Role of outer membrane protein T in pathogenicity of avian pathogenic Escherichia coli
An outer membrane protein T (OmpT) could play a vital role in the pathogenesis of the neonatal meningitisEscherichia coli(NMEC) in human and animals. However, whetherompTplays a role in avian pathogenicE. coli(APEC) infection remains unclear. In this study we evaluated the potential ofompTin APEC pathogenesis. AnompTgene was deleted from APEC mutant strain (TW-XM) was constructed and characterized. The inactivation ofompTreduced 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 ofompTgene 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 ofompTshowed 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 ofompTsignificantly decreased the expression levels ofompA,fimCandtshin the mutant strain ΔOmpT, when compared with TW-XM (p<0.01). Collectively, our data showed that inactivation ofompTdecreased adhesion, invasion, colonization, proliferation capacities, possibly by reduced expression levels ofompA,fimCandtsh, which may justify that,ompTis implicated in APEC pathogenicity..
| Medienart: |
Artikel |
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| Erscheinungsjahr: |
2017 |
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| Erschienen: |
2017 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:115 |
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| Enthalten in: |
Research in veterinary science - 115(2017), Seite 109-116 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Hejair, Hassan M.A [VerfasserIn] |
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| Links: |
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| doi: |
10.1016/j.rvsc.2017.01.026 |
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| Förderinstitution / Projekttitel: |
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| 245 | 1 | 0 | |a Role of outer membrane protein T in pathogenicity of avian pathogenic Escherichia coli |
| 264 | 1 | |c 2017 | |
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| 520 | |a An outer membrane protein T (OmpT) could play a vital role in the pathogenesis of the neonatal meningitisEscherichia coli(NMEC) in human and animals. However, whetherompTplays a role in avian pathogenicE. coli(APEC) infection remains unclear. In this study we evaluated the potential ofompTin APEC pathogenesis. AnompTgene was deleted from APEC mutant strain (TW-XM) was constructed and characterized. The inactivation ofompTreduced 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 ofompTgene 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 ofompTshowed 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 ofompTsignificantly decreased the expression levels ofompA,fimCandtshin the mutant strain ΔOmpT, when compared with TW-XM (p<0.01). Collectively, our data showed that inactivation ofompTdecreased adhesion, invasion, colonization, proliferation capacities, possibly by reduced expression levels ofompA,fimCandtsh, which may justify that,ompTis implicated in APEC pathogenicity. | ||
| 650 | 4 | |a Animals | |
| 650 | 4 | |a Mammals | |
| 650 | 4 | |a Animal models | |
| 650 | 4 | |a Membrane proteins | |
| 650 | 4 | |a Pathogenesis | |
| 650 | 4 | |a Strain | |
| 650 | 4 | |a Meningitis | |
| 650 | 4 | |a Reverse transcription | |
| 650 | 4 | |a Virulence | |
| 650 | 4 | |a Inactivation | |
| 650 | 4 | |a Endothelial cells | |
| 650 | 4 | |a Colonization | |
| 650 | 4 | |a Complementation | |
| 650 | 4 | |a Pathogenicity | |
| 650 | 4 | |a Polyclonal antibodies | |
| 650 | 4 | |a Escherichia coli | |
| 650 | 4 | |a Deactivation | |
| 650 | 4 | |a Infections | |
| 650 | 4 | |a Bacteria | |
| 650 | 4 | |a Microvasculature | |
| 650 | 4 | |a Experimental infection | |
| 650 | 4 | |a Deletion | |
| 650 | 4 | |a Clonal deletion | |
| 650 | 4 | |a Deoxyribonucleic acid--DNA | |
| 650 | 4 | |a Brain | |
| 650 | 4 | |a Enzymes | |
| 650 | 4 | |a Pathogens | |
| 650 | 4 | |a Plasmids | |
| 650 | 4 | |a Sepsis | |
| 650 | 4 | |a RNA polymerase | |
| 650 | 4 | |a Lungs | |
| 650 | 4 | |a Proteins | |
| 650 | 4 | |a Neonates | |
| 650 | 4 | |a E coli | |
| 650 | 4 | |a Biotechnology | |
| 700 | 1 | |a Ma, Jiale |4 oth | |
| 700 | 1 | |a Zhu, Yingchu |4 oth | |
| 700 | 1 | |a Sun, Min |4 oth | |
| 700 | 1 | |a Dong, Wenyang |4 oth | |
| 700 | 1 | |a Zhang, Yue |4 oth | |
| 700 | 1 | |a Pan, Zihao |4 oth | |
| 700 | 1 | |a Zhang, Wei |4 oth | |
| 700 | 1 | |a Yao, Huochun |4 oth | |
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| 773 | 1 | 8 | |g volume:115 |g year:2017 |g pages:109-116 |
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