Host-Protozoan Interactions Protect from Mucosal Infections through Activation of the Inflammasome
While conventional pathogenic protists have been extensively studied, there is an underappreciated constitutive protist microbiota that is an integral part of the vertebrate microbiome. The impact of these species on the host and their potential contributions to mucosal immune homeostasis remain poo...
- Autores:
- Tipo de recurso:
- Fecha de publicación:
- 2016
- Institución:
- Universidad del Rosario
- Repositorio:
- Repositorio EdocUR - U. Rosario
- Idioma:
- eng
- OAI Identifier:
- oai:repository.urosario.edu.co:10336/24790
- Acceso en línea:
- https://doi.org/10.1016/j.cell.2016.08.076
https://repository.urosario.edu.co/handle/10336/24790
- Palabra clave:
- Animals
Colitis
Dientamoeba
Host-Parasite Interactions
Immunity
Mucosal
Inflammasomes
Interleukin-18
Intestinal Mucosa
Mice
Mice
Inbred C57BL
Microbiota
Salmonella Infections
Salmonella typhimurium
Symbiosis
Th1 Cells
Th17 Cells
Trichomonas
Trichomonas Infections
- Rights
- License
- Abierto (Texto Completo)
Summary: | While conventional pathogenic protists have been extensively studied, there is an underappreciated constitutive protist microbiota that is an integral part of the vertebrate microbiome. The impact of these species on the host and their potential contributions to mucosal immune homeostasis remain poorly studied. Here, we show that the protozoan Tritrichomonas musculis activates the host epithelial inflammasome to induce IL-18 release. Epithelialderived IL-18 promotes dendritic cell-driven Th1 and Th17 immunity and confers dramatic protection from mucosal bacterial infections. Along with its role as a protistic'' antibiotic, colonization with T. musculis exacerbates the development of T-cell-driven colitis and sporadic colorectal tumors. Our findings demonstrate a novel mutualistic host-protozoan interaction that increases mucosal host defenses at the cost of an increased risk of inflammatory disease. |
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