Acinetobacter baumannii stimulates interleukin-22 production in CD4+ T cells and innate immune cells 3305

Abstract Description Acinetobacter baumannii is a Gram-negative, opportunistic pathogen whose multi-drug resistance (MDR) poses a threat to healthcare systems. Most A. baumannii studies focus on MDR, with few investigating this pathogen’s influence on the immune system. Our lab studies interleukin-22 (IL-22), a cytokine known to maintain the integrity of epithelial barriers and regulate inflammation. Understanding A. baumannii’s impact on IL-22 production in immune cells will likely provide immunological targets for therapeutics aiming to combat MDR A. baumannii infections. ELISA measured IL-22 levels in supernatants of CD4+ T cell cultures harvested from C57BL/6 mice spleens and activated in the presence or absence of heat-killed (HK) A. baumannii. All tested strains produced a significant increase in CD4 T cell IL-22 production. Intracellular staining (ICS) and flow cytometry (FACS) were used to see if cytokine production occurs within CD4+ T cells. Studies indicated less IFN-γ producing CD4+ T cells and elevated IL-22 producing CD4+ T cells when HK A. baumannii is present. ELISAs measuring IL-22 from splenocytes of Rag1-/- mice, which lack T and B cells, grown with HK A. baumannii showed elevations in IL-22, indicating innate cell contribution to IL-22 production. A likely candidate is type 3 innate lymphoid cells, known to secrete IL-22. Future studies will identify the innate immune cells producing IL-22 and determine the importance of IL-22 in clearing A. baumannii barrier infections. Funding Sources Funding for this project was supported by NIH Grant RO1AI173108 and the Robert Glenn Rapp Foundation’s Hyde Research Scholarship. Topic Categories Microbial, Parasitic, and Fungal Immunology (MPF)