Intestinal Microbiota Promotes Psoriasis-Like Skin Inflammation by Enhancing Th17 Response.
Zákostelská Z, Málková J, Klimešová K, Rossmann P, Hornová M, Novosádová I, Stehlíková Z, Kostovčík M, Hudcovic T, Štepánková R, Jůzlová K, Hercogová J, Tlaskalová-Hogenová H, Kverka M
PLoS One. 2016. doi: 10.1371/journal.pone.0159539
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.