Two HbpA-like proteins HbpA1 and HbpA2 from Actinobacillus pleuropneumoniae protect bacteria from sulfur source limitation, oxidative and cold stresses, but not essential to virulence.

Actinobacillus pleuropneumoniae GSH utilization HbpA1 HbpA2 Stress tolerance Virulence

Journal

Gene
ISSN: 1879-0038
Titre abrégé: Gene
Pays: Netherlands
ID NLM: 7706761

Informations de publication

Date de publication:
20 Aug 2024
Historique:
received: 20 05 2024
revised: 24 07 2024
accepted: 19 08 2024
medline: 23 8 2024
pubmed: 23 8 2024
entrez: 22 8 2024
Statut: aheadofprint

Résumé

Porcine pleuropneumonia is one of the respiratory diseases that pigs are susceptible to Actinobacillus pleuropneumoniae (A. pleuropneumoniae), poses a great threat to the global pig industry. Glutathione (GSH) is an important sulfur source, cellular antioxidant and virulence determinant of many pathogenic bacteria. In this study, roles of two HbpA-like proteins HbpA1 and HbpA2 of A. pleuropneumoniae were analyzed. A. pleuropneumoniae mutants without HbpA2 were basically unable to grow in chemically defined medium (CDM) with GSH as the sole sulfur source and had significantly reduced oxidative tolerance; whereas mutation in hbpA1 led to reduced survival under low-temperature environments. Neither HbpA1 nor HbpA2 affects utilization of heme. These two HbpA-like proteins are not associated with the virulence of A. pleuropneumoniae. Our results reveal the correlation of A. pleuropneumoniae HbpA1 and HbpA2 in GSH utilization, highlight the roles of HbpA1 in the cold stress resistance and HbpA2 in the anti-oxidative response. GSH limitation is not a way to attenuate colonization and pathogenicity of A. pleuropneumoniae.

Identifiants

pubmed: 39173979
pii: S0378-1119(24)00756-X
doi: 10.1016/j.gene.2024.148875
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

148875

Informations de copyright

Copyright © 2024. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Miao Zhang (M)

Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, Hubei 430079, China.

Zhuo Li (Z)

Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, Hubei 430079, China.

Hanwen Hu (H)

Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, Hubei 430079, China.

Jinlin Liu (J)

Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, Hubei 430079, China. Electronic address: liujinlin2009@126.com.

Chao Qi (C)

Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, Hubei 430079, China. Electronic address: qichao@mail.ccnu.edu.cn.

Classifications MeSH