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      The immunopathogenesis of sepsis in elderly patients.

      Clinical Infectious Diseases: An Official Publication of the Infectious Diseases Society of America
      Aged, Aging, genetics, immunology, physiology, Animals, B-Lymphocytes, Biological Evolution, Blood Coagulation, Clinical Trials as Topic, Cytokines, antagonists & inhibitors, Disease Susceptibility, Humans, Immunity, Cellular, Immunity, Innate, Plasma Cells, Risk Factors, Selection, Genetic, Sepsis, therapy, Shock, Septic

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          Abstract

          Prominent among the numerous events that contribute to the enhanced susceptibility of elderly patients to infection is the decline of immune function that accompanies aging. Elderly patients experience a marked decline in cell-mediated immune function and reduced humoral immune function. Age-dependent defects in T and B cell function are readily demonstrable in elderly patients, yet the essential elements of innate immunity are remarkably well preserved. The cytokine and chemokine signaling networks are altered in elderly patients and tends to favor a type 2 cytokine response over type 1 cytokine responses. The induction of proinflammatory cytokines after septic stimuli is not adequately controlled by anti-inflammatory mechanisms in elderly persons. This immune dysregulation is accompanied by a more pronounced procoagulant state in older patients. These molecular events function in concert to render elderly patients at excess risk for mortality from severe sepsis and septic shock.

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