A Bordetella pertussis MgtC homolog plays a role in the intracellular survival
Jazyk angličtina Země Spojené státy americké Médium electronic-ecollection
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
30161230
PubMed Central
PMC6117051
DOI
10.1371/journal.pone.0203204
PII: PONE-D-18-10137
Knihovny.cz E-zdroje
- MeSH
- bakteriální proteiny genetika metabolismus MeSH
- Bordetella pertussis účinky léků genetika růst a vývoj metabolismus MeSH
- Escherichia coli MeSH
- hořčík metabolismus MeSH
- inhibitory enzymů farmakologie MeSH
- kationty dvojmocné metabolismus MeSH
- koncentrace vodíkových iontů MeSH
- lidé MeSH
- makrofágy účinky léků mikrobiologie patologie MeSH
- makrolidy farmakologie MeSH
- mutace MeSH
- sekvenční homologie aminokyselin MeSH
- THP-1 buňky MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- bafilomycin A1 MeSH Prohlížeč
- bakteriální proteiny MeSH
- hořčík MeSH
- inhibitory enzymů MeSH
- kationty dvojmocné MeSH
- makrolidy MeSH
Bordetella pertussis, the causative agent of whooping cough, has the capability to survive inside the host cells. This process requires efficient adaptation of the pathogen to the intracellular environment and the associated stress. Among the proteins produced by the intracellular B. pertussis we identified a protein (BP0414) that shares homology with MgtC, a protein which was previously shown to be involved in the intracellular survival of other pathogens. To explore if BP0414 plays a role in B. pertussis intracellular survival a mutant strain defective in the production of this protein was constructed. Using standard in vitro growth conditions we found that BP0414 is required for B. pertussis growth under low magnesium availability or low pH, two environmental conditions that this pathogen might face within the host cell. Intracellular survival studies showed that MgtC is indeed involved in B. pertussis viability inside the macrophages. The use of bafilomycin A1, which inhibits phagosome acidification, abolished the survival defect of the mgtC deficient mutant strain suggesting that in intracellular B. pertussis the role of MgtC protein is mainly related to the bacterial adaptation to the acidic conditions found inside the of phagosomes. Overall, this work provides an insight into the importance of MgtC in B. pertussis pathogenesis and its contribution to bacterial survival within immune cells.
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