Role of outer membrane protein T in pathogenicity of avian pathogenic Escherichia coli. (December 2017)

• Record Type: Journal Article
• Authors: Hejair, Hassan M.A.; Ma, Jiale; Zhu, Yingchu; Sun, Min; Dong, Wenyang; Zhang, Yue; Pan, Zihao; Zhang, Wei; Yao, Huochun
• Is Part Of: Research in veterinary science. Volume 115(2017)
• Page Start: 109
• Page End: 116
• Publication Date: 2017-12
• Subjects: APEC -- ompT -- Adhesion -- Invasion -- Pathogenicity; Veterinary medicine -- Periodicals; Veterinary Medicine -- Periodicals; Médecine vétérinaire -- Périodiques; Médecine vétérinaire -- Recherche -- Périodiques; Diergeneeskunde; 636.089
• DOI: 10.1016/j.rvsc.2017.01.026
• Languages: English
• ISSNs: 0034-5288

Abstract

Abstract: An outer membrane protein T (OmpT) could play a vital role in the pathogenesis of the neonatal meningitis Escherichia coli (NMEC) in human and animals. However, whether ompT plays a role in avian pathogenic E. coli (APEC) infection remains unclear. In this study we evaluated the potential of ompT in APEC pathogenesis. An ompT gene was deleted from APEC mutant strain (TW-XM) was constructed and characterized. The inactivation of ompT reduced significantly the adherence and invasion capabilities of APEC to mouse brain microvascular endothelial cell (BMEC) bEnd.3 cells at the rates of 43.8% and 28.8% respectively, compared with the wild strain TW-XM. Further studies showed that deletion of ompT gene reduced the bacterial virulence with 15.2-fold in ducklings and 9.7-fold in mouse models based on the measurement of the LD50 . Furthermore, experimental infection of animals revealed that, loss of ompT showed reduced APEC colonization and invasion capacity in brains, lungs and blood by 2-fold, 1.96-fold, and 1.7-fold, respectively, compared with the wild-type strain TW-XM. 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 ompT significantly decreased the expression levels of ompA, fimC and tsh in the mutant strain ΔOmpT, when compared with TW-XM ( p < 0.01). Collectively, our data showed that inactivation of ompT decreased adhesion, invasion, colonization, proliferation capacities, possibly by reduced expression levels of ompA, fimC and tsh, which may justify that, ompT is implicated in APEC pathogenicity. Highlights: Deletion of ompT reduced the APEC adherence and invasion towards bEnd.3 cells. Deletion of ompT reduced the virulence of APEC in ducks and mouse models. Deletion of ompT decreased colonization and invasion capacity in brains, lungs and blood. Inactivation of ompT reduced expression level of ompA, fimC and tsh . ompT may be implicated in pathogenicity of APEC.