Apoptosis is the predominant mechanism responsible for ending a neutrophil-mediated inflammatory process. The life span of the neutrophil is among the shortest of all cells. The net effect of these influences in the setting of acute inflammation would appear to be prolongation of neutrophil survival as a result of the inhibition of apoptosis. Thus, the identification of signals that can cause the activated neutrophil to die an apoptotic death is important in understanding the mechanisms responsible for terminating an inflammatory response. Altered apoptosis appears to be responsible for some of the alterations in inflammatory and immune cell function seen after trauma and critical illness.
Lymphopenia is a common finding in the victim of trauma or critical surgical illness.
Thus, a functional correlate of systemic inflammation is a state of neutrophil refractoriness to the normal processes of cellular suicide, and the process of cell death is emerging as a new target for therapeutic intervention in an attempt to limit the adverse sequelae of inflammation. Conclusions Progress in biology generally occurs through a series of small advances that serve to amplify, refine or clarify an existing concept or paradigm. Changes in the underlying paradigm occur much less frequently, but when they do, they open grand new vistas on our understanding of disease. Such a paradigm shift has occurred with the recognition of programmed cell death as a process intrinsic to normal growth and development and to the host response to its environment. The scientific literature on apoptosis has grown exponentially, and the list of disease processes in which apoptosis plays a role continues to expand.