Imperial College London
Alternate

ProfessorPaulLangford

Faculty of Medicine, Department of Infectious Disease

Professor of Paediatric Infectious Diseases
 
 
 
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Contact

 

+44 (0)20 7594 3359p.langford Website

 
 
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Location

 

236Wright Fleming WingSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{Zhang:2022:10.1128/iai.00239-22,
author = {Zhang, Q and Tang, H and Yan, C and Han, W and Peng, L and Xu, J and Chen, X and Langford, PR and Bei, W and Huang, Q and Zhou, R and Li, L},
doi = {10.1128/iai.00239-22},
journal = {Infection and Immunity},
pages = {1--17},
title = {The metabolic adaptation in response to nitrate Is critical for Actinobacillus pleuropneumoniae growth and pathogenicity under the regulation of NarQ/P},
url = {http://dx.doi.org/10.1128/iai.00239-22},
volume = {90},
year = {2022}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Nitrate metabolism is an adaptation mechanism used by many bacteria for survival in anaerobic environments. As a by-product of inflammation, nitrate is used by the intestinal bacterial pathogens to enable gut infection. However, the responses of bacterial respiratory pathogens to nitrate are less well understood. Actinobacillus pleuropneumoniae is an important bacterial respiratory pathogen of swine. Previous studies have suggested that adaptation of A. pleuropneumoniae to anaerobiosis is important for infection. In this work, A. pleuropneumoniae growth and pathogenesis in response to the nitrate were investigated. Nitrate significantly promoted A. pleuropneumoniae growth under anaerobic conditions in vitro and lethality in mice. By using narQ and narP deletion mutants and single-residue-mutated complementary strains of ΔnarQ, the two-component system NarQ/P was confirmed to be critical for nitrate-induced growth, with Arg50 in NarQ as an essential functional residue. Transcriptome analysis showed that nitrate upregulated multiple energy-generating pathways, including nitrate metabolism, mannose and pentose metabolism, and glycerolipid metabolism via the regulation of NarQ/P. Furthermore, narQ, narP, and its target gene encoding the nitrate reductase Nap contributed to the pathogenicity of A. pleuropneumoniae. The Nap inhibitor tungstate significantly reduced the survival of A. pleuropneumoniae in vivo, suggesting that Nap is a potential drug target. These results give new insights into how the respiratory pathogen A. pleuropneumoniae utilizes the alternative electron acceptor nitrate to overcome the hypoxia microenvironment, which can occur in the inflammatory or necrotic infected tissues.
AU  - Zhang,Q
AU  - Tang,H
AU  - Yan,C
AU  - Han,W
AU  - Peng,L
AU  - Xu,J
AU  - Chen,X
AU  - Langford,PR
AU  - Bei,W
AU  - Huang,Q
AU  - Zhou,R
AU  - Li,L
DO  - 10.1128/iai.00239-22
EP  - 17
PY  - 2022///
SN  - 0019-9567
SP  - 1
TI  - The metabolic adaptation in response to nitrate Is critical for Actinobacillus pleuropneumoniae growth and pathogenicity under the regulation of NarQ/P
T2  - Infection and Immunity
UR  - http://dx.doi.org/10.1128/iai.00239-22
UR  - https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000838140000001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - https://journals.asm.org/doi/10.1128/iai.00239-22
UR  - http://hdl.handle.net/10044/1/102228
VL  - 90
ER  -
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