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• W3036229056 abstract "Background & Aims Intestinal epithelial cells (IECs) provide a barrier that separates the mucosal immune system from the luminal microbiota. IECs constitutively express low levels of major histocompatibility complex (MHC) class II proteins, which are upregulated upon exposure to interferon gamma. We investigated the effects of deleting MHCII proteins specifically in mice with infectious, dextran sodium sulfate (DSS)–, and T-cell–induced colitis. Methods We disrupted the histocompatibility 2, class II antigen A, beta 1 gene (H2-Ab1) in IECs of C57BL/6 mice (I-AbΔIEC) or Rag1–/– mice (Rag1–/–I-AbΔIEC); we used I-AbWT mice as controls. Colitis was induced by administration of DSS, transfer of CD4+CD45RBhi T cells, or infection with Citrobacter rodentium. Colon tissues were collected and analyzed by histology, immunofluorescence, xMAP, and reverse-transcription polymerase chain reaction and organoids were generated. Microbiota (total and immunoglobulin [Ig]A-coated) in intestinal samples were analyzed by16S amplicon profiling. IgA+CD138+ plasma cells from Peyer’s patches and lamina propria were analyzed by flow cytometry and IgA repertoire was determined by next-generation sequencing. Results Mice with IEC-specific loss of MHCII (I-AbΔIEC mice) developed less severe DSS- or T-cell transfer-induced colitis than control mice. Intestinal tissues from I-AbΔIEC mice had a lower proportion of IgA-coated bacteria compared with control mice, and a reduced luminal concentration of secretory IgA (SIgA) following infection with C rodentium. There was no significant difference in the mucosal IgA repertoire of I-AbΔIEC vs control mice, but opsonization of cultured C rodentium by SIgA isolated from I-AbΔIEC mice was 50% lower than that of SIgA from mAbWT mice. Fifty percent of I-AbΔIEC mice died after infection with C rodentium, compared with none of the control mice. We observed a transient but significant expansion of the pathogen in the feces of I-AbΔIEC mice compared with I-AbWT mice. Conclusions In mice with DSS or T-cell–induced colitis, loss of MHCII from IECs reduces but does not eliminate mucosal inflammation. However, in mice with C rodentium–induced colitis, loss of MHCII reduces bacterial clearance by decreasing binding of IgA to commensal and pathogenic bacteria. Intestinal epithelial cells (IECs) provide a barrier that separates the mucosal immune system from the luminal microbiota. IECs constitutively express low levels of major histocompatibility complex (MHC) class II proteins, which are upregulated upon exposure to interferon gamma. We investigated the effects of deleting MHCII proteins specifically in mice with infectious, dextran sodium sulfate (DSS)–, and T-cell–induced colitis. We disrupted the histocompatibility 2, class II antigen A, beta 1 gene (H2-Ab1) in IECs of C57BL/6 mice (I-AbΔIEC) or Rag1–/– mice (Rag1–/–I-AbΔIEC); we used I-AbWT mice as controls. Colitis was induced by administration of DSS, transfer of CD4+CD45RBhi T cells, or infection with Citrobacter rodentium. Colon tissues were collected and analyzed by histology, immunofluorescence, xMAP, and reverse-transcription polymerase chain reaction and organoids were generated. Microbiota (total and immunoglobulin [Ig]A-coated) in intestinal samples were analyzed by16S amplicon profiling. IgA+CD138+ plasma cells from Peyer’s patches and lamina propria were analyzed by flow cytometry and IgA repertoire was determined by next-generation sequencing. Mice with IEC-specific loss of MHCII (I-AbΔIEC mice) developed less severe DSS- or T-cell transfer-induced colitis than control mice. Intestinal tissues from I-AbΔIEC mice had a lower proportion of IgA-coated bacteria compared with control mice, and a reduced luminal concentration of secretory IgA (SIgA) following infection with C rodentium. There was no significant difference in the mucosal IgA repertoire of I-AbΔIEC vs control mice, but opsonization of cultured C rodentium by SIgA isolated from I-AbΔIEC mice was 50% lower than that of SIgA from mAbWT mice. Fifty percent of I-AbΔIEC mice died after infection with C rodentium, compared with none of the control mice. We observed a transient but significant expansion of the pathogen in the feces of I-AbΔIEC mice compared with I-AbWT mice. In mice with DSS or T-cell–induced colitis, loss of MHCII from IECs reduces but does not eliminate mucosal inflammation. However, in mice with C rodentium–induced colitis, loss of MHCII reduces bacterial clearance by decreasing binding of IgA to commensal and pathogenic bacteria." @default.
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• W3036229056 date "2020-10-01" @default.
• W3036229056 modified "2023-10-16" @default.
• W3036229056 title "Intestinal Epithelial Expression of MHCII Determines Severity of Chemical, T-Cell–Induced, and Infectious Colitis in Mice" @default.
• W3036229056 cites W113692232 @default.
• W3036229056 cites W1490919365 @default.
• W3036229056 cites W1578055160 @default.
• W3036229056 cites W1582329765 @default.
• W3036229056 cites W1885357042 @default.
• W3036229056 cites W1905496140 @default.
• W3036229056 cites W1967197195 @default.
• W3036229056 cites W1971279134 @default.
• W3036229056 cites W1979217507 @default.
• W3036229056 cites W1979475230 @default.
• W3036229056 cites W1980180441 @default.
• W3036229056 cites W1980343829 @default.
• W3036229056 cites W1984492299 @default.
• W3036229056 cites W1986005204 @default.
• W3036229056 cites W1994568522 @default.
• W3036229056 cites W2011006768 @default.
• W3036229056 cites W2011910303 @default.
• W3036229056 cites W2016948044 @default.
• W3036229056 cites W2018422387 @default.
• W3036229056 cites W2024164044 @default.
• W3036229056 cites W2024346860 @default.
• W3036229056 cites W2034285706 @default.
• W3036229056 cites W2035664677 @default.
• W3036229056 cites W2036125357 @default.
• W3036229056 cites W2055403920 @default.
• W3036229056 cites W2057044648 @default.
• W3036229056 cites W2068066862 @default.
• W3036229056 cites W2070834379 @default.
• W3036229056 cites W2084201164 @default.
• W3036229056 cites W2107066107 @default.
• W3036229056 cites W2111572119 @default.
• W3036229056 cites W2128743925 @default.
• W3036229056 cites W2134342374 @default.
• W3036229056 cites W2151558930 @default.
• W3036229056 cites W2166171121 @default.
• W3036229056 cites W2167269580 @default.
• W3036229056 cites W2169046908 @default.
• W3036229056 cites W2169355315 @default.
• W3036229056 cites W2170333722 @default.
• W3036229056 cites W2171045789 @default.
• W3036229056 cites W2174345167 @default.
• W3036229056 cites W2273601982 @default.
• W3036229056 cites W2291829437 @default.
• W3036229056 cites W2316161204 @default.
• W3036229056 cites W2342314812 @default.
• W3036229056 cites W2401404581 @default.
• W3036229056 cites W2408135904 @default.
• W3036229056 cites W2413669734 @default.
• W3036229056 cites W2604811621 @default.
• W3036229056 cites W2883466739 @default.
• W3036229056 cites W2888687530 @default.
• W3036229056 cites W2893091879 @default.
• W3036229056 cites W2899352054 @default.
• W3036229056 cites W2947508095 @default.
• W3036229056 cites W2973682581 @default.
• W3036229056 cites W2988261311 @default.
• W3036229056 doi "https://doi.org/10.1053/j.gastro.2020.06.049" @default.
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