Canine skin microbiota and allergies
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB25078 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Associations between canine skin microbiota, environment and allergies
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Project description:The maintenance of tissue-specific chronic inflammation results from the interplay of genetic and unidentified environmental factors. Here, we describe an immunoregulatory role for an environmentally driven microbial metabolite in Card14E138A/+-induced spontaneous psoriasis. Through metabolite screening, we demonstrate chronic skin inflammation is accompanied by alterations microbial metabolite. Notably, depletion of gut, not skin, microbes alleviates disease symptoms. We further identify indoxyl sulfate (I3S), a bacteriogenic metabolite, as a key driver of psoriatic inflammation and confirm that gut-resident indole-producing microbiota mediate this process. Mechanistically, indole-producing microbiota promote host I3S biothsynthesis via a metabolic relay, and I3S potentiates skin inflammation by reshaping chromatin accessibility in skin Th17 cells through AHR signaling. In human psoriasis cohorts, serum I3S levels correlate with disease severit. In summary, our study uncovers a mechanistic link between gut microbial factors and type 3 skin inflammation, highlighting targeting gut microbiota as a strategy for mitigating skin inflammation.
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Project description:Transcriptomic profiling of sheep skin lymph DC subsets after 16h in vitro culture in medium or stimulated by non replicative Canine Adenovirus serotype 2 Reference design: total enriched lymph dendritic cells- Biological replicates: 4 sheep (70958, 50274, 30066, 11261)- Samples: FACS sorted CD103 -type and CD11b type cultured in medium or with CAV2
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Project description:Host symbiosis with its microbiota can represent a liability for the host. Indeed, while these communities of microbes broadly control host physiology, the microbiota can also promote inflammation and represent a source of local and systemic infection. The unique strategies employed by each tissue to maintain and control coexistence with commensal microbes remain largely unclear. Here we uncover that, within the skin, host protection from its microbiota depends on the remarkable ability of the skin to act as an autonomous lymphoid organ. Notably, an encounter with a new skin microbe is associated with two parallel responses both, under the control of Langerhans cells. On one hand, skin commensal promotes the development of classical germinal centers within secondary lymphoid organs leading to IgG1 and IgG3 responses. On the other hand, microbial colonization also leads to the development of tertiary lymphoid organs that can locally sustain and mature IgG2b and IgG2c responses. The ability of the skin to develop as a lymphoid compartment is at least in part mediated by the ability of the local Treg pool to convert into T follicular helper cells accumulating within organized tertiary lymphoid organs surrounding the hair follicles. Remarkably, skin autonomous production of antibodies is sufficient to control both microbial colonization within the skin as well as subsequent infection with the same commensal. Collectively these results reveal a profound compartmentalization of humoral responses between the lymph nodes and the skin. Further, this work uncovers a previously unappreciated function for the skin as a compartment able to develop, in the absence of inflammation, powerful and long-lived antibody responses independently of secondary lymphoid organs.
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