Phagocytes

Macrophages secrete a complex array of inflammatory mediators that modulate inflammatory cell recruitment and the survival of leukocytes at the inflamed site. They kill bacteria, clear apoptotic cells, present antigen, activate resting T cells, and are central to appropriate wound healing. Despite their eclectic roles in inflammation and its resolution, macrophages have been implicated in the depressed immune function of critical illness. Because of their elaboration of prostaglandin E 2 and nitric oxide, which in high concentrations are both powerful immunodepressive agents, activated macrophages have been associated with impaired immunity. Critically ill patients have clear evidence of increased nitric oxide production with elevated nitrite and nitrate levels (the end-products of nitric oxide synthesis), and in animal models this is shown to be due to increased expression of inducible nitric oxide synthase ( A!bin.§ §Qd RelC.h.D.e.L.19.9.5).

Macrophages not only elaborate immunosuppressive factors but they also exhibit impaired function in response to critical illness. Antigen presentation by macrophages is depressed immediately after hemorrhage and remains so for up to 5 days. Macrophage capacity for release of proinflammatory cytokines is not demonstrably impaired.

Neutrophils are active phagocytes which can secrete tumor necrosis factor-a, IL-1b, and other important proinflammatory cytokines. Certain neutrophil functions are impaired in critical illness, and there is an association between the degree of neutrophil dysfunction and patient morbidity. Neutrophils exhibit reduced chemotaxis after burn injury, and some researchers have reported a reduction in bactericidal activity, the mechanisms of which are complex but are related to cellular hyperactivation, impaired neutrophil oxygen consumption, hydrogen peroxide production, lysosomal enzyme defects, and alterations in phagolysosome acidification (M.§Q.QlCk...1993.). Furthermore, serum from critically ill patients can have suppressive effects, depressing neutrophil chemotaxis and bactericidal function. Patients with major burns or trauma have neutrophil subgroups with markedly reduced capacity for phagocytosis and production of hydrogen peroxide. These cells can be identified by their relative lack of expression of CD16, loss of which is also associated with neutrophil apoptosis.

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