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. 2018 May 25;63(1):26–32. doi: 10.3164/jcbn.17-137

Table 1.

In vivo studies on the role of TLRs and MyD88 in I/R injury

Publications TLRs studied Beneficial or unbeneficial against intestinal I/R injury Findings
Tatum, J Pediatr Surg TLR2 TLR4 beneficial Neonatal mice deficient in TLR4, either alone or in concert with TLR2, were more susceptible to intestinal mucosal damage.
Watanabe, PLoS One TLR2 unbeneficial TLR2−/− mice exhibited less severe mucosal injury and decreased MPO and TNF-α and ICAM-1 mRNA expression.
Aprahamian, Pediatr Crit Care Med TLR2 beneficial In TLR2−/− mice, intestinal injury scores increased and the expression of IFN-γ, IL-4, and IL-6 mRNA decreased.
Chen, Shock TLR4 beneficial Lipopolysaccharide, a TLR4 ligand, decreased mesenteric I/R injury-induced gut damage through TNF-α signaling.
Zhu, Oncotarget TLR4 unbeneficial TLR4 mutation suppressed histological injuries and reduced cytokine expression in the intestine (TNF-α, IL-6, IL-1β, and NF-κB).
Pope, Mol Immunol TLR4 unbeneficial TLR4-deficient mice sustained less damage and inflammation after I/R than wild-type mice.
Moses, J Leukoc Biol TLR4 MyD88 unbeneficial The absence of TLR4 or MyD88 attenuated local mucosal damage and significantly decreased cytokine and eicosanoid secretion, including PGE2 production.
Wang, World J Gastroenterol TLR4 MyD88 unbeneficial Blocking HMGB1 and MyD88 reduced the levels of inflammatory cytokines (NF-κB, p65, and TNF-α) in serum.
Kojima, J Surg Res TLR4 unbeneficial Anti-HMGB1 antibody treatment significantly reduced the damage and improved the 48-h survival rates.
Slone, Am J Clin Exp Immunol TLR9 no effect TLR9 is not required for I/R-induced injury or inflammation of the intestine.
Watanabe, Am J Physiol Gastrointest Liver Physiol MyD88 beneficial The MyD88 signaling pathway inhibited I/R injury in the small intestine by inducing COX-2 expression.

TLR, Toll-like receptor; MyD88, myeloid differentiation primary response 88; I/R, ischemia/reperfusion; TNF, tumor necrosis factor; MPO, myeloperoxidase; ICAM, intercellular adhesion molecule; IFN, interferon; IL, interleukin; HMGB, high mobility group box; COX, cyclooxygenase.