1887

Abstract

Translocation of bacteria across the intestinal barrier is important in the pathogenesis of systemic sepsis. In inflammatory conditions, commensal bacteria exploit transcytotic pathways to cross the intestinal epithelium in a TLR4-dependent manner. The aim of this study was to test the hypothesis that ameliorates tumour necrosis factor-induced bacterial translocation by regulation of Toll-like receptor-4 expression.

strains were investigated to determine their capacity to inhibit the initial adhesion of B5 to Caco-2 cells. The inhibitory effects of on TNF-α-induced B5 translocation across Caco-2 cells were studied. Barrier function and integrity were simultaneously assessed by transepithelial electrical resistance, HRP permeability, LDH release and distribution of tight junctional proteins. Expression of TLR4 was assessed by RT-PCR.

Pretreatment of monolayers with L2 led to a significant decrease in B5 adhesion and cell internalization (<0.01). Exposure to TNF-α for six hours caused a significant increase in B5 translocation across Caco-2 cells, which was uncoupled from increases in paracellular permeability and disruption of tight junction proteins. Manipulations that induced bacterial translocation were associated with a marked increase in TLR4 mRNA expression and IL-8 secretion. L2 significantly abrogated TNF-α-induced bacterial translocation of B5, and also downregulated expression of TLR4 and IL-8 in intestinal epithelial cells.

Live L2 can inhibit TNF-α-induced transcellular bacterial translocation via regulation of TLR4 expression.

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2018-07-01
2024-04-20
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