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- W4313351688 abstract "Abstract Resident alveolar macrophages (rAM) play an important regulatory role in limiting excessive inflammatory responses in the respiratory tract. In a mouse model of allergic asthma we identified a new autofluohigh CD11c+ CD11b+ DEC205+ F4/80+ rAM population residing in the airways following the clearance of a prior allergic bronchial inflammation. Compared to naïve rAM, post-inflammation rAM feature a reduced basal phagocytosis along with an increased in vitro inflammatory response to LPS. Especially genes dependent for expression on the MyD88-independent signaling pathway and the type I interferon, IFN-β, showed strongly increased expression levels compared to the naïve rAM. A preferential enhancement of MyD88-independent signaling in post-inflammation rAM was also observed after in vivo LPS-challenge and resulted in a differential response pattern to TLR-3 and TLR-7 ligands. Using CD45 chimeric mice and intratracheal instilled fluorescent microparticles to distinguish resident from elicited AM, we observed a rapid and near complete disappearance of naïve rAM during allergen challenges. Furthermore, we showed that this inflammation-induced rAM turnover is a crucial event in the development of the post-inflammation rAM phenotype. This novel mechanism of innate imprinting may contribute to the increased sensitivity of the post-inflammation lung to inflammatory insults." @default.
- W4313351688 created "2023-01-06" @default.
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- W4313351688 date "2011-04-01" @default.
- W4313351688 modified "2023-09-30" @default.
- W4313351688 title "Innate imprinting of resident alveolar macrophages by a preceding allergic bronchial inflammation increases the inflammatory TLR-reactivity through an enhanced MyD88-independent signaling and the type I interferon, IFN-β. (55.5)" @default.
- W4313351688 doi "https://doi.org/10.4049/jimmunol.186.supp.55.5" @default.
- W4313351688 hasPublicationYear "2011" @default.
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