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The pathogenic bacterium  Pseudomonas aeruginosa  possesses high metabolic versatility, with its effectiveness to cause infections likely due to its well-regulated genetic content.  P. aeruginosa  PAO1 has at least six  fadD  paralogous genes, which have been implicated in fatty acid (FA) degradation and pathogenicity. In this study, we used mutagenesis and a functional approach in  P. aeruginosa  PAO1 to determine the roles of the  fadD4  gene in acyclic terpene (AT) and FA assimilation and on pathogenicity. The results indicate that  fadD4  encodes a terpenoyl-CoA synthetase utilized for AT and FA assimilation. Additionally, mutations in  fadD  paralogs led to the modification of the quorum-sensing  las / rhl  systems, as well as the content of virulence factors pyocyanin, biofilm, rhamnolipids, lipopolysaccharides (LPS), and polyhydroxyalkanoates. In a  Caenorhabditis elegans in vivo  pathogenicity model, culture supernatants from the 24-h-grown  fadD4  single mutant increased lethality compared to the PAO1 wild-type (WT) strain; however, the double mutants  fadD1/fadD2 ,  fadD1/fadD4 , and  fadD2/fadD4  and single mutant  fadD2  increased worm survival. A correlation analysis indicated an interaction between worm death by the PAO1 strain, the  fadD4  mutation, and the virulence factor LPS. Fatty acid methyl ester (FAME) analysis of LPS revealed that a proportion of the LPS and FA on lipid A were modified by the  fadD4  mutation, suggesting that FadD4 is also involved in the synthesis/degradation and modification of the lipid A component of LPS. LPS isolated from the  fadD4  mutant and double mutants  fadD1/fadD4  and  fadD2/fadD4  showed a differential behavior to induce an increase in body temperature in rats injected with LPS compared to the WT strain or from the  fadD1  and  fadD2  mutants. In agreement, LPS isolated from the  fadD4  mutant and double mutants  fadD1/fadD2  and  fadD2/fadD4  increased the induction of IL-8 in rat sera, but IL1-β cytokine levels decreased in the double mutants  fadD1/fadD2  and  fadD1/fadD4 . The results indicate that the  fadD  genes are implicated in the degree of pathogenicity of  P. aeruginosa  PAO1 induced by LPS-lipid A, suggesting that FadD4 contributes to the removal of acyl-linked FA from LPS, rendering modification in its immunogenic response associated to Toll-like receptor TLR4. The genetic redundancy of  fadD  is important for bacterial adaptability and pathogenicity over the host.

frontiers in microbiology

Participation of Acyl-Coenzyme A Synthetase FadD4 of Pseudomonas aeruginosa PAO1 in Acyclic Terpene/Fatty Acid Assimilation and Virulence by Lipid A Modification