TH1 and TH2 -signals by gene expression arrays in atopy and asthma
M. H. Brutsche, L. Joos, I. E. A. Carlen Brutsche, M. Crawen, P. Wood, A. Custovic, A. Woodcock (Basle, Switzerland; Manchester, United Kingdom)
Source: Annual Congress 2001 - Molecular and cellular pathology of asthma
Session: Molecular and cellular pathology of asthma
Session type: Poster Discussion
Number: 3557
Disease area: Airway diseases
Abstract Mast cells (MC[scquote]s) can be considered to be a tissue resident cell capable of playing a role in acute and chronic aspects of asthma via secretion and synthesis of a range of chemical mediators. Thus their distribution and activation in different airway wall compartments may relate to the pathophysiological features of asthma. Transverse sections of large and small airways from controls (CO), mild (nonfatal – NFA) and severe (fatal – FA) asthma, n=8 in each group, were stained with the AA1 (MC tryptase) monoclonal antibody. MC[scquote]s (intact and degranulated) were counted in the lumen (LU), epithelium (EPI), inner airway wall (WAi), smooth muscle (ASM), submucosal mucous glands (SMG) and outer airway wall (WAo) and expressed as cells per mm2 of the measured area. Degranulated MC[scquote]s were expressed as a % of total MC[scquote]s in the different airway compartments. MC density was 5 fold higher in small airways compared with large airways and highest on the ASM of all airway compartments. MC density was increased (p<0.05) in CO and NFA compared with FA in large airways and in NFA and FA compared with CO in small airways. MC density was highest in ASM and SMG in large airways and in the ASM and WAo in small airways. Degranulation was greater (P<0.05) in FA than in NFA and greater in NFA than CO in large and small airways. Degranulation was highest on ASM and SMG in FA and greater than in NFA and CO. We conclude that MC density varies between large and small airways and between airway compartments. Increased numbers of degranulated MC[scquote]s on ASM and Gland in FA is likely to play a role in excessive airway narrowing.
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M. H. Brutsche, L. Joos, I. E. A. Carlen Brutsche, M. Crawen, P. Wood, A. Custovic, A. Woodcock (Basle, Switzerland; Manchester, United Kingdom). TH1 and TH2 -signals by gene expression arrays in atopy and asthma. Eur Respir J 2001; 16: Suppl. 31, 3557
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