TLR7-dependent eosinophil degranulation links psoriatic skin inflammation to small intestinal inflammatory changes in mice
TLR7
DOI:
10.1038/s12276-024-01225-y
Publication Date:
2024-05-01T01:02:00Z
AUTHORS (14)
ABSTRACT
Recent evidence of gut microbiota dysbiosis in the context psoriasis and increased cooccurrence inflammatory bowel disease suggest a close relationship between skin immune responses. Using mouse model induced by Toll-like receptor (TLR) 7 ligand imiquimod, we found that psoriatic dermatitis was accompanied changes small intestine associated with eosinophil degranulation, which impaired intestinal barrier integrity. Inflammatory responses were mice prone to degranulation. Caco-2 human epithelial cells treated media containing granule proteins exhibited signs inflammation damage. Imiquimod-induced attenuated eosinophil-deficient mice, this attenuation counteracted transfer eosinophils. Imiquimod levels distribution eosinophils positively correlated intestine. TLR7-deficient did not exhibit degranulation but following imiquimod administration. These results TLR7-dependent bidirectional skin-to-gut communication occurs can accelerate psoriasis.
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