The Role of Leukocyte Endogenous Mediator (Endogenous Pyrogen) in Inflammation

Abstract

The term inflammation is generally employed to describe the localized response to cellular injury. However, if the extent of injury is sufficient there are systemic consequences as well. For example, even a simple surgical procedure such as venesection elicits modest increases in various plasma proteins (1), while severe injury induces marked alterations in trace metal, nitrogen, energy and hormone metabolism (2,3). In fact, there appears to be a proportionality between the extent of injury and a number of these metabolic alterations (4,5). Moreover, these systemic manifestations of inflammation evanesce if the injury is successfully treated or resolves itself (4,6). There is an increasing amount of evidence that many of these systemic sequelae of tissue injury interact with the local events usually associated with inflammation to protect the host against infection, as well as to limit and repair the injury (7–9). Thus it seems appropriate, at least for the purposes of this discussion, to include these systemic sequelae as part of the host’s comprehensive response to inflammation. If this is so, one would expect these systemic metabolic manifestations to occur whenever there is inflammation irrespective of the nature of the stimulus.