Abstract
BackgroundAvian pathogenic Escherichia coli strains cause extraintestinal diseases in birds, leading to substantial economic losses to the poultry industry worldwide. Bacteria that invade cells can overcome the host humoral immune response, resulting in a higher pathogenicity potential. Invasins are members of a large family of outer membrane proteins that allow pathogen invasion into host cells by interacting with specific receptors on the cell surface.ResultsAn in silico analysis of the genome of a septicemic APEC strain (SEPT362) demonstrated the presence of a putative invasin homologous to the ychO gene from E. coli str. K-12 substr. MG1655. In vitro and in vivo assays comparing a mutant strain carrying a null mutation of this gene, a complemented strain, and its counterpart wild-type strain showed that ychO plays a role in the pathogenicity of APEC strain SEPT362. In vitro assays demonstrated that the mutant strain exhibited significant decreases in bacterial adhesiveness and invasiveness in chicken cells and biofilm formation. In vivo assay indicated a decrease in pathogenicity of the mutant strain. Moreover, transcriptome analysis demonstrated that the ychO deletion affected the expression of 426 genes. Among the altered genes, 93.66 % were downregulated in the mutant, including membrane proteins and metabolism genes.ConclusionThe results led us to propose that gene ychO contributes to the pathogenicity of APEC strain SEPT362 influencing, in a pleiotropic manner, many biological characteristics, such as adhesion and invasion of in vitro cultured cells, biofilm formation and motility, which could be due to the possible membrane location of this protein. All of these results suggest that the absence of gene ychO would influence the virulence of the APEC strain herein studied.
Highlights
Avian pathogenic Escherichia coli strains cause extraintestinal diseases in birds, leading to substantial economic losses to the poultry industry worldwide
The lack of ychO gene decreases the virulence of strain SEPT362 after 48 h in the host, which indicates YchO has a role in survival of the strain in the host. This gene is found in non pathogenic E. coli strains, all of these results suggest that the absence of gene ychO influences the virulence of the avian pathogenic E. coli (APEC) strain studied in a direct way
The adhesion, invasion and biofilm formation results presented in this paper together with the presence of the three basic structures of the protein, allow us to suggest that gene Ycho protein plays roles as an adhesin/invasion in this specific strain
Summary
Avian pathogenic Escherichia coli strains cause extraintestinal diseases in birds, leading to substantial economic losses to the poultry industry worldwide. Invasins are members of a large family of outer membrane proteins that allow pathogen invasion into host cells by interacting with specific receptors on the cell surface. A large family of bacterial outer membrane proteins facilitates the entry of the pathogen into host cells by allowing tight adherence to and invasion of the cells. This family of proteins interacts with receptors displayed on the cell surface, triggering signaling cascades to rearrange the host cell cytoskeleton and induce the uptake of bacteria [11, 12]. The β-barrel structure is necessary for the passenger domain, which mediates interactions with host cells, to cross the outer membrane [20]
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