title: Immunosuppression following surgical and traumatic injury.
abstract: Severe sepsis and organ failure are still the major causes of postoperative morbidity and mortality after major hepatobiliary pancreatic surgery. Despite recent progress in understanding the immune conditions of abdominal sepsis, the postoperative incidence of septic complications after major visceral surgery remains high. This review focuses on the clinical and immunological parameters that determine the risk of the development and lethal outcome of postoperative septic complication following major surgery and trauma. A review of the literature indicates that surgical and traumatic injury profoundly affects the innate and adaptive immune responses, and that a marked suppression in cell-mediated immunity following an excessive inflammatory response appears to be responsible for the increased susceptibility to subsequent sepsis. The innate and adaptive immune responses are initiated and modulated by pathogen-associated molecular-pattern molecules and by damage-associated molecular-pattern molecules through the pattern-recognition receptors. Suppression of cell-mediated immunity may be caused by multifaceted cytokine/inhibitor profiles in the circulation and other compartments of the host, excessive activation and dysregulated recruitment of polymorphonuclear neutrophils, induction of alternatively activated or regulatory macrophages that have anti-inflammatory properties, a shift in the T-helper (Th)1/Th2 balance toward Th2, appearance of regulatory T cells, which are potent suppressors of the innate and adaptive immune system, and lymphocyte apoptosis in patients with sepsis. Recent basic and clinical studies have elucidated the functional effects of surgical and traumatic injury on the immune system. The research studies of interest may in future aid in the selection of appropriate therapeutic protocols.
authors.affiliation: Department of General Surgery, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
authors.forename: Fumio
authors.initials: F
authors.lastname: Kimura
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Shimizu
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Yoshidome
authors.forename: Masayuki
authors.initials: M
authors.lastname: Ohtsuka
authors.forename: Masaru
authors.initials: M
authors.lastname: Miyazaki
mesh_terms: D055371:Acute Lung Injury / Q000209:etiology / Q000276:immunology; D056704:Adaptive Immunity; D048868:Adaptor Proteins, Signal Transducing / Q000276:immunology; D000818:Animals; D006801:Humans; D007108:Immune Tolerance; D007111:Immunity, Cellular; D009102:Multiple Organ Failure / Q000209:etiology / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology; D011183:Postoperative Complications / Q000276:immunology*; D051192:Receptors, Pattern Recognition / Q000276:immunology; D018805:Sepsis / Q000209:etiology / Q000276:immunology*; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology / Q000276:immunology*; D051193:Toll-Like Receptors / Q000276:immunology; D014947:Wounds and Injuries / Q000150:complications* / Q000276:immunology
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D051192:Receptors, Pattern Recognition; D051193:Toll-Like Receptors