Quorum sensing and surface attachment in Acinetobacter baumannii

Acinetobacter baumannii is a Gram-negative nosocomial pathogen that causes a wide range of infections, including ventilator-associated pneumonia and soft tissue infections, mostly in seriously ill patients. Even though several virulence-associated factors have been described, the exact mechanisms of infection and the overall regulation of A. baumannii virulence are still poorly understood. One of the regulatory systems involved in virulence in many other pathogenic bacteria is quorum sensing (QS), a cell density-dependent bacterial communication system that relies in the accumulation of an extracellular signal. In Gram-negative bacteria, these are usually N-acyl-homoserine lactones (AHLs)) and they facilitate coordination of gene expression within a bacterial population. A. baumannii possesses a single LuxR/LuxI-type QS locus, named AbaR/AbaI, that, despite being reported in previous publications to be involved in surface motility and biofilm formation, remains poorly characterized. In this project the role of ABUW_3775 (here named abaM), a gene encoding an RsaM orthologue, and QS were investigated in the hypervirulent A. baumannii strain AB5075. AbaM and QS were phenotypically and genetically characterized, elucidating their role in attachment, surface motility, AHL production, virulence in G. mellonella and gene regulation (which included several genes involved in biofilm formation, such as de Csu pili operon). Further research involving Csu pili suggest that, despite being important in biofilm formation, they might not be the only factor involved in surface sensing and ‘deciding’ whether a surface is suitable for attachment and formation of biofilm or not. This work provides a deeper understanding of QS, gene regulation, attachment and virulence in A. baumannii, but more detailed future investigations will be required for a more comprehensive understanding of the virulence and physiology of this challenging pathogen