N-acyl-homoserine lactones-mediated quorum sensing promotes intestinal colonization of Aeromonas veronii through facilitating cheA gene expression

Abstract

Aeromonas veronii, which is a dominant bacterial species that causes economically adverse diseases in aquaculture, can colonize the gastrointestinal tracts of humans and animals, causing severe infections. Preceding studies have demonstrated that N-acyl-homoserine lactones (AHLs)-mediated quorum sensing (QS) stimulates the intestinal colonization of A. veronii, however, the mechanism involved remains unclear. Here, we performed transcriptomics analyses of the wild-type strain A. veronii Z12 and the AHLs synthase gene (ahyI) mutant strain Z12ΔahyI. The results suggested that the AHLs-mediated QS system regulated about 254 differentially expressed genes (DEGs), which contained 82 up-regulated and 172 down-regulated DEGs in strain Z12ΔahyI. Functional annotation and enrichment analyses of the DEGs revealed that the AHLs-mediated QS system primarily regulated chemotaxis gene expression. According to qRT-PCR validation and chemotaxis measurements, the deletion of the ahyI gene lowered the expression of chemotaxis genes, as well as the chemotaxis ability. Among the chemotaxis genes, the sensory histidine kinase gene cheA was determined as the critical gene to investigate as relates to its effects on intestinal colonization. The cheA gene mutant strain Z12ΔcheA was constructed, and it was determined that the expression levels of chemotaxis genes and chemotaxis ability of strain Z12ΔcheA were significantly lowered, as well as the intestinal ecological niche competition of Z12ΔcheA with intestinal bacteria. Furthermore, strain Z12ΔcheA exhibited lower dispersion and colonization levels in the intestine, in contrast to A. veronii Z12. Our findings confirmed that the regulation of the AHLs-mediated QS system on expression of the cheA gene that can contribute to colonizing the host with A. veronii Z12, which can further elucidate pathogenic colonization strategies.