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Intestinal Microbiota Promotes Psoriasis-Like Skin Inflammation by Enhancing Th17 Response

Psoriasis is a chronic inflammatory skin disease in which Th17 cells play a crucial role. Since indigenous gut microbiota influences the development and reactivity of immune cells, we analyzed the link among microbiota, T cells and the formation of psoriatic lesions in the imiquimod-induced murine m...

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Detalles Bibliográficos
Autores principales: Zákostelská, Zuzana, Málková, Jana, Klimešová, Klára, Rossmann, Pavel, Hornová, Michaela, Novosádová, Iva, Stehlíková, Zuzana, Kostovčík, Martin, Hudcovic, Tomáš, Štepánková, Renata, Jůzlová, Kateřina, Hercogová, Jana, Tlaskalová-Hogenová, Helena, Kverka, Miloslav
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4951142/
https://www.ncbi.nlm.nih.gov/pubmed/27434104
http://dx.doi.org/10.1371/journal.pone.0159539
Descripción
Sumario:Psoriasis is a chronic inflammatory skin disease in which Th17 cells play a crucial role. Since indigenous gut microbiota influences the development and reactivity of immune cells, we analyzed the link among microbiota, T cells and the formation of psoriatic lesions in the imiquimod-induced murine model of psoriasis. To explore the role of microbiota, we induced skin inflammation in germ-free (GF), broad-spectrum antibiotic (ATB)-treated or conventional (CV) BALB/c and C57BL/6 mice. We found that both mice reared in GF conditions for several generations and CV mice treated with ATB were more resistant to imiquimod-induced skin inflammation than CV mice. The ATB treatment dramatically changed the diversity of gut bacteria, which remained stable after subsequent imiquimod application; ATB treatment resulted in a substantial increase in the order Lactobacillales and a significant decrease in Coriobacteriales and Clostridiales. Moreover, as compared to CV mice, imiquimod induced a lower degree of local and systemic Th17 activation in both GF and ATB-treated mice. These findings suggest that gut microbiota control imiquimod-induced skin inflammation by altering the T cell response.