Abstract

BackgroundAcinetobacter species can occupy several ecological niches, including the mammalian intestine. Acinetobacter has been identified in the human fecal microbiota and it is speculated that the gut can serve as a reservoir for this pathobiont. The Acinetobacter calcoaceticus–Acinetobacter baumannii complex is a common cause of drug‐resistant pneumonia, urinary tract, skin and soft tissue infections. A. calcoaceticus has been considered to have relatively low virulence compared to its counterpart A. baumannii since colonization is more frequently noted more than infection clinically. However, few studies have dissected the interaction between A. calcoaceticus and the host, particularly in the gut. In this study, we sought to examine the ability of A. calcoaceticus strains to survive environmental stressors found in the gut. We also examined the reciprocal interactions of A. calcoaceticus strains on the host using colonic organoids.Methods & ResultsThree commercially available strains of A. calcoaceticus and four clinical isolates were grown aerobically in brain heart infusion (BHI) media, subcultured in a fully defined bacterial media termed ZMB1 and exposed to various concentrations of NaCl, ethanol, bile salts and pHs that were designed to mimic the gut. All A. calcoaceticusstrains grew robustly at NaCl concentrations that mirrored the small intestine, but differences were observed between strains at higher NaCl concentrations. Additionally, all strains grew well at pH 7 and pH 6, and exhibited growth reduction at pHs 5 and 4. All strains tolerated several concentrations of bile salts and ethanol; suggesting tolerance for intestinal stressors. Incubation of live A. calcoaceticus strains with inside‐out jejunum and colonic organoids significantly increased pro‐inflammatory cytokines (IL‐1α, KC/IL‐8, MCP‐1 and TNF) and decreased MUC2 and MUC13 transcripts, without altering tight junctions.ConclusionsCollectively, these data demonstrate that A. calcoaceticus is well adapted to the gastrointestinal tract and points to the potential for Acinetobacter to influence the gut epithelium. Of note, we observed differences between lab adapted strains and clinical isolates, highlighting strain variation and indicating that clinical isolate strains should be incorporated into future work.

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