The C. difficile clnRAB operon initiates adaptations to the host environment in response to LL-37.
PLoS Pathog
; 14(8): e1007153, 2018 08.
Article
em En
| MEDLINE
| ID: mdl-30125334
ABSTRACT
To cause disease, Clostridioides (Clostridium) difficile must resist killing by innate immune effectors in the intestine, including the host antimicrobial peptide, cathelicidin (LL-37). The mechanisms that enable C. difficile to adapt to the intestine in the presence of antimicrobial peptides are unknown. Expression analyses revealed an operon, CD630_16170-CD630_16190 (clnRAB), which is highly induced by LL-37 and is not expressed in response to other cell-surface active antimicrobials. This operon encodes a predicted transcriptional regulator (ClnR) and an ABC transporter system (ClnAB), all of which are required for function. Analyses of a clnR mutant indicate that ClnR is a pleiotropic regulator that directly binds to LL-37 and controls expression of numerous genes, including many involved in metabolism, cellular transport, signaling, gene regulation, and pathogenesis. The data suggest that ClnRAB is a novel regulatory mechanism that senses LL-37 as a host signal and regulates gene expression to adapt to the host intestinal environment during infection.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Óperon
/
Adaptação Fisiológica
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Regulação Bacteriana da Expressão Gênica
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Clostridioides difficile
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Evasão da Resposta Imune
Limite:
Animals
Idioma:
En
Revista:
PLoS Pathog
Ano de publicação:
2018
Tipo de documento:
Article
País de afiliação:
Estados Unidos