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Antigen-presenting characteristics of peritoneal cells of Salmonella enteritidis 11RX-infected mice
1Department of Microbiology and Immunology, University of Adelaide, South Australia.
Abstract:
Investigation of the possibility that infection with intracellular bacterial parasites such as Salmonellae may modulate the function of antigen-presenting cells (APC) revealed no major change in APC function of peritoneal cells (PC) harvested from the peritoneal cavity of mice 1-3 days after intraperitoneal immunization with S. enteritidis 11RX. Analysis of the phenotype of the Salmonella-primed T cells which responded when cultured with PC from either normal or infected mice and Salmonella-antigen showed that only L3T4+ T cells proliferated. This was also true when PC from normal and infected mice were compared for their ability to induce allogeneic responses; both L3T4+ and Lyt-2.2+ T cells were induced to proliferate, with the majority belonging to the class I restricted, Lyt-2.2+ phenotype. Significant levels of alloantigen-specific Lyt-2.2+ cytotoxic T-cell activity were also induced in both types of cultures. However, a minor population of adherent cells which inhibited Salmonella antigen-specific T-cell proliferation in vitro was detected in peritoneal cell suspensions harvested 3 days after intraperitoneal immunization with S. enteritidis 11RX. Further characterization of these peritoneal cells revealed that they also inhibited the induction of in vitro T-cell responses to alloantigens. It is likely that the cells mediating these inhibitory effects belonged to a macrophage-like subset.
Insights
Salmonella infection does not significantly alter antigen-presenting cell function in mice. However, a subset of peritoneal cells inhibits T-cell proliferation, suggesting a regulatory role for macrophages in immune responses.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Antigen-presenting cells (APCs) are crucial for initiating adaptive immune responses.
- Intracellular bacterial infections, like Salmonella, can influence APC function and host immunity.
- Understanding immune modulation during infection is vital for developing effective therapies.
Purpose of the Study:
- To investigate the impact of Salmonella enterica serovar Enteritidis (S. enteritidis) infection on murine peritoneal cell (PC) function.
- To analyze the T-cell response to Salmonella antigens presented by infected APCs.
- To identify any regulatory mechanisms affecting T-cell proliferation during Salmonella infection.
Main Methods:
- Mice were intraperitoneally immunized with S. enteritidis.
- Peritoneal cells (PCs) were harvested and analyzed for APC function.
- T-cell proliferation assays were performed using normal or infected PCs with Salmonella antigen.
- Allogeneic responses and cytotoxic T-cell activity were assessed.
- Inhibitory effects on T-cell proliferation were investigated.
Main Results:
- Salmonella infection did not cause major changes in APC function of peritoneal cells.
- L3T4+ T cells proliferated in response to Salmonella antigen presented by both normal and infected PCs.
- Both L3T4+ and Lyt-2.2+ T cells proliferated in allogeneic responses, with a majority of Lyt-2.2+ phenotype.
- Significant alloantigen-specific Lyt-2.2+ cytotoxic T-cell activity was induced.
- A minor population of adherent, macrophage-like cells inhibited Salmonella antigen-specific and alloantigen-specific T-cell proliferation in vitro.
Conclusions:
- Salmonella infection does not broadly impair APC function in the peritoneal cavity.
- A subset of peritoneal macrophages exhibits inhibitory properties, potentially regulating T-cell responses during Salmonella infection.
- These findings highlight a complex immunomodulatory role of macrophages during intracellular bacterial infections.