Functional modulation of human intestinal epithelial cell responses by Bifidobacterium infantis and Lactobacillus salivarius

Typeset version

 

TY  - JOUR
  - O'Hara, AM,O'Regan, P,Fanning, A,O'Mahony, C,MacSharry, J,Lyons, A,Bienenstock, J,O'Mahony, L,Shanahan, F
  - 2006
  - February
  - The Journal of Immunology
  - Functional modulation of human intestinal epithelial cell responses by Bifidobacterium infantis and Lactobacillus salivarius
  - Validated
  - ()
  - commensal bacteria flagellin interleukin-8 intestinal epithelium mucins INFLAMMATORY-BOWEL-DISEASE PLACEBO-CONTROLLED TRIAL TOLL-LIKE RECEPTOR-5 KAPPA-B ACTIVATION GENE-EXPRESSION DENDRITIC CELLS BACTERIAL FLAGELLIN DOUBLE-BLIND MUCOSAL INFLAMMATION PROBIOTIC STRAINS
  - 118
  - 202
  - 215
  - Intestinal epithelial cells (IECs) and dendritic cells (DCs) play a pivotal role in antigen sampling and the maintenance of gut homeostasis. However, the interaction of commensal bacteria with the intestinal surface remains incompletely understood. Here we investigated immune cell responses to commensal and pathogenic bacteria. HT-29 human IECs were incubated with Bifidobacterium infantis 35624, Lactobacillus salivarius UCC118 or Salmonella typhimurium UK1 for varying times, or were pretreated with a probiotic for 2 hr prior to stimulation with S. typhimurium or flagellin. Gene arrays were used to examine inflammatory gene expression. Nuclear factor (NF)-kappa B activation, interleukin (IL)-8 secretion, pathogen adherence to IECs, and mucin-3 (MUC3) and E-cadherin gene expression were assayed by TransAM assay, enzyme-linked immunosorbent assay (ELISA), fluorescence, and real-time reverse transcriptase-polymerase chain reaction (RT-PCR), respectively. IL-10 and tumour necrosis factor (TNF)-alpha secretion by bacteria-treated peripheral blood-derived DCs were measured using ELISA. S. typhimurium increased expression of 36 of the 847 immune-related genes assayed, including NF-kappa B and IL-8. The commensal bacteria did not alter expression levels of any of the 847 genes. However, B. infantis and L. salivarius attenuated both IL-8 secretion at baseline and S. typhimurium-induced pro-inflammatory responses. B. infantis also limited flagellin-induced IL-8 protein secretion. The commensal bacteria did not increase MUC3 or E-cadherin expression, or interfere with pathogen binding to HT-29 cells, but they did stimulate IL-10 and TNF-alpha secretion by DCs. The data demonstrate that, although the intestinal epithelium is immunologically quiescent when it encounters B. infantis or L. salivarius, these commensal bacteria exert immunomodulatory effects on intestinal immune cells that mediate host responses to flagellin and enteric pathogens.
  - DOI 10.1111/j.1365-2567.2006.02358.x
DA  - 2006/02
ER  - 
@article{V119869220,
   = {O'Hara,  AM and O'Regan,  P and Fanning,  A and O'Mahony,  C and MacSharry,  J and Lyons,  A and Bienenstock,  J and O'Mahony,  L and Shanahan,  F },
   = {2006},
   = {February},
   = {The Journal of Immunology},
   = {Functional modulation of human intestinal epithelial cell responses by Bifidobacterium infantis and Lactobacillus salivarius},
   = {Validated},
   = {()},
   = {commensal bacteria flagellin interleukin-8 intestinal epithelium mucins INFLAMMATORY-BOWEL-DISEASE PLACEBO-CONTROLLED TRIAL TOLL-LIKE RECEPTOR-5 KAPPA-B ACTIVATION GENE-EXPRESSION DENDRITIC CELLS BACTERIAL FLAGELLIN DOUBLE-BLIND MUCOSAL INFLAMMATION PROBIOTIC STRAINS},
   = {118},
  pages = {202--215},
   = {{Intestinal epithelial cells (IECs) and dendritic cells (DCs) play a pivotal role in antigen sampling and the maintenance of gut homeostasis. However, the interaction of commensal bacteria with the intestinal surface remains incompletely understood. Here we investigated immune cell responses to commensal and pathogenic bacteria. HT-29 human IECs were incubated with Bifidobacterium infantis 35624, Lactobacillus salivarius UCC118 or Salmonella typhimurium UK1 for varying times, or were pretreated with a probiotic for 2 hr prior to stimulation with S. typhimurium or flagellin. Gene arrays were used to examine inflammatory gene expression. Nuclear factor (NF)-kappa B activation, interleukin (IL)-8 secretion, pathogen adherence to IECs, and mucin-3 (MUC3) and E-cadherin gene expression were assayed by TransAM assay, enzyme-linked immunosorbent assay (ELISA), fluorescence, and real-time reverse transcriptase-polymerase chain reaction (RT-PCR), respectively. IL-10 and tumour necrosis factor (TNF)-alpha secretion by bacteria-treated peripheral blood-derived DCs were measured using ELISA. S. typhimurium increased expression of 36 of the 847 immune-related genes assayed, including NF-kappa B and IL-8. The commensal bacteria did not alter expression levels of any of the 847 genes. However, B. infantis and L. salivarius attenuated both IL-8 secretion at baseline and S. typhimurium-induced pro-inflammatory responses. B. infantis also limited flagellin-induced IL-8 protein secretion. The commensal bacteria did not increase MUC3 or E-cadherin expression, or interfere with pathogen binding to HT-29 cells, but they did stimulate IL-10 and TNF-alpha secretion by DCs. The data demonstrate that, although the intestinal epithelium is immunologically quiescent when it encounters B. infantis or L. salivarius, these commensal bacteria exert immunomodulatory effects on intestinal immune cells that mediate host responses to flagellin and enteric pathogens.}},
   = {DOI 10.1111/j.1365-2567.2006.02358.x},
  source = {IRIS}
}
AUTHORSO'Hara, AM,O'Regan, P,Fanning, A,O'Mahony, C,MacSharry, J,Lyons, A,Bienenstock, J,O'Mahony, L,Shanahan, F
YEAR2006
MONTHFebruary
JOURNAL_CODEThe Journal of Immunology
TITLEFunctional modulation of human intestinal epithelial cell responses by Bifidobacterium infantis and Lactobacillus salivarius
STATUSValidated
TIMES_CITED()
SEARCH_KEYWORDcommensal bacteria flagellin interleukin-8 intestinal epithelium mucins INFLAMMATORY-BOWEL-DISEASE PLACEBO-CONTROLLED TRIAL TOLL-LIKE RECEPTOR-5 KAPPA-B ACTIVATION GENE-EXPRESSION DENDRITIC CELLS BACTERIAL FLAGELLIN DOUBLE-BLIND MUCOSAL INFLAMMATION PROBIOTIC STRAINS
VOLUME118
ISSUE
START_PAGE202
END_PAGE215
ABSTRACTIntestinal epithelial cells (IECs) and dendritic cells (DCs) play a pivotal role in antigen sampling and the maintenance of gut homeostasis. However, the interaction of commensal bacteria with the intestinal surface remains incompletely understood. Here we investigated immune cell responses to commensal and pathogenic bacteria. HT-29 human IECs were incubated with Bifidobacterium infantis 35624, Lactobacillus salivarius UCC118 or Salmonella typhimurium UK1 for varying times, or were pretreated with a probiotic for 2 hr prior to stimulation with S. typhimurium or flagellin. Gene arrays were used to examine inflammatory gene expression. Nuclear factor (NF)-kappa B activation, interleukin (IL)-8 secretion, pathogen adherence to IECs, and mucin-3 (MUC3) and E-cadherin gene expression were assayed by TransAM assay, enzyme-linked immunosorbent assay (ELISA), fluorescence, and real-time reverse transcriptase-polymerase chain reaction (RT-PCR), respectively. IL-10 and tumour necrosis factor (TNF)-alpha secretion by bacteria-treated peripheral blood-derived DCs were measured using ELISA. S. typhimurium increased expression of 36 of the 847 immune-related genes assayed, including NF-kappa B and IL-8. The commensal bacteria did not alter expression levels of any of the 847 genes. However, B. infantis and L. salivarius attenuated both IL-8 secretion at baseline and S. typhimurium-induced pro-inflammatory responses. B. infantis also limited flagellin-induced IL-8 protein secretion. The commensal bacteria did not increase MUC3 or E-cadherin expression, or interfere with pathogen binding to HT-29 cells, but they did stimulate IL-10 and TNF-alpha secretion by DCs. The data demonstrate that, although the intestinal epithelium is immunologically quiescent when it encounters B. infantis or L. salivarius, these commensal bacteria exert immunomodulatory effects on intestinal immune cells that mediate host responses to flagellin and enteric pathogens.
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DOI_LINKDOI 10.1111/j.1365-2567.2006.02358.x
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