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
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
148875Informations 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.