title: Stress proteins in inflammation.
abstract: Inflammation provides those searching in the field with a number of "models" allowing them to study, in vivo, in humans and in animals, the regulation and the functions of HSP, which are being considered as a new and promising marker for the severity and the prognosis of inflammatory diseases. HSP are differentially regulated according to the type of inflammation, whether acute or chronic, whether self-limiting (inflammatory cell elimination by apoptosis) or self-perpetuating (inflammatory cell death by necrosis). We propose that mitochondria are a key organelle in determining the outcome of inflammation, because they are both the cellular "switchboard" for apoptosis and a selective target for the protective effects of HSP against the cytotoxic effects of TNF alpha and ROS. On the other hand, HSP exert multiple protective effects in inflammation, including self/non-self discrimination, enhancement of immune responses, immune protection, thermotolerance and protection against the cytotoxicity of inflammatory mediators. The latter protective effects against the deleterious effects of the mediators of inflammation, including ROS and cytokines, open new avenues for the development of original anti-inflammatory therapies, such as non-toxic inducers of a complete HS response. It may well be that the "beneficial effects of fever" already described by Hippocrates actually relate to increased HSP expression during fever, and to their protective effects....
authors.affiliation: Laboratoire de Physiologie Respiratoire, UFR Cochin Port-Royal, Université Paris V, France.
authors.forename: B S
authors.initials: BS
authors.lastname: Polla
authors.forename: A
authors.initials: A
authors.lastname: Cossarizza
mesh_terms: D000818:Animals; D016207:Cytokines / Q000378:metabolism / Q000494:pharmacology; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000235:genetics; D006360:Heat-Shock Proteins / Q000378:metabolism*; D006801:Humans; D007239:Infections / Q000378:metabolism; D007249:Inflammation / Q000378:metabolism*; D050356:Lipid Metabolism; D008954:Models, Biological; D010587:Phagocytosis / Q000502:physiology; D011493:Protein Kinase C / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D016207:Cytokines; D006360:Heat-Shock Proteins; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D011493:Protein Kinase C