The stressed host response to infection: the disruptive signals and rhythms of systemic inflammation.
The cognate signals from sterile or pathogen-induced sources converge on the same recognition or response pathways. In the surgical patient, a systemic response to infection most often occurs in the context of ongoing inflammatory stress. Such an inflammatory response is modulated initially by the magnitude of injury and by patient-specific (endogenous) factors, such as confounding illness, age, and genetic variation. Over an extended period of stress, treatmentrelated (exogenous) factors add unpredictability to host responses to subsequent challenges, such as acquired infection. The host response is discussed in the context of how existing sterile stressors may modify the response to acquired infection in surgical patients.
Lowry
Stephen F
SF
Department of Surgery, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA. lowrysf@umdnj.edu
D003428:Cross Infection / Q000276:immunology* / Q000503:physiopathology / Q000628:therapy; D006706:Homeostasis / Q000276:immunology / Q000502:physiology; D006801:Humans; D009490:Neurosecretory Systems / Q000276:immunology / Q000503:physiopathology; D010641:Phenotype; D012307:Risk Factors; D013312:Stress, Physiological / Q000276:immunology*; D013530:Surgical Wound Infection / Q000276:immunology* / Q000503:physiopathology / Q000628:therapy; D018746:Systemic Inflammatory Response Syndrome / Q000276:immunology* / Q000503:physiopathology / Q000628:therapy