Killing of Escherichia coli in the peritoneal cavity of convalescent mice; role of specific and non-specific immune mechanisms.
Mice surviving a sublethal E. coli O18:K1 infection possess a greatly increased resistance to a subsequent lethal E. coli O18:K1 peritonitis. A similar increase in resistance can also be achieved by LPS pretreatment. The early course of the infection in the convalescent mice at day 1 was identical to that in LPS-pretreated mice. At this time, the convalescent mice were also able to restrict the growth of the heterologous E. coli O78(ColV) strain, suggesting that non-specific phagocyte activation was responsible for the increased destruction of the bacteria. At day 4, the kinetics of infection in convalescent mice were identical to those in mice passively immunised with specific anti-K1 capsule antiserum. A rapid decline in the numbers of viable homologous, but not heterologous, bacteria took place in the peritoneal cavity suggesting effective antibody-mediated opsonisation followed by phagocytosis and killing of the bacteria.
D000818:Animals; D003289:Convalescence; D004926:Escherichia coli / Q000276:immunology / Q000302:isolation & purification; D004927:Escherichia coli Infections / Q000276:immunology*; D007109:Immunity; D007116:Immunization, Passive; D007700:Kinetics; D008070:Lipopolysaccharides / Q000276:immunology; D051379:Mice; D008815:Mice, Inbred Strains; D009345:Neisseria meningitidis / Q000276:immunology; D010538:Peritonitis / Q000276:immunology* / Q000382:microbiology; D013045:Species Specificity
D008070:Lipopolysaccharides