title: Intestinal Microbiota Promotes Psoriasis-Like Skin Inflammation by Enhancing Th17 Response.
abstract: 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.
authors.affiliation: Institute of Microbiology of the Czech Academy of Sciences, v.v.i., Prague, Czech Republic.
authors.forename: Zuzana
authors.initials: Z
authors.lastname: Zákostelská
authors.affiliation: Institute of Microbiology of the Czech Academy of Sciences, v.v.i., Prague, Czech Republic.
authors.forename: Jana
authors.initials: J
authors.lastname: Málková
authors.affiliation: Institute of Microbiology of the Czech Academy of Sciences, v.v.i., Prague, Czech Republic.|Institute of Molecular Genetics of the Czech Academy of Sciences, v.v.i., Prague, Czech Republic.
authors.forename: Klára
authors.initials: K
authors.lastname: Klimešová
authors.affiliation: Institute of Microbiology of the Czech Academy of Sciences, v.v.i., Prague, Czech Republic.
authors.forename: Pavel
authors.initials: P
authors.lastname: Rossmann
authors.affiliation: Institute of Microbiology of the Czech Academy of Sciences, v.v.i., Prague, Czech Republic.
authors.forename: Michaela
authors.initials: M
authors.lastname: Hornová
authors.affiliation: Institute of Microbiology of the Czech Academy of Sciences, v.v.i., Prague, Czech Republic.
authors.forename: Iva
authors.initials: I
authors.lastname: Novosádová
authors.affiliation: Institute of Microbiology of the Czech Academy of Sciences, v.v.i., Prague, Czech Republic.
authors.forename: Zuzana
authors.initials: Z
authors.lastname: Stehlíková
authors.affiliation: Institute of Microbiology of the Czech Academy of Sciences, v.v.i., Prague, Czech Republic.
authors.forename: Martin
authors.initials: M
authors.lastname: Kostovčík
authors.affiliation: Institute of Microbiology of the Czech Academy of Sciences, v.v.i., Nový Hrádek, Czech Republic.
authors.forename: Tomáš
authors.initials: T
authors.lastname: Hudcovic
authors.affiliation: Institute of Microbiology of the Czech Academy of Sciences, v.v.i., Nový Hrádek, Czech Republic.
authors.forename: Renata
authors.initials: R
authors.lastname: Štepánková
authors.affiliation: Department of Dermatology, 2nd Medical Faculty, Charles University in Prague and Bulovka Hospital, Prague, Czech Republic.
authors.forename: Kateřina
authors.initials: K
authors.lastname: Jůzlová
authors.affiliation: Department of Dermatology, 2nd Medical Faculty, Charles University in Prague and Bulovka Hospital, Prague, Czech Republic.
authors.forename: Jana
authors.initials: J
authors.lastname: Hercogová
authors.affiliation: Institute of Microbiology of the Czech Academy of Sciences, v.v.i., Prague, Czech Republic.
authors.forename: Helena
authors.initials: H
authors.lastname: Tlaskalová-Hogenová
authors.affiliation: Institute of Microbiology of the Czech Academy of Sciences, v.v.i., Prague, Czech Republic.|Institute of Experimental Medicine of the Czech Academy of Sciences, v.v.i., Prague, Czech Republic.
authors.forename: Miloslav
authors.identifier: http://orcid.org/0000-0002-1335-5252
authors.initials: M
authors.lastname: Kverka
mesh_terms: D039903:Actinobacteria / Q000187:drug effects / Q000502:physiology; D000634:Aminoquinolines / Q000494:pharmacology; D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D000068016:Eubacteriales / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D005260:Female; D000069196:Gastrointestinal Microbiome / Q000187:drug effects / Q000502:physiology*; D015870:Gene Expression; D005856:Germ-Free Life; D006801:Humans; D000077271:Imiquimod; D020381:Interleukin-17 / Q000235:genetics / Q000276:immunology; D056546:Lactobacillales / Q000187:drug effects / Q000502:physiology; D008213:Lymphocyte Activation / Q000187:drug effects; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000235:genetics / Q000276:immunology; D011565:Psoriasis / Q000139:chemically induced / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000235:genetics / Q000276:immunology; D012867:Skin / Q000187:drug effects / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D013045:Species Specificity; D058504:Th17 Cells / Q000187:drug effects / Q000276:immunology* / Q000382:microbiology
chemical_list: D000634:Aminoquinolines; D000900:Anti-Bacterial Agents; D020381:Interleukin-17; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D016692:Receptors, Antigen, T-Cell, gamma-delta; C539901:Rorc protein, mouse; D000077271:Imiquimod