Reactive airway dysfunction syndrome (RADS) has a clinical manifestation similar to asthma, but some features are different between both the diseases. To probe the effect of CD19+ cells in RADS pathogenesis by inhalation of sulfur dioxide (SO2), rats were exposed to SO2 at 600 ppm for 2 h per day for 7 days and the CD19 expression in lung tissue was detected both at mRNA and protein levels by RT-PCR and western blot. The percentages of CD19+ and CD19+ CD23+ cells were measured by flow cytometry. IgG, IgA, and IgE in serum and bronchoalveolar lavage fluid (BALF) were detected by enzyme-linked immunosorbent assay (ELISA). Histological analysis was performed. The results showed that expression of CD19 in SO2 exposure group was lower than that in the control both at mRNA and protein levels ( P < 0.05). Flow cytometry analysis showed that the percentages of CD19+ and CD19+ CD23+ were significantly lower in the SO2 exposed group than that in the control ( P < 0.05). There was no difference between the control and SO2 exposed groups in both serum and BALF levels of IgG, IgA, and IgE. Pathological changes, such as chronic bronchitis, local alveolar hemorrhage, and lymphocytes infiltration were observed in SO2 exposed. RADS is a non-immunogenicity, chronic airway inflammatory disease caused by irritation of harmful factor and manifests as airway hyperresposiveness.
Reactive airway dysfunction syndrome: Are we missing these patients?
