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Quantification of Innate Lymphoid Cell Subsets in a Mouse Model of Chronic Obstructive Pulmonary Disease
Description
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A4757 - Quantification of Innate Lymphoid Cell Subsets in a Mouse Model of Chronic Obstructive Pulmonary Disease
Author Block: E. Blomme, S. Provoost, K. R. Bracke, G. F. Joos, G. G. Brusselle, T. Maes, Laboratory for Translational Research in Obstructive Pulmonary Diseases; Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium.
Rationale
Innate lymphoid cells (ILCs) are tissue-resident immune cells that participate in many physiological processes. Three main subsets can be distinguished, namely ILC1, ILC2 and ILC3. Upon activation, ILCs proliferate and secrete effector cytokines, such as IFNγ by ILC1 and IL-17 by ILC3. We hypothesize that ILCs contribute to the pathogenesis of chronic obstructive pulmonary disease (COPD). Therefore, we investigated whether the number and cytokine production of mouse pulmonary ILCs was altered upon (sub)acute cigarette smoke (CS) exposure.
Methods
Wild type C57BL/6 mice were exposed to air or cigarette smoke for 5 consecutive days (acute) or for 4 weeks (subacute). ILC subsets in lung tissue and bronchoalveolar lavage (BAL) were discriminated by flow cytometry using several surface markers and transcription factors. For investigating ILC cytokine production, BAL cells were stimulated ex vivo with phorbol myristate acetate/ionomycin, followed by intracellular cytokine staining and flow cytometry.
Results
CS exposure induced a neutrophilic inflammatory response. All BAL ILC subsets (CD45+, Lin-, CD90+), i.e. ST2+ ILC2, RORγt+ ILC3 and T-BET+ ILC1, increased significantly in the smoking group at both time points. Percentage and total cell numbers of IFNγ+ ILCs and IL-17+ ILCs were significantly elevated in BAL of CS-exposed mice compared to air-exposed mice after 4 weeks. No double-positive IL-17+/IFNγ+ cells were observed within the ILC population. In lung tissue, no difference was seen in ILC numbers between air-exposed and CS-exposed mice.
Conclusion
CS exposure in mice increases the number of all ILC subsets in BAL. In addition, CS exposure increases the number of IFNγ or IL-17-producing ILCs in BAL, indicative for increased activation of ILC1 and ILC3.
Author Block: E. Blomme, S. Provoost, K. R. Bracke, G. F. Joos, G. G. Brusselle, T. Maes, Laboratory for Translational Research in Obstructive Pulmonary Diseases; Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium.
Rationale
Innate lymphoid cells (ILCs) are tissue-resident immune cells that participate in many physiological processes. Three main subsets can be distinguished, namely ILC1, ILC2 and ILC3. Upon activation, ILCs proliferate and secrete effector cytokines, such as IFNγ by ILC1 and IL-17 by ILC3. We hypothesize that ILCs contribute to the pathogenesis of chronic obstructive pulmonary disease (COPD). Therefore, we investigated whether the number and cytokine production of mouse pulmonary ILCs was altered upon (sub)acute cigarette smoke (CS) exposure.
Methods
Wild type C57BL/6 mice were exposed to air or cigarette smoke for 5 consecutive days (acute) or for 4 weeks (subacute). ILC subsets in lung tissue and bronchoalveolar lavage (BAL) were discriminated by flow cytometry using several surface markers and transcription factors. For investigating ILC cytokine production, BAL cells were stimulated ex vivo with phorbol myristate acetate/ionomycin, followed by intracellular cytokine staining and flow cytometry.
Results
CS exposure induced a neutrophilic inflammatory response. All BAL ILC subsets (CD45+, Lin-, CD90+), i.e. ST2+ ILC2, RORγt+ ILC3 and T-BET+ ILC1, increased significantly in the smoking group at both time points. Percentage and total cell numbers of IFNγ+ ILCs and IL-17+ ILCs were significantly elevated in BAL of CS-exposed mice compared to air-exposed mice after 4 weeks. No double-positive IL-17+/IFNγ+ cells were observed within the ILC population. In lung tissue, no difference was seen in ILC numbers between air-exposed and CS-exposed mice.
Conclusion
CS exposure in mice increases the number of all ILC subsets in BAL. In addition, CS exposure increases the number of IFNγ or IL-17-producing ILCs in BAL, indicative for increased activation of ILC1 and ILC3.
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