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• W2896571328 abstract "Chemoattractant receptor homologous with T-helper cell type 2 cells (CRTH2), a receptor for prostaglandin D2, is preferentially expressed on T-helper cell type 2 lymphocytes, group 2 innate lymphoid cells, eosinophils, and basophils, and elicits the production of type 2 cytokines, including profibrotic IL-13. We hypothesized that lack of CRTH2 might protect against fibrotic lung disease, and we tested this hypothesis using a bleomycin-induced lung inflammation and fibrosis model in CRTH2-deficient (CRTH2-/-) or wild-type BALB/c mice. Compared with wild-type mice, CRTH2-/- mice treated with bleomycin exhibited significantly higher mortality, enhanced accumulation of inflammatory cells 14-21 days after bleomycin injection, reduced pulmonary compliance, and increased levels of collagen and total protein in the lungs. These phenotypes were associated with decreased levels of IFN-γ, IL-6, IL-10, and IL-17A in BAL fluid. Adoptive transfer of splenocytes from wild-type, but not CRTH2-/-, mice 2 days before injection of bleomycin resolved the sustained inflammation as well as the increased collagen and protein accumulation in the lungs of CRTH2-/- mice. We consider that the disease model is driven by γδT cells that express CRTH2; thus, the adoptive transfer of γδT cells could ameliorate bleomycin-induced alveolar inflammation and fibrosis." @default.
• W2896571328 created "2018-10-26" @default.
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• W2896571328 date "2019-03-01" @default.
• W2896571328 modified "2023-10-18" @default.
• W2896571328 title "Deficiency of CRTH2, a Prostaglandin D₂ Receptor, Aggravates Bleomycin-induced Pulmonary Inflammation and Fibrosis" @default.
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• W2896571328 doi "https://doi.org/10.1165/rcmb.2017-0397oc" @default.
• W2896571328 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30326727" @default.
• W2896571328 hasPublicationYear "2019" @default.
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