Local expression of epsilon germline gene transcripts and RNA for the epsilon heavy chain of IgE in the bronchial mucose in atonic and nonatopic asthma
S. Ying et al., Local expression of epsilon germline gene transcripts and RNA for the epsilon heavy chain of IgE in the bronchial mucose in atonic and nonatopic asthma, J ALLERG CL, 107(4), 2001, pp. 686-692
Background: The demonstration of epsilon germline gene (C epsilon) transcri
pts and mature mRNA for the epsilon heavy chain gene (I epsilon) in the nas
al mucosa suggested that IgE synthesis may occur in allergic rhinitis.
Objective: In view of our previous demonstration of increases in IL-4 mRNA(
+) cells in asthmatic subjects, we assessed whether local IgE synthesis may
also be a feature of bronchial asthma.
Methods: Fiberoptic bronchoscopic mucosa biopsy specimens were obtained fro
m 9 atopic asthmatic subjects and 10 nonatopic normal (intrinsic) control s
ubjects. To control for atopy, we also studied 9 nonatopic asthmatic subjec
ts and 10 atopic nonasthmatic control subjects. Tissue was processed for im
munohistochemistry for B cells (CD20) and in situ hybridization for I epsil
on and C epsilon RNA(+) cells and IL-4 mRNA(+) cells.
Results: B-cell numbers in the bronchial mucosa were similar for asthmatic
subjects compared with control subjects, whereas significantly higher numbe
rs of I epsilon RNA(+) (P =.02 and P =.04, respectively), C epsilon RNA(+)
(P =.01 and P =.03, respectively), and IL-4 mRNA(+) (P =.001 and P =.001, r
espectively) cells were observed in atopic asthmatic subjects and nonatopic
asthmatic subjects, respectively, but not in atopic control subjects compa
red with nonatopic control subjects. In asthmatic subjects there H ere sign
ificant correlations between I epsilon RNA(+) tells (r = 0.53, P =.02) and
CE RNA+ cells (r = 0.48, P = .05) when compared with the number of IL-4 mRN
A(+) cells.
Conclusion: Increases in I epsilon and C epsilon RNA(+) cells, but not B-ce
ll numbers, in the bronchial mucosa provide evidence for local IgE synthesi
s in both atopic and nonatopic asthma. These changes appear to relate to as
thma rather than atopy per se and, at least in part, may be under the regul
ation of IL-4.