Thorax 62:8-15 doi:10.1136/thx.2006.062141
  • Asthma

Inflammation of bronchial smooth muscle in allergic asthma

  1. H Begueret1,
  2. P Berger1,
  3. J M Vernejoux2,
  4. L Dubuisson3,
  5. R Marthan1,
  6. J M Tunon-de-Lara1,2
  1. 1Université Bordeaux 2, Laboratoire de Physiologie Cellulaire Respiratoire, F-33076, Bordeaux; Inserm E356 F-23076, Bordeaux, France
  2. 2CHU de Bordeaux, Service des Maladies Respiratoires, F-33076, Bordeaux, France
  3. 3Université Bordeaux 2, Service de Microscopie Electronique, F-33076, Bordeaux, France
  1. Correspondence to:
    Dr J M Tunon-de-Lara
    Laboratoire de Physiologie Cellulaire Respiratoire, INSERM E356 Université Bordeaux 2, 146 rue Léo Saignat, 33076 Bordeaux, France; manuel.tunondelara{at}
  • Received 9 March 2006
  • Accepted 14 July 2006


Background: Recent observations in asthma suggest that bronchial smooth muscle is infiltrated by inflammatory cells including mast cells. Such an infiltration may contribute to airway remodelling that is partly due to an increase in smooth muscle mass. Whether muscle increase is the result of smooth muscle cell hypertrophy remains controversial and has not been studied by ultrastructural analysis. A morphometric analysis of airway smooth muscle (ASM) was undertaken in asthmatic patients using electron microscopy to examine the interactions between ASM cells and inflammatory cells.

Methods: ASM specimens were obtained from 14 asthmatic subjects and nine non-asthmatic controls undergoing fibreoptic endoscopy. Inflammatory cell counts were assessed by immunohistochemistry, and ultrastructural parameters were measured using electron microscopy in a blinded fashion on smooth muscle cells and inflammatory cells.

Results: ASM from asthmatic patients was infiltrated by an increased number of mast cells and lymphocytes. Smooth muscle cells and their basal lamina were thicker in asthmatic patients (9.5 (0.8) and 1.4 (0.2) μm) than in controls (6.7 (0.4) and 0.7 (0.1) μm). In asthmatics the extracellular matrix was frequently organised in large amounts between ASM cells. Myofibroblasts within smooth muscle bundles were only observed in asthmatics, some of them displaying a close contact with ASM cells.

Conclusion: In asthma, airway myositis is characterised by a direct interaction between ASM cells and mast cells and lymphocytes. Smooth muscle remodelling was present, including cell hypertrophy and abnormal extracellular matrix deposition moulding ASM cells.


  • This study was supported by a grant PHRC (Programme Hospitalier de Recherche Clinique) 2002 from the CHU de Bordeaux and a grant from FRM (Fondation Recherche Médicale) DAL2005120574.

  • Competing interests: none declared.