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

Lumin Yu,Jingtian Ni,Li Yu,Wenchang Li,Ming Zhang,Ting Xue,Yunmei Cui,Fei Shang,Xiaolin Chen

doi:10.1002/mbo3.582

Lumin Yu, Jingtian Ni + Show 7 more

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https://doi.org/10.1002/mbo3.582

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Abstract

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.

Highlights

Avian pathogenic Escherichia coli (APEC) is known to possess specific virulence attributes associated with colibacillosis in birds, and it is responsible for severe economic losses for the poultry industry worldwide (Dhomoulin & Fairbrother, 1999; Gross, 1994; Zhao et al, 2005)
Previous studies reported that autoinducer 2 (AI-2) is an important Quorum sensing (QS) signal molecule in gram- negative and -positive bacteria, including E. coli, suggesting that AI-2 could play an important role in the physiological activity or regulation of E. coli (Ahmed et al, 2009; Vendeville et al, 2005; Xue et al, 2009)
Our previous study demonstrated that exogenous AI-2 increased the antibiotic resistance of a clinical E. coli strain isolated from a dairy cow with mastitis by upregulating the expression of resistance gene TEM, and the regulation was directly related to LsrR which is the receptor of AI-2 (Xue et al, 2016)

Summary

| INTRODUCTION

Avian pathogenic Escherichia coli (APEC) is known to possess specific virulence attributes associated with colibacillosis in birds, and it is responsible for severe economic losses for the poultry industry worldwide (Dhomoulin & Fairbrother, 1999; Gross, 1994; Zhao et al, 2005). In the past few years, both the morbidity and mortality of APEC infections have increased rapidly and have become a major problem in the poultry industry (Altekruse et al, 2002; Blanco, Blanco, Mora, & Blanco, 1997). It has necessitated the use of antimicrobial chemotherapy to prevent and control outbreaks of APEC infections (Aggad, Ammar, Hammoudi, & Kihal, 2010; Watts, Salmon, Yancey, Nersessian, & Kounev, 1993). We reported that exogenous AI-2 increses the susceptibility of APEC strains to trimethoprim-sulfamethoxazole (SXT) in a folate synthesis- dependent pathway but not in the LsrR-dependent manner. Primer name g-folA-f g-folA-r g-folC-f g-folC-r g-metE-f g-metE-r g-metH-f g-metH-r rt-16s-f rt-16s-r rt-lsrR-f rt-lsrR-r rt-folA-f rt-folA-r rt-folC-f rt-folC-r rt-luxS-f rt-luxS-r rt-metE-f rt-metE-r rt-metH-f rt-metH-r p-folA-f p-folA-r p-folC-f p-folC-r

| MATERIALS AND METHODS

| DISCUSSION