Functional role of ompF and ompC porins in pathogenesis of avian pathogenic Escherichia coli. (June 2017)

• Record Type: Journal Article
• Authors: Hejair, Hassan M.A.; Zhu, Yinchu; Ma, Jiale; Zhang, Yue; Pan, Zihao; Zhang, Wei; Yao, Huochun
• Is Part Of: Microbial pathogenesis. Volume 107(2017)
• Page Start: 29
• Page End: 37
• Publication Date: 2017-06
• Subjects: APEC -- ompF -- ompC -- Adhesion -- Invasion -- Pathogenesis; Pathogenic microorganisms -- Periodicals; Pathology, Molecular -- Periodicals; Communicable Diseases -- microbiology -- Periodicals; Communicable Diseases -- parasitology -- Periodicals; Micro-organismes pathogènes -- Périodiques; Pathologie moléculaire -- Périodiques; Electronic journals; 616.9041
• DOI: 10.1016/j.micpath.2017.02.033
• Languages: English
• ISSNs: 0882-4010

Abstract

Abstract: Avian pathogenic Escherichia coli is an important pathogen causes systemic infections in avian species and large economic losses in poultry industry worldwide. The functional role of porins during the infection and their mechanisms of interaction with host tissues for adhesion to and invasion are poorly understood. However, whether porins play a role in infection remains unclear. In this study we evaluated the potential of ompF and ompC outer membrane porins in the pathogenesis of avian pathogenic E. coli (APEC) strain TW-XM. The ompF and ompC were deleted to generate a series of mutants. We found that, Δ ompF and Δ ompC reduced significantly the adherence by 41.3% and 46.1% and invasion capabilities of APEC to mouse brain microvascular endothelial cell (BMEC) bEnd.3 cells in vitro by 51.9% and 49.7% respectively, compared with the wild strain TW-XM. I n vivo experiment based on the measurement of the LD50 have also shown that, Δ ompF and Δ ompC reduced the bacterial virulence by 9.8-fold, 12.3-fold in ducklings and 9-fold, 10.2-fold in mouse models. Animal infection experiments further revealed that, loss of ompF and ompC reduced TW-XM colonization and invasion capacity in brains, lungs and blood compared to wild-type strain TW-XM ( P > 0.01). These virulence-related phenotypes were partially recoverable by genetic complementation. The results of the quantitative real-time reverse transcription-PCR (qRT-PCR) indicated that, the loss of ompF and ompC significantly decreased the expression levels of ompA, fimC and iBeA genes in the mutant strains, compared to wild-type strainTW-XM ( P < 0.01). Collectively, our data demonstrate that inactivation of these two porins decreased adhesion, invasion, colonization, proliferation capacities, possibly by reduced expression levels of ompA, fimC and iBeA, which may indicate the involvement of ompF and ompC in APEC pathogenesis. Highlights: Deletion of ompF and ompC reduced the APEC adherence and invasion towards bEnd.3 cells. Deletion of ompF and ompC reduced the virulence of APEC in ducks and mouse models. Deletion of ompF and ompC decreased colonization and invasion capacity in brains, lungs and blood. Inactivation of ompF and ompC reduced expression level of ompA, fimC and iBeA. ompF and ompC may be implicated in pathogenicity of APEC.