Matches in SemOpenAlex for { <https://semopenalex.org/work/W2007579654> ?p ?o ?g. }
- W2007579654 endingPage "1288.e2" @default.
- W2007579654 startingPage "1278" @default.
- W2007579654 abstract "Background & AimsReduced generation of all-trans retinoic acid (RA) by CD103+ intestinal dendritic cells (DCs) is linked to intestinal inflammation in mice. However, the role of RA in intestinal inflammation in humans is unclear. We investigated which antigen-presenting cells (APCs) produce RA in the human intestine and whether generation of RA is reduced in patients with Crohn's disease (CD).MethodsIleal and colonic tissues were collected from patients with CD during endoscopy or surgery, and healthy tissues were collected from subjects who were undergoing follow-up because of rectal bleeding, altered bowel habits, or cancer (controls). Cells were isolated from the tissue samples, and APCs were isolated by flow cytometry. Retinaldehyde dehydrogenase (RALDH) activity was assessed by Aldefluor assay, and ALDH1A expression was measured by quantitative real-time polymerase chain reaction. Macrophages were derived by incubation of human blood monocytes with granulocyte-macrophage colony–stimulating factor (GM-CSF).ResultsCD103+ and CD103− DCs and CD14+ macrophages from healthy human intestine had RALDH activity. Although ALDH1A1 was not expressed by DCs, it was the predominant RALDH enzyme isoform expressed by intestinal CD14+ macrophages and their putative precursors, CD14+ monocytes. RALDH activity was up-regulated in all 3 populations of APCs from patients with CD; in CD14+ macrophages, it was associated with local induction of ALDH1A1 expression. Blocking of RA receptor signaling during GM-CSF–mediated differentiation of monocytes into macrophages down-regulated CD14 and HLA-DR expression and reduced the development of tumor necrosis factor α–producing inflammatory macrophages.ConclusionsRA receptor signaling promotes differentiation of human tumor necrosis factor α–producing inflammatory macrophages in vitro. In vivo, more CD14+ macrophages from the intestinal mucosa of patients with CD than from controls are capable of generating RA, which might increase the inflammatory phenotype of these cells. Strategies to reduce the generation of RA by CD14+ macrophages could provide new therapeutic options for patients with CD. Reduced generation of all-trans retinoic acid (RA) by CD103+ intestinal dendritic cells (DCs) is linked to intestinal inflammation in mice. However, the role of RA in intestinal inflammation in humans is unclear. We investigated which antigen-presenting cells (APCs) produce RA in the human intestine and whether generation of RA is reduced in patients with Crohn's disease (CD). Ileal and colonic tissues were collected from patients with CD during endoscopy or surgery, and healthy tissues were collected from subjects who were undergoing follow-up because of rectal bleeding, altered bowel habits, or cancer (controls). Cells were isolated from the tissue samples, and APCs were isolated by flow cytometry. Retinaldehyde dehydrogenase (RALDH) activity was assessed by Aldefluor assay, and ALDH1A expression was measured by quantitative real-time polymerase chain reaction. Macrophages were derived by incubation of human blood monocytes with granulocyte-macrophage colony–stimulating factor (GM-CSF). CD103+ and CD103− DCs and CD14+ macrophages from healthy human intestine had RALDH activity. Although ALDH1A1 was not expressed by DCs, it was the predominant RALDH enzyme isoform expressed by intestinal CD14+ macrophages and their putative precursors, CD14+ monocytes. RALDH activity was up-regulated in all 3 populations of APCs from patients with CD; in CD14+ macrophages, it was associated with local induction of ALDH1A1 expression. Blocking of RA receptor signaling during GM-CSF–mediated differentiation of monocytes into macrophages down-regulated CD14 and HLA-DR expression and reduced the development of tumor necrosis factor α–producing inflammatory macrophages. RA receptor signaling promotes differentiation of human tumor necrosis factor α–producing inflammatory macrophages in vitro. In vivo, more CD14+ macrophages from the intestinal mucosa of patients with CD than from controls are capable of generating RA, which might increase the inflammatory phenotype of these cells. Strategies to reduce the generation of RA by CD14+ macrophages could provide new therapeutic options for patients with CD." @default.
- W2007579654 created "2016-06-24" @default.
- W2007579654 creator A5021652535 @default.
- W2007579654 creator A5050579181 @default.
- W2007579654 creator A5055734737 @default.
- W2007579654 creator A5061019212 @default.
- W2007579654 creator A5062418600 @default.
- W2007579654 creator A5073349527 @default.
- W2007579654 creator A5075419127 @default.
- W2007579654 creator A5079489754 @default.
- W2007579654 date "2014-05-01" @default.
- W2007579654 modified "2023-10-01" @default.
- W2007579654 title "Increased Production of Retinoic Acid by Intestinal Macrophages Contributes to Their Inflammatory Phenotype in Patients With Crohn's Disease" @default.
- W2007579654 cites W1579553066 @default.
- W2007579654 cites W1965256830 @default.
- W2007579654 cites W1967369695 @default.
- W2007579654 cites W1967949491 @default.
- W2007579654 cites W1968138311 @default.
- W2007579654 cites W1984378291 @default.
- W2007579654 cites W1988712793 @default.
- W2007579654 cites W1991072797 @default.
- W2007579654 cites W1991579347 @default.
- W2007579654 cites W1994107743 @default.
- W2007579654 cites W1995535600 @default.
- W2007579654 cites W2006044429 @default.
- W2007579654 cites W2008859777 @default.
- W2007579654 cites W2010011171 @default.
- W2007579654 cites W2012428888 @default.
- W2007579654 cites W2016525543 @default.
- W2007579654 cites W2029686125 @default.
- W2007579654 cites W2031551895 @default.
- W2007579654 cites W2033119740 @default.
- W2007579654 cites W2037259928 @default.
- W2007579654 cites W2040307290 @default.
- W2007579654 cites W2044286043 @default.
- W2007579654 cites W2055641051 @default.
- W2007579654 cites W2070111160 @default.
- W2007579654 cites W2092488865 @default.
- W2007579654 cites W2094979669 @default.
- W2007579654 cites W2101875461 @default.
- W2007579654 cites W2102293117 @default.
- W2007579654 cites W2104299175 @default.
- W2007579654 cites W2105221079 @default.
- W2007579654 cites W2107631420 @default.
- W2007579654 cites W2108244474 @default.
- W2007579654 cites W2110178990 @default.
- W2007579654 cites W2110957620 @default.
- W2007579654 cites W2115138114 @default.
- W2007579654 cites W2123129546 @default.
- W2007579654 cites W2126000068 @default.
- W2007579654 cites W2127035465 @default.
- W2007579654 cites W2129284543 @default.
- W2007579654 cites W2134422149 @default.
- W2007579654 cites W2139972156 @default.
- W2007579654 cites W2141083396 @default.
- W2007579654 cites W2144836936 @default.
- W2007579654 cites W2150781849 @default.
- W2007579654 cites W2161722835 @default.
- W2007579654 cites W2171898230 @default.
- W2007579654 cites W4234615218 @default.
- W2007579654 doi "https://doi.org/10.1053/j.gastro.2014.01.057" @default.
- W2007579654 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24503130" @default.
- W2007579654 hasPublicationYear "2014" @default.
- W2007579654 type Work @default.
- W2007579654 sameAs 2007579654 @default.
- W2007579654 citedByCount "71" @default.
- W2007579654 countsByYear W20075796542014 @default.
- W2007579654 countsByYear W20075796542015 @default.
- W2007579654 countsByYear W20075796542016 @default.
- W2007579654 countsByYear W20075796542017 @default.
- W2007579654 countsByYear W20075796542018 @default.
- W2007579654 countsByYear W20075796542019 @default.
- W2007579654 countsByYear W20075796542020 @default.
- W2007579654 countsByYear W20075796542021 @default.
- W2007579654 countsByYear W20075796542022 @default.
- W2007579654 countsByYear W20075796542023 @default.
- W2007579654 crossrefType "journal-article" @default.
- W2007579654 hasAuthorship W2007579654A5021652535 @default.
- W2007579654 hasAuthorship W2007579654A5050579181 @default.
- W2007579654 hasAuthorship W2007579654A5055734737 @default.
- W2007579654 hasAuthorship W2007579654A5061019212 @default.
- W2007579654 hasAuthorship W2007579654A5062418600 @default.
- W2007579654 hasAuthorship W2007579654A5073349527 @default.
- W2007579654 hasAuthorship W2007579654A5075419127 @default.
- W2007579654 hasAuthorship W2007579654A5079489754 @default.
- W2007579654 hasBestOaLocation W20075796541 @default.
- W2007579654 hasConcept C126322002 @default.
- W2007579654 hasConcept C17991360 @default.
- W2007579654 hasConcept C202751555 @default.
- W2007579654 hasConcept C203014093 @default.
- W2007579654 hasConcept C2776914184 @default.
- W2007579654 hasConcept C2777478134 @default.
- W2007579654 hasConcept C2778260677 @default.
- W2007579654 hasConcept C2778513237 @default.
- W2007579654 hasConcept C2778690821 @default.
- W2007579654 hasConcept C2779134260 @default.
- W2007579654 hasConcept C2779244956 @default.
- W2007579654 hasConcept C2781121885 @default.