Journal
JOURNAL OF LEUKOCYTE BIOLOGY
Volume 105, Issue 1, Pages 143-150Publisher
WILEY
DOI: 10.1002/JLB.3AB0518-178R
Keywords
COPD; emphysema; ILC2s; inflammation; remodelling; T cells
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Funding
- National Health and Medical Research Council of Australia (NHMRC)
- NHMRC
- Australian Research Council Discovery Early Career Research Award
- Lung Foundation Australia/Boehringer Ingelheim Chronic Obstructive Pulmonary Disease Research Fellowship
- MRC UK [U105178805]
- Wellcome Trust [100963/Z/13/Z]
- National Health and Medical Research Council of Australia
- Faculty of Health and Medicine, The University of Newcastle
- Australian Research Council
- MRC [MC_U105178805] Funding Source: UKRI
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Pulmonary inflammation in chronic obstructive pulmonary disease (COPD) is characterized by both innate and adaptive immune responses; however, their specific roles in the pathogenesis of COPD are unclear. Therefore, we investigated the roles of T and B lymphocytes and group 2 innate lymphoid cells (ILC2s) in airway inflammation and remodelling, and lung function in an experimental model of COPD using mice that specifically lack these cells (Rag1(-/-) and Rora(fl/fl)Il7r(Cre) [ILC2-deficient] mice). Wild-type (WT) C57BL/6 mice, Rag1(-/-), and Rora(fl/fl)Il7r(Cre) mice were exposed to cigarette smoke (CS; 12 cigarettes twice a day, 5 days a week) for up to 12 weeks, and airway inflammation, airway remodelling (collagen deposition and alveolar enlargement), and lung function were assessed. WT, Rag1(-/-), and ILC2-deficient mice exposed to CS had similar levels of airway inflammation and impaired lung function. CS exposure increased small airway collagen deposition in WT mice. Rag1(-/-) normal air- and CS-exposed mice had significantly increased collagen deposition compared to similarly exposed WT mice, which was associated with increases in IL-33, IL-13, and ILC2 numbers. CS-exposed Rora(fl/fl)Il7r(Cre) mice were protected from emphysema, but had increased IL-33/IL-13 expression and collagen deposition compared to WT CS-exposed mice. T/B lymphocytes and ILC2s play roles in airway collagen deposition/fibrosis, but not inflammation, in experimental COPD.
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