Myofibroblasts are increased in the lung parenchyma in asthma

PLoS One. 2017 Aug 7;12(8):e0182378. doi: 10.1371/journal.pone.0182378. eCollection 2017.

Abstract

Background: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

MeSH terms

  • Actins / metabolism
  • Adolescent
  • Adult
  • Asthma / pathology*
  • Cell Count
  • Female
  • Humans
  • Lung / pathology*
  • Male
  • Middle Aged
  • Myocytes, Smooth Muscle / metabolism
  • Myocytes, Smooth Muscle / pathology
  • Myofibroblasts / pathology*
  • Parenchymal Tissue / pathology*
  • Young Adult

Substances

  • Actins

Grants and funding

This work was supported by Health Canada, Alberta Lung Association, Herron Foundation of Alberta, Alberta Innovates Health Solutions (AIHS), Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), and National Health and Medical Research Council, Australia, Project Grant ID 618700. The funders provided support in the form of salaries for authors GS and AC funded in part by ALA. EC and BBA were funded by CNPq, but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific roles of these authors are articulated in the 'author contributions' section. No funder played a direct role in this study.