Acinetobacter baumannii defends against oxidative stress through a Mn²⁺-dependent small RNA-mediated suppression of type VI secretion system

SUMMARY

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.