Innate immune crosstalk in asthmatic airways: Innate lymphoid cells coordinate polarization of lung macrophages.


Journal

The Journal of allergy and clinical immunology
ISSN: 1097-6825
Titre abrégé: J Allergy Clin Immunol
Pays: United States
ID NLM: 1275002

Informations de publication

Date de publication:
05 2019
Historique:
received: 15 03 2018
revised: 21 09 2018
accepted: 09 10 2018
pubmed: 12 11 2018
medline: 12 5 2020
entrez: 12 11 2018
Statut: ppublish

Résumé

Recent studies have emphasized the role of innate lymphoid cells (ILCs) in the development of asthma. The involvement of group 2 innate lymphoid cells (ILC2s) in asthma is well studied: however, the participation of other types of ILCs in the development of asthma remains unclear. This study aims to understand the role of various ILCs in patients with asthma, especially their effect on macrophage polarization. Each subset of ILCs and macrophages in induced sputum from 51 steroid-naive patients with asthma and 18 healthy donors was analyzed by using flow cytometry. Alveolar macrophages (AM) were sorted and cocultured with each subset of ILCs to determine whether the polarization of macrophages could be regulated by ILCs. In addition to ILC2s, numbers of group 1 innate lymphoid cells (ILC1s) and group 3 innate lymphoid cells (ILC3s) were increased in induced sputum from asthmatic patients when compared with those in healthy control subjects. The dominance of macrophages in induced sputum was more prominent in asthmatic patients than in healthy control subjects. A positive correlation between numbers of ILC2s and numbers of M2 macrophages and those of ILC1s/ILC3s and M1 macrophages was observed. Coculture of ILC2s with AMs induced expression of M2 macrophage-related genes, whereas coculture of ILC1s and ILC3s with AMs induced expression of M1 macrophage-related genes through cytokine secretion, as well as cell-cell contact. According to the inflammatory signature, patients with eosinophilic asthma have more ILC2s and M2 macrophages, and those with noneosinophilic asthma have an M1 macrophage-dominant profile. A different subset of ILCs regulates macrophage polarization, contributing to developing the distinct phenotype of asthma.

Sections du résumé

BACKGROUND
Recent studies have emphasized the role of innate lymphoid cells (ILCs) in the development of asthma. The involvement of group 2 innate lymphoid cells (ILC2s) in asthma is well studied: however, the participation of other types of ILCs in the development of asthma remains unclear.
OBJECTIVE
This study aims to understand the role of various ILCs in patients with asthma, especially their effect on macrophage polarization.
METHODS
Each subset of ILCs and macrophages in induced sputum from 51 steroid-naive patients with asthma and 18 healthy donors was analyzed by using flow cytometry. Alveolar macrophages (AM) were sorted and cocultured with each subset of ILCs to determine whether the polarization of macrophages could be regulated by ILCs.
RESULTS
In addition to ILC2s, numbers of group 1 innate lymphoid cells (ILC1s) and group 3 innate lymphoid cells (ILC3s) were increased in induced sputum from asthmatic patients when compared with those in healthy control subjects. The dominance of macrophages in induced sputum was more prominent in asthmatic patients than in healthy control subjects. A positive correlation between numbers of ILC2s and numbers of M2 macrophages and those of ILC1s/ILC3s and M1 macrophages was observed. Coculture of ILC2s with AMs induced expression of M2 macrophage-related genes, whereas coculture of ILC1s and ILC3s with AMs induced expression of M1 macrophage-related genes through cytokine secretion, as well as cell-cell contact. According to the inflammatory signature, patients with eosinophilic asthma have more ILC2s and M2 macrophages, and those with noneosinophilic asthma have an M1 macrophage-dominant profile.
CONCLUSION
A different subset of ILCs regulates macrophage polarization, contributing to developing the distinct phenotype of asthma.

Identifiants

pubmed: 30414858
pii: S0091-6749(18)31582-3
doi: 10.1016/j.jaci.2018.10.040
pii:
doi:

Substances chimiques

Cytokines 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1769-1782.e11

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2018 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.

Auteurs

Jihyun Kim (J)

Laboratory of Mucosal Immunology in the Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.

Yuna Chang (Y)

Laboratory of Mucosal Immunology in the Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.

Boram Bae (B)

Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, Korea.

Kyoung-Hee Sohn (KH)

Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, Korea; Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.

Sang-Heon Cho (SH)

Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, Korea; Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.

Doo Hyun Chung (DH)

Department of Pathology, Seoul National University College of Medicine, Seoul, Korea; Laboratory of Immune Regulation in the Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.

Hye Ryun Kang (HR)

Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, Korea; Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea. Electronic address: helenmed@snu.ac.kr.

Hye Young Kim (HY)

Laboratory of Mucosal Immunology in the Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea; Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, Korea. Electronic address: hykim11@snu.ac.kr.

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