Innate Myeloid Cell Subset-Specific Gene Expression Patterns in the Human Colon are Altered in Crohn's Disease Patients.


Journal

Digestion
ISSN: 1421-9867
Titre abrégé: Digestion
Pays: Switzerland
ID NLM: 0150472

Informations de publication

Date de publication:
2019
Historique:
received: 19 03 2018
accepted: 12 06 2018
pubmed: 22 10 2018
medline: 27 8 2019
entrez: 22 10 2018
Statut: ppublish

Résumé

There is a heterogeneous subset innate myeloid cells, such as macrophages and dendritic cells, in the human intestinal lamina propria. Several studies have demonstrated that these cells contribute to the maintenance of gut homeostasis through the induction of inflammatory responses and tolerance via cell type-specific mechanisms; whereas, disrupted innate immune responses are implicated in the pathogenesis of Crohn's disease (CD). However, the detailed mechanisms by which each innate myeloid subset regulates gut homeostasis and inflammation largely remain unknown. We aimed to clarify the comprehensive gene expression profiles of innate myeloid cell -subsets in the lamina propria from normal human colons (NC) and the inflamed colon sites from patients with Crohn's disease (CDi). We performed RNA-sequencing analysis and precise bioinformatics analysis on 3 innate myeloid cell subsets, CD14-CD11c-, CD14-CD11c+, and CD14+CD11c+CD163low cells from NC and CDi. Transcriptional analysis of the 3 subsets from the NC showed distinct gene expression patterns and gene ontology (GO) enrichment analysis revealed the associated innate myeloid subset-specific biological process (BP) terms. In addition, changes in gene expression patterns were observed in innate myeloid subsets from CDi. Furthermore, the core GO-BP terms for the genes upregulated in the innate myeloid cells from CDi were distinct from those found in NC. Our data identified the innate myeloid cell subset-specific transcriptomes and the associated enriched GO-BP terms in the NC and found these patterns were altered in CDi.

Sections du résumé

BACKGROUND/AIMS OBJECTIVE
There is a heterogeneous subset innate myeloid cells, such as macrophages and dendritic cells, in the human intestinal lamina propria. Several studies have demonstrated that these cells contribute to the maintenance of gut homeostasis through the induction of inflammatory responses and tolerance via cell type-specific mechanisms; whereas, disrupted innate immune responses are implicated in the pathogenesis of Crohn's disease (CD). However, the detailed mechanisms by which each innate myeloid subset regulates gut homeostasis and inflammation largely remain unknown. We aimed to clarify the comprehensive gene expression profiles of innate myeloid cell -subsets in the lamina propria from normal human colons (NC) and the inflamed colon sites from patients with Crohn's disease (CDi).
METHODS METHODS
We performed RNA-sequencing analysis and precise bioinformatics analysis on 3 innate myeloid cell subsets, CD14-CD11c-, CD14-CD11c+, and CD14+CD11c+CD163low cells from NC and CDi.
RESULTS RESULTS
Transcriptional analysis of the 3 subsets from the NC showed distinct gene expression patterns and gene ontology (GO) enrichment analysis revealed the associated innate myeloid subset-specific biological process (BP) terms. In addition, changes in gene expression patterns were observed in innate myeloid subsets from CDi. Furthermore, the core GO-BP terms for the genes upregulated in the innate myeloid cells from CDi were distinct from those found in NC.
CONCLUSION CONCLUSIONS
Our data identified the innate myeloid cell subset-specific transcriptomes and the associated enriched GO-BP terms in the NC and found these patterns were altered in CDi.

Identifiants

pubmed: 30343293
pii: 000490890
doi: 10.1159/000490890
doi:

Types de publication

Journal Article

Langues

eng

Pagination

194-204

Informations de copyright

© 2018 S. Karger AG, Basel.

Auteurs

Yuki Sekido (Y)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.

Yoshiaki Yasumizu (Y)

Department of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita, Japan.

Junichi Nishimura (J)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan, jnishimura@gesurg.med.osaka-u.ac.jp.
Department of Gastroenterological Surgery, Osaka International Cancer Institute, Osaka, Japan, jnishimura@gesurg.med.osaka-u.ac.jp.

Hisako Kayama (H)

Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Suita, Japan.
Laboratory of Mucosal Immunology, Immunology Frontier Research Center, Osaka University, Suita, Japan.
Core Research for Evolutional Science and Technology, Japan Agency for Medical Research and Development, Tokyo, Japan.

Hiroshi Matsuno (H)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.

Takayuki Ogino (T)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.

Norikatsu Miyoshi (N)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.

Hidekazu Takahashi (H)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.

Naotsugu Haraguchi (N)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.

Taishi Hata (T)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.

Chu Matsuda (C)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.

Yuichiro Doki (Y)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.

Masaki Mori (M)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.

Kiyoshi Takeda (K)

Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Suita, Japan.
Laboratory of Mucosal Immunology, Immunology Frontier Research Center, Osaka University, Suita, Japan.
Core Research for Evolutional Science and Technology, Japan Agency for Medical Research and Development, Tokyo, Japan.

Naganari Ohkura (N)

Department of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita, Japan.

Shimon Sakaguchi (S)

Department of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita, Japan.

Tsunekazu Mizushima (T)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.
Department of Therapeutics for Inflammatory Bowel Diseases, Graduate School of Medicine, Osaka University, Suita, Japan.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH