Toll-like receptor 2 is protective of ischemia–reperfusion-mediated small-bowel injury in a murine model

Abstract

TLR2-/- mice have a dysregulated mucosal innate immune response and fail to mount a protective response after ischemia-reperfusion compared with wild-type mice. This murine model of intestinal injury may correlate with the early postnatal course of premature infants who may have decreased TLR2 expression and/or decreased luminal commensal bacteria secondary to antibiotic therapy, thus decreasing TLR2-mediated signaling.

Molecular Mediators of Liver Ischemia and Reperfusion Injury: A Brief Review

“…TLRs have important roles in the pathophysiology of IRI in other organ systems. In a neonatal murine model of small-bowel IRI, TLR2-deficient mice sustained greater intestinal damage (18); in contrast, TLR2 deficiency was shown to be protective in a murine renal IRI model (19), and involves both MyD88-dependent and -independent signaling pathways (20). However, a recent study points to TLR4-and selective MyD88-mediated signaling (23).…”

Changes in intestinal Toll-like receptors and cytokines precede histological injury in a rat model of necrotizing enterocolitis

“…Some studies indicated that TLR2 may provide protective signaling. Evidence was that C57BL/6 TLR2-deficient mice, compared with wild-type mice, have a dysregulated mucosal innate immune response and fail to mount a protective response after ischemia-reperfusion injury (1). TLR2 stimulation in intestinal epithelial cells effectively preserves tight junction (TJ)-associated barrier assembly against stress-induced damage, and inflammatory stress in mice deficient of TLR2 induced early TJ-associated disruption (8).…”

“…Recent studies found that TLR2 mRNA were also increased together with TLR4 mRNA in NEC (25). However, C57BL/6 TLR2-deficient mice, when studied in an intestinal ischemia model, were found to have a dysregulated mucosal innate immune response, with reduced cytokine production and increased injury score (1). Differences in the expression of TLRs may alter a host's response to a commensal or pathogenic microorganism.…”

Estudo da reatividade vascular em ratos submetidos à isquemia e reperfusão instestinal: mecanismos envolvidos e papel protetor da sinvastatina.

“…O sistema linfático é um importante componente do sistema imunológico, transportando células desse sistema provenientes do espaço intersticial para circulação sistêmica. Sabe-se que, durante a iIR, além de linfócitos serem ativados (Aprahamian et al, 2008, Edgerton et al, 2009), citocinas como TNF-α, IL-1β, -6, -8 e -10, mediadores lipídicos e radicais livres estão incluídos na fisiopatologia das lesões teciduais ocasionadas por essa doença (Bhatia et al, 2004).…”