Roles for T/B lymphocytes and ILC2s in experimental chronic obstructive pulmonary disease

Autor: Andrew N. J. McKenzie, Paul S. Foster, Chantal Donovan, Bernadette Jones, Peter A. B. Wark, Richard Kim, Prema M. Nair, Philip M. Hansbro, Tatt Jhong Haw, Jillian L. Barlow, Kurtis F. Budden, Guy J. M. Cameron, Malcolm R. Starkey, Batika M. J. Rana, Jay C. Horvat
Rok vydání: 2018
Předmět:
0301 basic medicine
T-Lymphocytes
Cell Count
Pathogenesis
Pulmonary Disease
Chronic Obstructive
0302 clinical medicine
Fibrosis
Immunology and Allergy
remodelling
COPD
B-Lymphocytes
Innate lymphoid cell
respiratory system
3. Good health
emphysema
030220 oncology & carcinogenesis
Airway Remodeling
Collagen
medicine.symptom
medicine.medical_specialty
Immunology
T cells
Pulmonary disease
Inflammation
Brief Conclusive Report
Biology
ILC2s
03 medical and health sciences
Immune system
Internal medicine
medicine
Respiratory Hypersensitivity
Animals
Homeodomain Proteins
Airway Resistance
Interleukins
Inflammation
Extracellular Mediators
& Effector Molecules
Body Weight
Cell Biology
Pneumonia
medicine.disease
Immunity
Innate
respiratory tract diseases
Mice
Inbred C57BL
Pulmonary Alveoli
030104 developmental biology
Endocrinology
inflammation
Airway
Zdroj: Journal of Leukocyte Biology
ISSN: 1938-3673
Popis: 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 Rorafl/flIl7rCre [ILC2-deficient] mice). Wild-type (WT) C57BL/6 mice, Rag1−/−, and Rorafl/flIl7rCre 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 Rorafl/flIl7rCre 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. T/B lymphocytes and ILC2s play roles in airway fibrosis but not inflammation in a mouse model of experimental COPD.
Databáze: OpenAIRE
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