Autoinducer2 affects trimethoprim-sulfamethoxazole susceptibility in avian pathogenic Escherichia coli dependent on the folate synthesis-associate pathway.

Avian pathogenic Escherichia coli (APEC) causes airsacculitis, polyserositis, septicemia, and other mainly extraintestinal diseases in chickens, ducks, geese, pigeons, and other avian species, and is responsible for great economic losses in the avian industry. The autoinducer 2 (AI-2) quorum sensing system is widely present in many species of gram-negative and gram-positive bacteria and has been proposed to be involved in interspecies communication. In clinical APEC strains, whether or not AI-2 affects the expression of antibiotic-related genes has not been reported. In this study, we have reported that exogenous AI-2 increase the susceptibility of APEC strains to trimethoprim-sulfamethoxazole (SXT) in a folate synthesis-dependent pathway but not in the LsrR-dependent manner. Our results further explained that exogenous AI-2 can down regulate the transcription of the folate synthetase encoding genes folA and folC, and the folate synthesis-related genes luxS, metE, and metH. Gel shift assays confirmed that LsrR, the AI-2 receptor, did not bind to the promoters of folA and folC, suggesting that exogenous AI-2 might influence folate metabolism by a feedback inhibition effect but not in the LsrR-dependent pathway. This study might provide further information in the search for potential drug targets for prophylaxis of avian colibacillosis and for auxiliary antibiotics in the treatment of avian colibacillosis.