Exposure to diverse airborne bacterial communities following Klebsiella pneumoniae infection elicits distinct host response mechanisms in mice

BACKGROUND: Air harbors diverse microorganisms. However, the influence of airborne microbial communities on the recovery phase of pneumonia patients remains inadequately explored. METHOD: We randomly generated five distinct bacterial communities with varying compositions from a pool of 16 bacteria. Following infection with Klebsiella pneumoniae, convalescent BALB/c mice were exposed to either saline (control group, G1) or one of the five artificially constructed microbial communities (H1-H5 groups) during their recovery period. Body weight, lung tissue pathology, inflammatory cytokines, metabolomics, and fecal flora were analyzed. RESULTS: Exposure to varied microbial communities induced inflammatory cell infiltration around pulmonary blood vessels and bronchi. Overall, after microbiota exposure, peripheral neutrophil percentages showed a significant increase (p < 0.05). Concurrently, IL-1β was increased in bronchoalveolar lavage fluid (BALF), while IL-6 and IFN-γ were decreased in plasma (p < 0.05). Additionally, varying levels of inflammatory factors and hematological parameters were observed among different exposure groups. Metabolomic analysis revealed joint alterations in nucleotide metabolism and Nicotinate and nicotinamide metabolism in BALF, as well as broader metabolic pathway changes in plasma. Moreover, there were significant differences in metabolic pathways between the different exposure groups. Significant differences in the composition and richness of the gut microbiota were observed among the experimental groups. Pearson correlation analysis established a potential correlation between lung metabolites, gut microbiota, and plasma metabolites, suggesting a potential link within the lung-gut axis. CONCLUSIONS: Our findings demonstrate that varied airborne bacterial communities exposure exert differential effects on convalescent pneumonia in mice. This influence may be mediated, at least in part, by modulating disease progression through the lung-gut axis.