Myofibroblasts are increased in the lung parenchyma in asthma

• Published in: PloS one Vol. 12; no. 8; p. e0182378
• Main Authors: Boser, Stacey R., Mauad, Thais, Araújo-Paulino, Bianca Bergamo de, Mitchell, Ian, Shrestha, Grishma, Chiu, Andrea, Butt, John, Kelly, Margaret M., Caldini, Elia, James, Alan, Green, Francis H. Y.
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 07.08.2017; Public Library of Science (PLoS)
• Subjects: Acetylcysteine; Actin; Actins - metabolism; Adolescent; Adult; Airway management; Alveoli; Asthma; Asthma - pathology; Biology and Life Sciences; Cell Count; Chronic illnesses; Development and progression; Female; Fibroblasts; Forensic pathology; Genetic aspects; Humans; Inflammation; Lung - pathology; Lungs; Male; Medicine; Medicine and Health Sciences; Middle Aged; Muscle proteins; Myocytes, Smooth Muscle - metabolism; Myocytes, Smooth Muscle - pathology; Myofibroblasts - pathology; Parenchyma; Parenchymal Tissue - pathology; Physiological aspects; Respiratory tract; Smooth muscle; Young Adult; Brazil; Australia; Canada; Calgary Alberta Canada
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0182378

Increased airway smooth muscle is observed in large and small airways in asthma. Semi-quantitative estimates suggest that cells containing alpha smooth muscle actin (α-SMA) are also increased in the lung parenchyma. This study quantified and characterized α-SMA positive cells (α-SMA+) in the lung parenchyma of non-asthmatic and asthmatic individuals. Post-mortem sections of peripheral lung from cases of fatal asthma (FA), persons with asthma dying of non-respiratory causes (NFA) and non-asthma control subjects (NAC) were stained for α-SMA, quantified using point-counting and normalised to alveolar basement membrane length and interstitial area. α-SMA+ fractional area was increased in alveolar parenchyma in both FA (14.7 ± 2.8% of tissue area) and NFA (13.0 ± 1.2%), compared with NAC (7.4 ± 2.4%), p < 0.05 The difference was greater in upper lobes compared with lower lobes (p < 0.01) in both asthma groups. Similar changes were observed in alveolar ducts and alveolar walls. The electron microscopic features of the α-SMA+ cells were characteristic of myofibroblasts. We conclude that in asthma there is a marked increase in α-SMA+ myofibroblasts in the lung parenchyma. The physiologic consequences of this increase are unknown.