Effect of B cell deficiency in mice during Acientobacter baumannii respiratory infection

Role of B cells against pulmonary infection caused by Acinetobacter baumannii is poorly understood. In this study we performed RNA-seq of whole lung tissue to compare the gene expression profile of WT C57BL/6 and B cell deficient mice (muMT) at 4 hours post infection (4hpi). We also compared the gene expression profile of naive WT and muMT mice. Here we report that naive WT mice had significantly higher expression of numerous genes related to antimicrobial peptide production, leukocyte chemotaxis and activation. We also found that the B cell deficiency lead to higher expression of genes associated with decreased pulmonary respiratory rate, increased pulmonary ventillation rate, and increased recruitment of pulmonary eosinophils at 4hpi. This observation suggests a higher pulmonary infammatory response in B cell deficient mice. Taken together, this study expands our current understanding about the role of B cells in controlling A. baumannii at the early stages of respiratory infection. Overall design: WT and muMT mice were intranasally infected with 10^8 cfu of Acinetobacter baumannii AB5075 strain. At 4 hours post infectiopn, lung tissues were aseptically harvested and total RNA was extracted from the lungs for RNA-sequencing. Lung tissues were also harvested from uninfected mice for RNA-sequencing. We then performed comparative gene expression profiling analysis using the data obtained from RNA-seq.