TABLE 2

Studies of extracellular matrix composition in mild, moderate and severe asthma

MethodsPopulationFindings[Ref.]
Post mortem specimen: large airways (Pi >6 mm) and small airways (Pi <6 mm)Fatal asthma (n=18)
Control (n=10)
Inner airway wall area: proteoglycans (versican increased)
Outer airway wall area: proteoglycans (decorin and lumican decreased)
[58]
Post mortem specimen: small airways (Pi <6 mm)Fatal asthma (n=15)
Control (n=9)
Outer airway wall area: elastic fibre content decreased[59]
Post mortem specimen: two large airways (Pi >6 mm) and three small airways (Pi <6 mm) from each subjectFatal asthma (n= 35)
Nonfatal asthma (n=10)
Nonasthmatic control (n=22)
Within ASM: fractional area of elastic fibre was increased in fatal asthma versus nonfatal asthma, but not to nonasthmatic control
Collagen I and III, fibronectin, versican, MMP (1, 2, 9 and 12) and TIMP (1 and 2) were not significantly different in fatal asthma versus nonasthmatic control
[60]
Post mortem specimen: central versus peripheral airways were defined according to presence of cartilageFatal asthma (n=31)
Control (n=10)
Inner airway wall area: elastic fibre content nonsignificant[61]
Post mortem specimen: large airways (Pi >6 mm) and small airways (Pi <6 mm)Fatal asthma (n=24)
Control (n=11)
Inner airway wall area: collagen type I increased, collagen type III decreased
Outer airway wall area: collagen type III decreased and collagen type I, fibronectin, MMP-1, MMP-2, MMP-9 all increased
TIMP 1 and 2 were not significantly different
[62]
Transbronchial biopsy specimen: alveolar tissueMild asthma (n=11)
Control (n=12)
Collagen expression increased
Proliferation rate of distally derived fibroblasts decreased
Versican increased, biglycan and decorin decreased, and perlecan was nonsignificant from distally derived fibroblasts
[63]
Surgical lung biopsies: small airways and alveolar parenchymaSevere asthma only (n=5)
Severe asthma with autoimmune disease (n=5)
Severe asthma with asthmatic granulomatosis (n=9)
Severe asthma with asthmatic granulomatosis and autoimmune disease (n=10)
Submucosal fibrosis and subbasement membrane thickening was observed[38]
Post mortem specimen: small airways (Pi 2–10 mm)Fatal asthma (n=25)
Control (n=11)
Inner airway wall area: increased collagen[64]
Bronchial and transbronchial biopsies: alveolar parenchymaUncontrolled atopic asthma (n=16)
Controlled atopic asthma (n=9)
Control (n=8)
Increased collagen in uncontrolled atopic asthma versus control
Decreased versican in controlled atopic asthma versus control
Increased decorin in uncontrolled atopic asthma versus control
Decreased biglycan in controlled atopic asthma versus control and uncontrolled atopic asthma
Decreased MMP-9 in controlled atopic asthma versus control and uncontrolled atopic asthma
Increased TIMP-3 in uncontrolled and controlled atopic asthma versus control
Decreased myofibroblasts in controlled atopic asthma versus control and uncontrolled atopic asthma
Fibronectin: nonsignificant difference between the three groups
[65]

Findings for small airways are presented. Pi: perimeter; ASM: airway smooth muscle; MMP: matrix metalloproteinase; TIMP: tissue inhibitors of matrix metalloproteinase.