Abstract
Acinetobacter baumannii is an important pathogen of nosocomial infection worldwide, which can primarily cause pneumonia, bloodstream infection, and urinary tract infection. The increasing drug resistance rate of A. baumannii and the slow development of new antibacterial drugs brought great challenges for clinical treatment. Host immunity is crucial to the defense of A. baumannii infection, and understanding the mechanisms of immune response can facilitate the development of new therapeutic strategies. To characterize the system-level changes of host proteome in immune response, we used tandem mass tag (TMT) labeling quantitative proteomics to compare the proteome changes of lungs from A. baumannii infected mice with control mice 6 h after infection. A total of 6,218 proteins were identified in which 6,172 could be quantified. With threshold p < 0.05 and relative expression fold change > 1.2 or < 0.83, we found 120 differentially expressed proteins. Bioinformatics analysis showed that differentially expressed proteins after infection were associated with receptor recognition, NADPH oxidase (NOX) activation and antimicrobial peptides. These differentially expressed proteins were involved in the pathways including leukocyte transendothelial migration, phagocyte, neutrophil degranulation, and antimicrobial peptides. In conclusion, our study showed proteome changes in mouse lung tissue due to A. baumannii infection and suggested the important roles of NOX, neutrophils, and antimicrobial peptides in host response. Our results provide a potential list of protein candidates for the further study of host-bacteria interaction in A. baumannii infection. Data are available via ProteomeXchange with identifier PXD020640.
Highlights
Acinetobacter baumannii is a hazardous Gram-negative opportunistic pathogen of nosocomial infection that represent serious health risk worldwide
Ferrer-Navarro et al compared the proteome profiles of mouse lungs infected by Streptococcus pneumoniae (Gram-positive bacteria) with control mice at 24 and 48 h postinfection by 2D-differential gel electrophoresis (2D-DIGE). 91 differentially expressed proteins were identified, and the analysis showed that the cytoskeleton of host lung tissue cells is modified in S. pneumoniae infection (Ferrer-Navarro et al, 2018)
Mice were randomly separated into two categories: the proteomic and bacteria counting categories. 18 mice were designated into proteomic category and separated into control group (CON, n = 9) and infection group (INF, n = 9)
Summary
Acinetobacter baumannii is a hazardous Gram-negative opportunistic pathogen of nosocomial infection that represent serious health risk worldwide. Some studies about the pathogenesis and host immune defense mechanisms against A. baumannii have been reported (Bruhn et al, 2015). Some other molecular/signaling mechanisms of infection response were under investigation, such as neutrophil extracellular traps (NETs) (Kamoshida et al, 2015), IL-17 signaling pathway (Breslow et al, 2011), and inflammasome NLRP3 (Dikshit et al, 2018). Most of these studies focused on specific proteins or pathways, ignoring the complicated networks of the human immune response. Analyzing the global level responses will advance our understanding of host-pathogen interactions
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