Phase Variation in HMW1A Controls a Phenotypic Switch in Haemophilus influenzae Associated with Pathoadaptation during Persistent Infection.
Haemophilus influenzae
allelic variant
biofilm
chronic obstructive pulmonary disease (COPD)
epithelial hyperinvasion
high-molecular-weight (HMW)
lifestyle switch
pathoadaptation
persistence
phase variation
Journal
mBio
ISSN: 2150-7511
Titre abrégé: mBio
Pays: United States
ID NLM: 101519231
Informations de publication
Date de publication:
29 06 2021
29 06 2021
Historique:
pubmed:
23
6
2021
medline:
12
11
2021
entrez:
22
6
2021
Statut:
ppublish
Résumé
Genetic variants arising from within-patient evolution shed light on bacterial adaptation during chronic infection. Contingency loci generate high levels of genetic variation in bacterial genomes, enabling adaptation to the stringent selective pressures exerted by the host. A significant gap in our understanding of phase-variable contingency loci is the extent of their contribution to natural infections. The human-adapted pathogen nontypeable Haemophilus influenzae (NTHi) causes persistent infections, which contribute to underlying disease progression. The phase-variable high-molecular-weight (HMW) adhesins located on the NTHi surface mediate adherence to respiratory epithelial cells and, depending on the allelic variant, can also confer high epithelial invasiveness or hyperinvasion. In this study, we characterize the dynamics of HMW-mediated hyperinvasion in living cells and identify a specific HMW binding domain shared by hyperinvasive NTHi isolates of distinct pathological origins. Moreover, we observed that HMW expression decreased over time by using a longitudinal set of persistent NTHi strains collected from chronic obstructive pulmonary disease (COPD) patients, resulting from increased numbers of simple-sequence repeats (SSRs) downstream of the functional P2
Identifiants
pubmed: 34154422
doi: 10.1128/mBio.00789-21
pmc: PMC8262952
doi:
Substances chimiques
Adhesins, Bacterial
0
HMW1 protein, bacteria
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0078921Subventions
Organisme : NIDCD NIH HHS
ID : R01 DC002148
Pays : United States
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