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In a recent paper published in Gut Sharif and co-workers have investigated the role of toll-like receptor 4 (TLR4) and its co-receptor CD14 in experimental pancreatitis. Using genetically modified strains of mice in which TLR4 or CD14 had been deleted the authors found significantly less pancreatic injury and systemic inflammation in the milder, caerulein-induced pancreatitis as well as the more severe L-arginine-induced variety.1 Toll-like receptors belong to a family of pattern recognition receptors that mediate innate immune recognition and inflammatory responses. They are activated by products of microbial metabolism and for TLR4 the best established ligand is lipopolysaccharide (LPS), a major component of Gram-negative bacteria. Surprisingly, the beneficial effect of TLR4 or CD14 deletion on pancreatitis was completely independent of either the presence of LPS, or the translocation of bacteria.1 If TLR4 were to have a similar …
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