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Cited by 335

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Enhanced translocation of bacteria across metabolically stressed epithelia is reduced by butyrate†

Lewis, Kimberley, Lutgendorff, Femke, Phan, Van, Söderholm, Johan D., Sherman, Philip M., McKay, Derek M.·2010·Inflammatory Bowel Diseases
DOI 10.1002/ibd.21177
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Abstract

Background: The gut microflora in some patients with Crohn's disease can be reduced in numbers of butyrate-producing bacteria and this could result in metabolic stress in the colonocytes. Thus, we hypothesized that the short-chain fatty acid, butyrate, is important in the maintenance and regulation of the barrier function of the colonic epithelium. Methods: Confluent monolayers of the human colon-derived T84 or HT-29 epithelial cell lines were exposed to dinitrophenol (DNP (0.1 mM), uncouples oxidative phosphorylation) + Escherichia coli (strain HB101, 106 cfu) ± butyrate (3–50 mM). Transepithelial resistance (TER), and bacterial internalization and translocation were assessed over a 24-hour period. Epithelial ultrastructure was assessed by transmission electron microscopy. Results: Epithelia under metabolic stress display decreased TER and increased numbers of pseudopodia that is consistent with increased internalization and translocation of the E. coli. Butyrate (but not acetate) significantly reduced the bacterial translocation across DNP-treated epithelia but did not ameliorate the drop in TER in the DNP+E. coli exposed monolayers. Inhibition of bacterial transcytosis across metabolically stressed epithelia was associated with reduced I-κB phosphorylation and hence NF-κB activation. Conclusions: Reduced butyrate-producing bacteria could result in increased epithelial permeability particularly in the context of concomitant exposure to another stimulus that reduces mitochondria function. We speculate that prebiotics, the substrate for butyrate synthesis, is a valuable prophylaxis in the regulation of epithelial permeability and could be of benefit in preventing relapses in IBD. (Inflamm Bowel Dis 2010)

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Metadata

Authors
Lewis, K., Lutgendorff, F., Phan, V., Söderholm, J. D., Sherman, P. M., & McKay, D. M.
Venue
Inflammatory Bowel Diseases
Publisher
Oxford University Press (OUP)
Published
2009-12-18
Volume
16
Issue
7
Pages
1138-1148
ISSN
  • 1078-0998 (ISSN-L)
  • 1536-4844
DOI
10.1002/ibd.21177
OpenAlex
W1974546936
Cited by
335
References
3
FWCI
4.32
Type
journal article
Language
en
Open access
closed

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