Dual roles of commensal bacteria after intestinal ischemia and reperfusion
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In brief
In brief
This study reveals commensal gut bacteria play dual roles after intestinal ischemia-reperfusion injury: they worsen early inflammatory damage but are essential for epithelial healing. Bacterial lipopolysaccharides promote intestinal epithelial cell proliferation through TLR4-mediated PGE2 production and EGFR/PI3K/Akt pathway activation.
Written by the GCMD Library team from the article.
Abstract
Purpose
The roles of commensal bacteria after intestinal ischemia and reperfusion (IIR) are unclear. In current study, we aim to investigate the effects and underlying mechanisms of commensal bacteria in injury and epithelial restitution after IIR.
Methods
Commensal gut bacteria were deleted by broad-spectrum antibiotics in mice. IIR was induced by clamping superior mesenteric artery. Intestinal injury, permeability, epithelial proliferation, and proinflammatory activity of mesenteric lymph were investigated.
Results
Commensals deletion improved mice survival in the early phase, but failed to improve the overall survival at 96 h after IIR. Commensals deletion reduced proliferation of intestinal epithelial cells (IEC) and augmented proinflammatory activity of mesenteric lymph after IIR. Lipopolysaccharides (LPS) supplement promoted IEC proliferation and improved survival in mice with commensals deletion after IIR. LPS induced production of prostaglandin E2 (PGE2) in mucosa via toll-like receptor 4-NFκB-cyclooxygenase 2 pathway. PGE2 enhanced IEC proliferation in vivo, which was preceded by activation of Akt and extracellular signal-regulated kinase (ERK) 1/2. Blocking of EGFR, PI3K/Akt activity abolished LPS-induced IEC proliferation.
Conclusions
Commensal bacteria are essential for epithelial restitution after IIR, which enhance IEC proliferation via induction of PGE2.