Editorial: Hemopexin: newest member of the anti-inflammatory mediator club Mitchell P. Fink 1 Departments of Critical Care Medicine, Surgery and Pharmacology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA 1. Correspondence: Departments of Critical Care Medicine, University of Pittsburgh, 3550 Terrace St., Pittsburgh PA 15261, USA. E-mail: finkmp@ccm.upmc.edu innate immunity acute-phase reactions Certain aspects of the systemic inflammatory response to infection are beneficial to the host. The most obvious example is fever. The febrile response is orchestrated by the CNS in response to the presence of certain proinflammatory cytokines (endogenous pyrogens), notably, IL-1β and TNF, in the bloodstream. As the classic experiments were carried out more than 30 years ago by Kluger et al. [ 1 , 2 ] , it has been apparent that relatively slight increases in body temperature increase the resistance of the host to infection. This notion has been confirmed recently in a study of the effects of fever on the survival of sheep with polymicrobial bacterial peritonitis and septic shock [ 3 ] . It is clear, however, that the systemic inflammatory response to infection also can be deleterious to the host, especially if potent mediators, such as TNF or HMGB1, are secreted into the
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Editorial: Hemopexin: newest member of the anti-inflammatory mediator club
Fink, Mitchell P.
Follow Journal of Leukocyte Biology
, Volume 86 (2): 203
Fed of American Socs for Experimental Biology – Aug 1, 2009
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