PloS one, 2016-07, Vol.11 (7), p.e0159539-e0159539
2016
Details
- Autor(en) / Beteiligte
- Titel
- Intestinal Microbiota Promotes Psoriasis-Like Skin Inflammation by Enhancing Th17 Response
- Ist Teil von
- PloS one, 2016-07, Vol.11 (7), p.e0159539-e0159539
- Ort / Verlag
- United States: Public Library of Science
- Erscheinungsjahr
- 2016
- Link zum Volltext
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- 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.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1932-6203eISSN: 1932-6203DOI: 10.1371/journal.pone.0159539Titel-ID: cdi_plos_journals_1805485515
- Format
- –
- Schlagworte
- Acne, Actinobacteria - drug effects, Actinobacteria - physiology, Aminoquinolines - pharmacology, Animal experimentation, Animal models, Animals, Anti-Bacterial Agents - pharmacology, Antibiotics, Arthritis, Bacteria, Biology and Life Sciences, Clostridiales, Clostridiales - drug effects, Clostridiales - physiology, Dermatology, Digestive system, Digestive tract, Disease Models, Animal, Dosage and administration, Drinking water, Drug therapy, Experiments, Female, Gastrointestinal Microbiome - drug effects, Gastrointestinal Microbiome - physiology, Gene Expression, Germ-Free Life, Germfree, Health aspects, Helper cells, Humans, Imiquimod, Immune system, Inflammation, Inflammatory bowel disease, Inflammatory diseases, Interleukin-17 - genetics, Interleukin-17 - immunology, Intestinal microflora, Intestine, Lactobacillales - drug effects, Lactobacillales - physiology, Lesions, Lymphocyte Activation - drug effects, Lymphocytes, Lymphocytes T, Medical research, Medicine and Health Sciences, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Microbiota, Microbiota (Symbiotic organisms), Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics, Nuclear Receptor Subfamily 1, Group F, Member 3 - immunology, Probiotics, Psoriasis, Psoriasis - chemically induced, Psoriasis - immunology, Psoriasis - microbiology, Psoriasis - pathology, Receptors, Antigen, T-Cell, gamma-delta - genetics, Receptors, Antigen, T-Cell, gamma-delta - immunology, Research and Analysis Methods, Risk factors, Rosacea, Skin - drug effects, Skin - immunology, Skin - microbiology, Skin - pathology, Skin diseases, Skin resistance, Species Specificity, Systems development, Th17 Cells - drug effects, Th17 Cells - immunology, Th17 Cells - microbiology