Studies of Cachexia in Parasitic Infection

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Abstract
Chronic illness caused by infection with parasites, viruses, or bacteria is frequently associated with a potentially fatal syndrome termed “cachexia.” The stricken host dies from progressive weight loss, anemia, immune suppression, and terminal organ injury, even when the invasive burden may be relatively small. Until recently the biochemical basis of these harmful effects of infection‐associated cachexia was not understood. They are now known to be mediated primarily by endogenous factors released in response to invasive infection. The search for these mediators led to the identification, isolation, and cloning of the cytokine known as cachectin/TNF (tumor necrosis factor).Investigation of the biological effects of cachectin/TNF subsequently confirmed its role as a mediator of cachexia. Further studies revealed that cachectin is also an important mediator of septic shock, another syndrome of injurious host responses elicited by acute bacterial infection. The realization that endogenous factors, produced acutely or chronically during infection and inflammation, may mediate lethal syndromes in the host has advanced our understanding of the pathophysiology of infectious illnesses, and led to the investigation of novel treatment modalities. In this paper we will briefly review the history of cachectin/TNF, and discuss its role as an endogenous mediator of the hosts' responses to infection.