Inner membrane protein TolA facilitates the antibiotic resistance, environment adaptability, biofilm formation and virulence of avian pathogenic Escherichia coli

Abstract

Highlights 1. TolA enhances the antibiotic resistance and environment adaptability of APEC. 2. TolA promotes the biofilm formation and interbacterial competition of APEC. 3. TolA facilitates the infection and virulence of APEC. Abstract Avian pathogenic Escherichia coli (APEC) could cause colibacillosis, which is economically devastating to poultry industries worldwide. The bacterial membrane is critical to its environment adaptability and virulence. The inner membrane protein TolA maintains membrane integrity, but the roles of which in fitness and pathogenesis of APEC are not completely understood. Thus, the tolA gene mutant and complemented strains of APEC were constructed and characterized. We found that mutant strain ΔtolA was damaged in inner and outer membranes, and showed altered morphology, impaired flagella production, reduced motility, increased outer membrane vesicles (OMVs) production, decreased resistance to antibiotics and environmental stress. Deletion of tolA gene resulted in a significant decrease in biofilm formation and interbacterial competition, due to the downregulated expression of biofilm-associated genes and type VI secretion system (T6SS) genes, respectively. In addition, the mutant strain exhibited diminished serum bactericidal resistance, reduced cell infection capacity, Journal of Integrative Agriculture decreased intracellular survival, consequently, leading to attenuated bacterial survival and virulence in mice. Compared with the wild-type and complemented strains, mutant strain induced less expression of inflammatory cytokine interleukin 1 beta (IL-1β) in HD-11 macrophages, consistent with the pathological damage in mice. In conclusion, inner membrane protein TolA contributed to the antibiotic resistance, environment adaptability, biofilm formation and virulence of APEC.