Deciphering the virulence factors, regulation, and immune response to Acinetobacter baumannii infectionAcinetobacter baumannii is a gram-negative multidrug-resistant nosocomial pathogen and a major cause of hospital acquired infetions. Carbapenem resistant A. baumannii has been categorised as a Priority1 critial pathogen by the World Health Organisation. A. baumannii is responsible for infections in hospital settings, clinical sectors, ventilator-associated pneumonia, and bloodstream infections with a mortality rates up to 35%. With the development of advanced genome sequencing, molecular mechanisms of manipulating bacterial genomes, and animal infection studies, it has become more convenient to identify the factors that play a major role in A. baumannii infection and its persistence. In the present review, we have explored the mechanism of infection, virulence factors, and various other factors associated with the pathogenesis of this organism. Additionally, the role of the innate and adaptive immune response, and the current progress in the development of innovative strategies to combat this multidrug-resistant pathogen is also discussed.

Acinetobacter baumannii employs a plethora of strategies during infection to compete with other pathogens and mitigate host-mediated oxidative stress. A. baumannii utilizes the type VI secretion system (T6SS) to induce contact-dependent killing off the competitor microbes. However, the role of T6SS during host-induced oxidative stress is not explored in A. baumannii. Here, we show that A. baumannii T6+ cells cannot cope with phagocytic cell-mediated oxidative stress due to inadequate uptake of Mn2+, which is crucial for bacterial physiology and reactive oxygen species (ROS) breakdown. Deleting the Mn2+-uptake system (MntH) causes a significant increase in the T6+ population, stipulating a deleterious effect on T6SS modulation in A. baumannii. Intriguingly, we identify a bonafide sRNA, AbsR28, that meditates the crosstalk between MntH and T6SS. This work elucidates a detailed mechanism of Mn2+-dependent AbsR28-mediated post-transcriptional repression of T6SS, exploited by A. baumannii to survive in the host and establish pathogenesis.