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Published on: March 1, 2024
Crucial Role of Microbiota in Experimental Psoriasis Revealed by a Gnotobiotic Mouse Model
Zuzana Stehlikova1,2, Klara Kostovcikova1,3, Miloslav Kverka1,4
1Institute of Microbiology of the Czech Academy of Sciences, v.v.i., Prague, Czechia.
Abstract:
Psoriatic patients have altered microbiota, both in the intestine and on the skin. It is not clear, however, whether this is a cause or consequence of the disease. In this study, using an experimental mouse model of psoriasis induced by imiquimod (IMQ), we show that oral treatment with a broad spectrum of antibiotics (MIX) or metronidazole (MET) alone mitigates the severity of skin inflammation through downregulation of Th17 immune response in conventional mice. Since some antibiotics, including MET, can influence immune system reactivity, we also evaluated the effect of MIX in the same model under germ-free (GF) conditions. GF mice treated with MET did not show milder signs of imiquimod-induced skin inflammation (IISI) which supports the conclusion that the therapeutic effect is mediated by changes in microbiota composition. Moreover, compared to controls, mice treated with MIX had a significantly higher abundance of the genus Lactobacillus in the intestine and on the skin. Mice treated with MET had a significantly higher abundance of the genera Bifidobacterium and Enterococcus both on the skin and in the intestine and of Parabacteroides distasonis in the intestine. Additionally, GF mice and mice monocolonized with either Lactobacillus plantarum or segmented filamentous bacteria (SFB) were more resistant to IISI than conventional mice. Interestingly, compared to GF mice, IMQ induced a higher degree of systemic Th17 activation in mice monocolonized with SFB but not with L. plantarum. The present findings provide evidence that intestinal and skin microbiota directly regulates IISI and emphasizes the importance of microbiota in the pathogenesis of psoriasis.
Insights
Altering gut and skin microbiota with antibiotics reduced psoriasis severity in mice. Specific bacteria like Lactobacillus and Bifidobacterium showed increased abundance, suggesting microbiota
Area of Science:
- Microbiology
- Immunology
- Dermatology
Background:
- Psoriatic patients exhibit altered intestinal and skin microbiota, but causality remains unclear.
- The role of microbiota in the pathogenesis of imiquimod-induced skin inflammation (IISI) requires further investigation.
Purpose of the Study:
- To investigate the causal role of gut and skin microbiota in the development of experimental psoriasis.
- To determine the impact of antibiotic-induced microbiota modulation on skin inflammation and immune responses.
Main Methods:
- Utilized a mouse model of psoriasis induced by imiquimod (IMQ).
- Administered broad-spectrum antibiotics (MIX) or metronidazole (MET) orally to conventional and germ-free (GF) mice.
- Assessed skin inflammation severity, Th17 immune response, and microbial composition (intestinal and skin).
Main Results:
- Antibiotic treatment (MIX or MET) mitigated skin inflammation in conventional mice by downregulating Th17 responses.
- Therapeutic effects were microbiota-dependent, as MET did not alleviate inflammation in germ-free mice.
- Specific bacterial genera (Lactobacillus, Bifidobacterium, Enterococcus, Parabacteroides distasonis) increased with antibiotic treatment.
- Germ-free mice and those colonized with Lactobacillus plantarum or segmented filamentous bacteria (SFB) showed resistance to IISI.
- SFB colonization, but not L. plantarum, enhanced systemic Th17 activation compared to GF mice.
Conclusions:
- Intestinal and skin microbiota directly regulate imiquimod-induced skin inflammation (IISI).
- The findings highlight the critical role of microbiota composition in psoriasis pathogenesis.
- Targeting specific microbial communities may offer therapeutic strategies for psoriasis.
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