Comparison of CD30, HLA-DR and CD23 expression in bronchial biopsies obtained from patients with atopic asthma and sarcoidosis

Th2-type cells play a crucial role in the regulation of inflammatory process in atopic disorders. In contrast, the importance of Th1-type response during granulomatous inflammation is postulated. There is some evidence that CD30 cell surface molecule is associated with the differentiation/activation pathway of human Th2-type cells.
The aim of this study was to evaluate the spontaneous expression of CD30 in comparison with the other cell activation markers - HLA-DR, CD23 - in bronchial biopsy specimens recovered from patients suffering from atopic bronchial asthma or sarcoidosis.
For this purpose 13 patients with episodic atopic bronchial asthma during asymptomatic period of the disease (FEV₁ >80% predicted) diagnosed according to ATS criteria were included into the trial.
The bronchial mucosa slides obtained from 5 patients with sarcoidosis were studied.
A few biopsy specimens of bronchial mucosa and submucosa were taken from a peripheral bronchus of the inferior lobe during the fiberoptic bronchoscopy. The deparaffinized sections were processed in three stages method (ABC) using mouse monoclonal antibody labelled by isotype specific biotinylated rabbit anti-mouse immunoglobulins and subsequently by streptavidin-peroxydase complex amplified. Studies were evaluated semiquantitatively.
In patients with asthma the CD 30+ mononuclear cells in the epithelium (slight and moderate positive reaction) in 38 % of patients were observed. The expression of CD23 on mononuclear cells in the epithelium (slight positive reaction) in only three subjects was noticed. In contrast, strong and moderate HLA-DR expression in all specimens studied both in the epithelium and in submucosa was observed. In patients with Sarcoidosis there was moderate positive reaction with CD30 in three patients. Like in asthma strong positive reaction of HLA-DR antigen was observed in all subjects. CD23 was slightly and moderately positive in three patients.
We conclude that:
1. CD30⁺ cells cannot be considered as an useful differentiative marker between bronchial asthma and sarcoidosis.
2. It cannot be excluded that some stages of inflammation during sarcoidosis are Th-2-dependent.
3. The spontaneous increased expression of HLA-DR molecule in bronchial biopsy specimens from asymptomatic asthmatics and sarcoid patients during remission support the notion that mucosal inflammation persists in the airways irrespectively to the stadium of the diseases