Abstract
An immunosuppressed state develops following traumatic injury, which makes patients more prone to develop infection. A variety of disturbances accompany injury that affect both specific and nonspecific components of host defense. Many clinical studies have attempted to evaluate the many deficits that follow injury and place the patient at a higher risk for infection. Several components of host defense are affected simultaneously and include (1) cellular changes (decreased activation of T-lymphocyte subsets with decreased helper cells, increased suppressor T-cell function, increased but abnormal activity of macrophages, activation of polymorphonuclear leukocytes with depressed chemotaxis and killing); (2) depressed nonspecific and specific serum immunity (e.g., depressed fibronectin and immunoglobulin levels); (3) the presence of altered cytokine levels (interleukin-1 [IL-1], IL-2, IL-6, tumor necrosis factor) levels; (4) ongoing serum proteolytic activity; and (5) the generation of serum suppressive peptides. An in-depth understanding of the deficits that occur following injury in host defense will provide the basis for therapeutic intervention.
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