Editorial: A recipe for inflammation Marco E. Bianchi 1 San Raffaele University and San Raffaele Research Institute, Department of Genetics and Cell Biology, Milano, Italy 1. Correspondence: San Raffaele University and San Raffaele Research Institute, Department of Genetics and Cell Biology, via Olgettina 58, 20132 Milano, Italy. E-mail: bianchi.marco@hsr.it N-ε-carboxymethyl-lysine (CML) receptor for advanced glycation endproducts (RAGE) inflammation diabetes sepsis Diabetes is cause and effect of a diffuse, low-grade inflammation, and no one in life-threatening conditions would like being injected with compounds that play a role in diabetes. Yet, this has apparently happened all too often until now, as reported in this issue [ 1 ] . Humpert et al. [ 1 ] found that batches of HSA, which is used frequently in patients with burns or severe blood loss, often contain post-translational modifications that accumulate in diabetes and cause inflammation. Such modified HSA increases lethality in a mouse model of sepsis and may possibly have increased lethality in patients as well, or at least wiped out any therapeutic effect expected from HSA infusion. Glucose and other reducing carbohydrates can react nonenzymatically with proteins, generating what are known variously and rather inconsistently as Amadori, Schiff base, and Maillard
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