Pseudomonas aeruginosaによる生体防御調節機構 ： 抗リステリア活性の誘導

Abstract

Subcutaneous inoculation of Pseudomonas aeruginosa, either mucoid type or non-mucoid type, 72h before a lethal infection with Listeria monocytogenes induced antilisterial resistance in mice. Non-mucoid P. aeruginosa was more efficient in inducing the resistance than mucoid. Formalin, acetone, or heat-killed cells of P. aeruginosa induced the protection as effective in as did viable organisms of P. aeruginosa. Endotoxin low-responder C3H/HeJ mice were not protected from listerial lethal infection by this treatment. These results indicate that anti-listerial resistance conferred by P. aeruginosa is attributed to lipopolysaccharide (LPS). This resistance was adoptively transferred to naive mice by peritoneal cells from the mice pretreated intraperitoneally with heat-killed P. aeruginosa. These peritoneal cells were able to produce tumor necrosis factor-α upon stimulation with heat-killed L. monocytogenes and also to exhibit enhanced phagocytic activity. Macrophages are predominant in the peritoneal cells, as determined by the negative selection. Moreover, endogenous interferon-γ (IFN-γ), which is a strong macrophage activator, was induced to a significant extent in the bloodstream of mice pretreated with P. aeruginosa 72h after infection with L. monocytogenes. Pretreatment with monoclonal anti IFN-γ antibody resulted in significant reduction in anti-listerial resistance conferred by P. aeruginosa. Thus, it is assumed that peritoneal macrophages stimulated by LPS of P. aeruginosa could be fully activated by IFN-γ produced upon listerial infection, thereby exerting high magnitude anti-listerial activity.