculosis may mediate mucosal damage and that B. infantis can exert immunomodulatory effects on IECs that mediate host responses to flagellin and flagellated enteric pathogens.Language
enISSN
1471-2172ae974a485f413a2113503eed53cd6c53
10.1186/1471-2172-10-54