Vol.65 No.6 November 2017
Infection by Acinetobacter baumannii and host immunity A novel bacterial transport mechanism "Bacterial immunity taxi"
Department of Microbiology and Immunology, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo, Japan
Abstract
Hospital-acquired infections due to Acinetobacter baumannii have become problematic because of high rates of drug resistance. A. baumannii is usually harmless, but it causes sepsis resulting in a high mortality rate in compromised hosts. Therefore, we must consider its interaction with host cells to understand diseases resulting from A. baumannii infection. Neutrophils play a critical role in infective protection against the extracellular growth of bacteria. However, their interactions with A. baumannii remain largely unknown. Recently, a new biological defense mechanism called neutrophil extracellular traps (NETs) has been attracting attention. In the present study, we investigated the responsiveness of human neutrophils to A. baumannii focusing on NET formation. The results demonstrated that infective protection against Pseudomonas aeruginosa via NETs formation was observed, but for A. baumannii NETs formation did not occur. It seems that the innate infective protection against A. baumannii does not work normally and this bacterium was not killed by neutrophils. To elucidate the interactions between A. baumannii and neutrophils, we performed a more detailed analysis. A. baumannii seems to spread throughout the body by calling and hijacking neutrophils like a taxi; therefore, the mechanism behind this novel bacterial transport will be referred to as the "Bacterial immunity taxi." In the future, we aim to clarify in more detail the interactions between A. baumannii and host cells, and hopefully thus identify infection control, diagnosis and treatment.
Key word
Acinetobacter baumannii, neutrophil, neutrophil extracellular traps（NETs）, Bacterial immunity taxi, sepsis
Received
January 5, 2017
Accepted
May 10, 2017
Jpn. J. Chemother. 65 (6): 794-802, 2017
