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Toll-like receptor 4 polymorphisms in German and US patients are not associated with occurrence or severity of acute pancreatitis
  1. Annett Guenther1,
  2. Ali Aghdassi1,
  3. Venkata Muddana2,
  4. Bettina Rau3,
  5. Hans-Ulrich Schulz1,
  6. Julia Mayerle1,
  7. Matthias Kraft1,
  8. David C Whitcomb2,
  9. Markus M Lerch1,
  10. Frank U Weiss1
  1. 1Department of Medicine A, Ernst-Moritz-Arndt Universität Greifswald, Germany
  2. 2Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
  3. 3Department of Surgery, University of Rostock, Rostock, Germany
  4. 4Department of Surgery, Otto-von-Guericke Universität Magdeburg, Germany
  1. Correspondence to Professor Markus M Lerch Department of Medicine A, Ernst-Moritz-Arndt Universität Greifswald, Germany. lerch{at}uni-greifswald.de

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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 …

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