Surgical stress, bacteria, and mucosal immune function.
Bacteria share a benign coexistence with host mucosal surfaces in the gastrointestinal tract during periods of health. Both host epithelial defense function and bacterial virulence phenotypes are significantly affected by stress. Via discreet and specific sensory input signals to bacteria, the molecular machinery of otherwise commensal strains of bacteria can shift the phenotypes of residential colonizers to more virulent and invasive strains. This occurs at a time when the host may be relatively immunosuppressed by the injury. This adaptive response demonstrates the duplicitous nature of bacteria residing on mucosal surfaces whose ability to shift their virulence characteristics may play an important role in infectious-related morbidity following surgical stress.
Alverdy
J C
JC
Department of Surgery, University of Chicago, Illinois, USA.
Rocha
F
F
D000818:Animals; D001419:Bacteria / Q000472:pathogenicity*; D001422:Bacterial Adhesion; D018988:Bacterial Translocation; D004064:Digestive System / Q000276:immunology / Q000382:microbiology; D005938:Glucocorticoids / Q000494:pharmacology; D006801:Humans; D007108:Immune Tolerance; D018928:Immunity, Mucosal; D007070:Immunoglobulin A / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000276:immunology* / Q000382:microbiology*; D009490:Neurosecretory Systems / Q000502:physiology; D011183:Postoperative Complications / Q000276:immunology*; D013312:Stress, Physiological / Q000276:immunology* / Q000503:physiopathology; D014774:Virulence
D005938:Glucocorticoids; D007070:Immunoglobulin A