Colitis-Induced Th17 Cells Increase the Risk for Severe Subsequent Clostridium difficile Infection.
Cell Host Microbe
; 25(5): 756-765.e5, 2019 May 08.
Article
en En
| MEDLINE
| ID: mdl-31003940
ABSTRACT
Clostridium difficile infection (CDI) is the number one hospital-acquired infection in the United States. CDI is more common and severe in inflammatory bowel disease patients. Here, we studied the mechanism by which prior colitis exacerbates CDI. Mice were given dextran sulfate sodium (DSS) colitis, recovered for 2 weeks, and then were infected with C. difficile. Mortality and CDI severity were increased in DSS-treated mice compared to controls. Severe CDI is dependent on CD4+ T cells, which persist after colitis-associated inflammation subsides. Adoptive transfer of Th17 cells to naive mice is sufficient to increase CDI-associated mortality through elevated IL-17 production. Finally, in humans, the Th17 cytokines IL-6 and IL-23 associate with severe CDI, and patients with high serum IL-6 are 7.6 times more likely to die post infection. These findings establish a central role for Th17 cells in CDI pathogenesis following colitis and identify them as a potential target for preventing severe disease.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Clostridioides difficile
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Infecciones por Clostridium
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Colitis
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Susceptibilidad a Enfermedades
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Células Th17
Tipo de estudio:
Etiology_studies
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Prognostic_studies
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Risk_factors_studies
Límite:
Adolescent
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Adult
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Aged
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Animals
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Child
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
Cell Host Microbe
Asunto de la revista:
MICROBIOLOGIA
Año:
2019
Tipo del documento:
Article
País de afiliación:
Estados Unidos