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Pseudomonas aeruginosa  is an opportunistic bacteria and a major cause of nosocomial pneumonia.  P. aeruginosa  has many virulence factors contributing to its ability to colonize the host. LoxA is a lipoxygenase enzyme secreted by  P. aeruginosa  that oxidizes polyunsaturated fatty acids. Based on previous  in vitro  biochemical studies, several biological roles of LoxA have been hypothesized, including interference of the host lipid signaling, and modulation of bacterial invasion properties. However, the contribution of LoxA to  P. aeruginosa  lung pathogenesis  per se  remained unclear. In this study, we used complementary  in vitro  and  in vivo  approaches, clinical strains of  P. aeruginosa  as well as lipidomics technology to investigate the role of LoxA in lung infection. We found that several  P. aeruginosa  clinical isolates express LoxA. When secreted in the lungs, LoxA processes a wide range of host polyunsaturated fatty acids, which further results in the production of bioactive lipid mediators (including lipoxin A 4 ). LoxA also inhibits the expression of major chemokines (e.g., MIPs and KC) and the recruitment of key leukocytes. Remarkably, LoxA promotes  P. aeruginosa  persistence in lungs tissues. Hence, our study suggests that LoxA-dependent interference of the host lipid pathways may contribute to  P. aeruginosa  lung pathogenesis.

Pseudomonas aeruginosa Lipoxygenase LoxA Contributes to Lung Infection by Altering the Host Immune Lipid Signaling