Transcriptomic Analysis and High-dimensional Phenotypic Mapping of Mononuclear Phagocytes in Mesenteric Lymph Nodes Reveal Differences Between Ulcerative Colitis and Crohn's Disease.


Journal

Journal of Crohn's & colitis
ISSN: 1876-4479
Titre abrégé: J Crohns Colitis
Pays: England
ID NLM: 101318676

Informations de publication

Date de publication:
13 Mar 2020
Historique:
pubmed: 22 9 2019
medline: 5 1 2021
entrez: 22 9 2019
Statut: ppublish

Résumé

Crohn's disease [CD] and ulcerative colitis [UC] are distinct forms of inflammatory bowel disease. Heterogeneity of HLA-DR+SIRPα + mononuclear phagocytes [MNPs], including macrophages [MΦ], monocyte-derived [Mono] cells, and dendritic cells [DCs], was reported in gut tissue but not yet investigated in mesenteric lymph nodes [MLNs] of IBD patients. We here compared the phenotype, function, and molecular profile of HLA-DR+SIRPα + MNPs in CD and UC MLNs. Cell distribution, morphology, immune function, and transcriptomic [bulk RNAseq] and high-dimensional protein expression profiles [CyTOF] of HLA-DR+SIRPα + MNPs were examined in MLNs of UC [n = 14], CD [n = 35], and non-IBD [n = 12] patients. Elevated frequencies of CD14+CD64+CD163+ [Mono/MΦ-like] MNPs displaying monocyte/MΦ morphology and phagocytic function were a distinct feature of UC MLNs. In CD, the proportion of CD14-CD64-CD163- [DC-like] cells was augmented relative to Mono/MΦ-like cells; DC-like cells drove naïve T cell proliferation, Th1 polarisation, and Th17 TCM plasticity. Gene expression profile corroborated the nature of DC-like cells, best represented by BTLA, SERPINF, IGJ and, of Mono/MΦ-like cells, defined by CD163, MARCO, MAFB, CD300E, S100A9 expression. CyTOF analysis showed that CD123+ plasmacytoid cells predominated over conventional DCs in DC-like cells. Four CD163+ clusters were revealed in Mono/MΦ-like cells, two of which were enriched in MARCO-CD68dimHLA-DRdim monocyte-like cells and MARCOhiCD68hiHLA-DRhi Mɸ, whose proportion increased in UC relative to CD. Defining the landscape of MNPs in MLNs provided evidence for expansion of CD163+ Mono/MΦ-like cells in UC only, highlighting a distinction between UC and CD, and thus the potential contribution of monocyte-like cells in driving colitis.

Sections du résumé

BACKGROUND AND AIMS OBJECTIVE
Crohn's disease [CD] and ulcerative colitis [UC] are distinct forms of inflammatory bowel disease. Heterogeneity of HLA-DR+SIRPα + mononuclear phagocytes [MNPs], including macrophages [MΦ], monocyte-derived [Mono] cells, and dendritic cells [DCs], was reported in gut tissue but not yet investigated in mesenteric lymph nodes [MLNs] of IBD patients. We here compared the phenotype, function, and molecular profile of HLA-DR+SIRPα + MNPs in CD and UC MLNs.
METHODS METHODS
Cell distribution, morphology, immune function, and transcriptomic [bulk RNAseq] and high-dimensional protein expression profiles [CyTOF] of HLA-DR+SIRPα + MNPs were examined in MLNs of UC [n = 14], CD [n = 35], and non-IBD [n = 12] patients.
RESULTS RESULTS
Elevated frequencies of CD14+CD64+CD163+ [Mono/MΦ-like] MNPs displaying monocyte/MΦ morphology and phagocytic function were a distinct feature of UC MLNs. In CD, the proportion of CD14-CD64-CD163- [DC-like] cells was augmented relative to Mono/MΦ-like cells; DC-like cells drove naïve T cell proliferation, Th1 polarisation, and Th17 TCM plasticity. Gene expression profile corroborated the nature of DC-like cells, best represented by BTLA, SERPINF, IGJ and, of Mono/MΦ-like cells, defined by CD163, MARCO, MAFB, CD300E, S100A9 expression. CyTOF analysis showed that CD123+ plasmacytoid cells predominated over conventional DCs in DC-like cells. Four CD163+ clusters were revealed in Mono/MΦ-like cells, two of which were enriched in MARCO-CD68dimHLA-DRdim monocyte-like cells and MARCOhiCD68hiHLA-DRhi Mɸ, whose proportion increased in UC relative to CD.
CONCLUSIONS CONCLUSIONS
Defining the landscape of MNPs in MLNs provided evidence for expansion of CD163+ Mono/MΦ-like cells in UC only, highlighting a distinction between UC and CD, and thus the potential contribution of monocyte-like cells in driving colitis.

Identifiants

pubmed: 31541232
pii: 5572419
doi: 10.1093/ecco-jcc/jjz156
pmc: PMC7068244
doi:

Substances chimiques

Antigens, CD 0
Antigens, Differentiation, Myelomonocytic 0
CD163 antigen 0
Lipopolysaccharide Receptors 0
Receptors, Cell Surface 0
Receptors, IgG 0
Receptors, Scavenger 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

393-405

Informations de copyright

Copyright © 2019 European Crohn’s and Colitis Organisation (ECCO). Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.

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Auteurs

Laurence Chapuy (L)

Immunoregulation Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal [CRCHUM], Montréal, QC, Canada.

Marwa Bsat (M)

Immunoregulation Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal [CRCHUM], Montréal, QC, Canada.

Manuel Rubio (M)

Immunoregulation Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal [CRCHUM], Montréal, QC, Canada.

François Harvey (F)

Department of Biomedical Informatics, Centre de Recherche du Centre Hospitalier de l'Université de Montréal [CRCHUM], Montréal, QC, Canada.

Vinicius Motta (V)

McGill Goodman Research Center, McGill University, Montréal, QC, Canada.

Frank Schwenter (F)

Digestive Surgery Department, Centre Hospitalier de l'Université de Montréal [CHUM], Montréal, QC, Canada.

Ramses Wassef (R)

Digestive Surgery Department, Centre Hospitalier de l'Université de Montréal [CHUM], Montréal, QC, Canada.

Carole Richard (C)

Digestive Surgery Department, Centre Hospitalier de l'Université de Montréal [CHUM], Montréal, QC, Canada.

Colette Deslandres (C)

Division of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, CHU Sainte-Justine, Université de Montreal, QC, Canada.

Bich N Nguyen (BN)

Pathology Department, Centre Hospitalier de l'Université de Montréal [CHUM], Montréal, QC, Canada.

Geneviève Soucy (G)

Pathology Department, Centre Hospitalier de l'Université de Montréal [CHUM], Montréal, QC, Canada.

Nir Hacohen (N)

Broad Institute of MIT and Harvard, Cambridge, MA USA.

Jorge Fritz (J)

Department of Microbiology and Immunology, McGill University, Montréal, Qc, Canada.

Alexandra-Chloé Villani (AC)

Broad Institute of MIT and Harvard, Cambridge, MA USA.
Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, MA, USA.

Heena Mehta (H)

Immunoregulation Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal [CRCHUM], Montréal, QC, Canada.

Marika Sarfati (M)

Immunoregulation Laboratory, Centre de Recherche du Centre Hospitalier de l'Université de Montréal [CRCHUM], Montréal, QC, Canada.

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