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• W2783626024 abstract "Abstract The TLR4 co-receptor CD14 was identified as an IBD candidate gene. Here, its influence on the intestinal barrier was addressed utilizing E. coli Nissle (EcN), which induces severe inflammation in germfree TLR4 −/− mice. After monoassociation, EcN was detected in spleens and livers of TLR4 −/− and CD14 −/− but not wildtype mice. Barrier impairment was characterized by increased apoptosis and decreased epithelial junction (EJ) expression and was reversed by TLR2 stimulation in CD14 −/− mice. Bone marrow (BM) transplantation revealed contribution of hematopoietic and non-hematopoietic cells towards intestinal homeostasis. EcN inoculated WT mice showed B cell activation, CD14 −/− and TLR4 −/− mice cytotoxic T cell and impaired B cell responses. The latter was characterized by absence of B cells in TLR4 −/− mice, decreased levels of EcN induced immunoglobulins and downregulation of their transporter pIgR. EcN colonization of mice with genetically or antibody induced impaired B cell response resulted in dissemination of EcN and downregulation of EJ. BM chimeras indicated that CD14 originating from radiation resistant cells is sufficient to restore EJ-function. Overall, CD14/TLR4 signalling seems to be critical for intestinal barrier function and for the crosstalk between B cells and the epithelium, underlining that CD14 serves as a protective modulator of intestinal homeostasis." @default.
• W2783626024 created "2018-01-26" @default.
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• W2783626024 date "2018-01-15" @default.
• W2783626024 modified "2023-10-13" @default.
• W2783626024 title "Loss of CD14 leads to disturbed epithelial-B cell crosstalk and impairment of the intestinal barrier after E. coli Nissle monoassociation" @default.
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• W2783626024 doi "https://doi.org/10.1038/s41598-017-19062-7" @default.
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