Interference of Pseudomonas aeruginosa with immunospecific host defenses.
Pseudomonas aeruginosa, an important nosocomial pathogen, has numerous virulence factors that may interfere with unspecific host defense mechanisms (complement components, neutrophils, macrophages). Furthermore, Pseudomonas aeruginosa or substances derived from it can inhibit lymphocyte proliferative responses and alter immune responses, especially cell-mediated immune responses as evidenced by prolonged survival of skin homografts and suppression of DTH skin reaction in humans and laboratory animals. Acquired cellular resistance to Listeria monocytogenes is also suppressed by P. aeruginosa. Likely more than one mechanism is responsible for these depressed immune responses. Nevertheless, P. aeruginosa is able to interfere with macrophages and T-lymphocyte activities. The relevance of the immunosuppression with respect to host defenses against infections is discussed in the context of evidence in favor of cell-mediated immunity of P. aeruginosa.
D000818:Animals; D000917:Antibody Formation; D002455:Cell Division; D006023:Glycoproteins / Q000502:physiology; D006168:Guinea Pigs; D006801:Humans; D007108:Immune Tolerance; D007111:Immunity, Cellular; D008214:Lymphocytes / Q000166:cytology / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D011135:Polysaccharides, Bacterial / Q000502:physiology; D011552:Pseudomonas Infections / Q000276:immunology; D011550:Pseudomonas aeruginosa / Q000276:immunology*; D051381:Rats; D050378:T-Lymphocytes, Regulatory / Q000276:immunology
D006023:Glycoproteins; D011135:Polysaccharides, Bacterial