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Innate immune crosstalk in asthmatic airways: innate lymphoid cells coordinate the polarization of lung macrophage.
Journal of Allergy and Clinical Immunology 2018 November 9
BACKGROUND: Recent studies have emphasized the role of innate lymphoid cells (ILCs) in the development of asthma. The involvement of group 2 ILCs (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 the patients with asthma, especially their effect on the polarization of macrophages.
METHODS: Each subset of ILCs and macrophages in induced sputum from 51 steroid-naïve asthma patients and 18 healthy donors analyzed by flow cytometry. To determine whether the polarization of macrophages could be regulated by ILCs, alveolar macrophages (AM) were sorted; and co-cultured with each subset of ILCs.
RESULTS: In addition to ILC2s, ILC1s and ILC3s were increased in the induced sputum from asthmatics when compared with the healthy controls. The dominance of macrophages in induced sputum was more prominent in asthmatics than healthy controls. A positive correlation between ILC2s and M2 macrophages and that of ILC1s/ILC3s and M1 macrophages observed. Co-culture of ILC2s with AMs induced the expression of M2 macrophage-related genes, whereas co-culture of ILC1s and ILC3s with AMs induced the expression of M1 macrophage-related genes via cytokine secretion as well as cell-cell contact. According to the inflammatory signature, patients with eosinophilic asthma have more ILC2s and M2 macrophages while those with non-eosinophilic asthma present are M1 macrophages dominant profile.
CONCLUSION: A different subset of ILCs regulates the polarization of macrophages, contributing to developing the distinct phenotype of asthma.
OBJECTIVE: This study aims to understand the role of various ILCs in the patients with asthma, especially their effect on the polarization of macrophages.
METHODS: Each subset of ILCs and macrophages in induced sputum from 51 steroid-naïve asthma patients and 18 healthy donors analyzed by flow cytometry. To determine whether the polarization of macrophages could be regulated by ILCs, alveolar macrophages (AM) were sorted; and co-cultured with each subset of ILCs.
RESULTS: In addition to ILC2s, ILC1s and ILC3s were increased in the induced sputum from asthmatics when compared with the healthy controls. The dominance of macrophages in induced sputum was more prominent in asthmatics than healthy controls. A positive correlation between ILC2s and M2 macrophages and that of ILC1s/ILC3s and M1 macrophages observed. Co-culture of ILC2s with AMs induced the expression of M2 macrophage-related genes, whereas co-culture of ILC1s and ILC3s with AMs induced the expression of M1 macrophage-related genes via cytokine secretion as well as cell-cell contact. According to the inflammatory signature, patients with eosinophilic asthma have more ILC2s and M2 macrophages while those with non-eosinophilic asthma present are M1 macrophages dominant profile.
CONCLUSION: A different subset of ILCs regulates the polarization of macrophages, contributing to developing the distinct phenotype of asthma.
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