Non-dystrophic 129 REJ mice are susceptible to i.p. infection with Listeria monocytogenes despite an ability to recruit inflammatory neutrophils to the peritoneal cavity.
In this study we compared the host response to Listeria monocytogenes in 129 REJ mice with listeria-resistant (C57Bl/6j) and susceptible (Balb/c) mouse strains. In all experiments mice were inoculated by the i.p. route. 129 REJ mice and Balb/c mice were sensitive to listeriosis whilst C57Bl/6j mice were relatively resistant to i.p. infection. Relatively large numbers of viable bacteria could be detected in the spleens of 129 REJ mice as early as 6 h following i.p. inoculation suggesting that dissemination of listeria from the peritoneal cavity is rapid in this mouse strain. This contrasted with Balb/c mice which exhibited an early lag phase during which only low numbers of bacteria could be isolated from the spleens of infected animals. In response to both proteose peptone and live listeria, 129 REJ mice demonstrated a greater capacity to recruit neutrophils to the peritoneal cavity than Balb/c and C57Bl/6j mice. In addition, inflammatory phagocytes from 129 REJ mice were as bactericidal in vitro as phagocytes from the Balb/c and C57Bl/6j strains. However, in vivo, inflammatory neutrophils elicited by proteose peptone prior to i.p. infection with L. monocytogenes were not protective in the three mouse strains tested. Despite the apparent inadequacy of peritoneal neutrophils in controlling early bacterial proliferation, depletion of neutrophils in 129 REJ mice severely exacerbated i.p. infection with L. monocytogenes. The results indicate that neutrophils provide an inefficient but essential means of controlling early outgrowth of listeria in the peritoneal cavity of 129 REJ mice. The excessive inflammatory response seen in 129 REJ mice may facilitate the early dissemination of L. monocytogenes from the peritoneal cavity to peripheral sites.
D000818:Animals; D000907:Antibodies, Bacterial; D000911:Antibodies, Monoclonal; D002364:Caseins / Q000494:pharmacology; D004198:Disease Susceptibility; D007113:Immunity, Innate; D008089:Listeria monocytogenes / Q000254:growth & development / Q000472:pathogenicity*; D008088:Listeriosis / Q000276:immunology* / Q000382:microbiology; D017737:Macrophages, Peritoneal / Q000276:immunology; D051379:Mice; D008815:Mice, Inbred Strains; D009504:Neutrophils / Q000276:immunology*; D010446:Peptide Fragments / Q000494:pharmacology; D010529:Peritoneal Cavity / Q000166:cytology / Q000382:microbiology*; D013154:Spleen / Q000382:microbiology
D000907:Antibodies, Bacterial; D000911:Antibodies, Monoclonal; D002364:Caseins; D010446:Peptide Fragments; C018135:proteose-peptone