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

0464813 - MBÚ 2017 RIV US eng J - Článek v odborném periodiku
Zákostelská, Zuzana - Málková, Jana - Klimešová, Klára - Rossmann, Pavel - Hornová, Michaela - Novosádová, Iva - Stehlíková, Zuzana - Kostovčík, Martin - Hudcovic, Tomáš - Štěpánková, Renata - Jůzlová, K. - Herzogová, J. - Tlaskalová-Hogenová, Helena - Kverka, Miloslav
Intestinal Microbiota Promotes Psoriasis-Like Skin Inflammation by Enhancing Th17 Response.
PLoS ONE. Roč. 11, č. 7 (2016), s. 0159539. ISSN 1932-6203. E-ISSN 1932-6203
Grant CEP: GA MZd(CZ) NV15-30782A; GA MŠMT(CZ) ED1.1.00/02.0109; GA ČR(CZ) GAP303/12/0535
Institucionální podpora: RVO:61388971
Klíčová slova: ALTERED GUT MICROBIOTA * DELTA T-CELLS * BACTERIAL OVERGROWTH
Kód oboru RIV: EE - Mikrobiologie, virologie
Impakt faktor: 2.806, rok: 2016

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.
Trvalý link: http://hdl.handle.net/11104/0263742