R X Zhang1, S Q Yu, J Z Jiang, G J Liu. 1. Department of Otolaryngology, Huadong Hospital, Fudan University, Shanghai, China. rxzhang@x263.net
Abstract
OBJECTIVE: To analyze the roles of chemokines and their receptors in the pathogenesis of allergic rhinitis by observing the complementary DNA (cDNA) expression of the chemokines and their receptors in the nasal mucosa of patients with and without allergic rhinitis, using gene chips. METHODS: The total RNAs were isolated from the nasal mucosa of 20 allergic rhinitis patients and purified to messenger RNAs, and then reversely transcribed to cDNAs and incorporated with samples of fluorescence-labeled with Cy5-dUPT (rhinitis patient samples) or Cy3-dUTP (control samples of nonallergic nasal mucosa). Thirty-nine cDNAs of chemokines and their receptors were latticed into expression profile chips, which were hybridized with probes and then scanned with the computer to study gene expression according to the different fluorescence intensities. RESULTS: The cDNAs of the following chemokines were upregulated: CCL1, CCL2, CCL5, CCL7, CCL8, CCL11, CCL13, CCL14, CCL17, CCL18, CCL19, CCL24, and CX3CL1 in most of the allergic rhinitis sample chips. CCR2, CCR3, CCR4, CCR5, CCR8 and CX3CR1 were the highly expressed receptor genes. Low expression of CXCL4 was found in these tissues. CONCLUSION: The T helper cell (T(H)) immune system is not well regulated in allergic rhinitis. Most of the upregulated genes we identified are of chemokines and their receptors that play important roles in T(H)2 response, and some are involved in the induction of allergic reaction, accumulation of inflammatory cells, and degranulation of sensitized cells. These findings can point to new strategies for allergic rhinitis immunotherapy.
OBJECTIVE: To analyze the roles of chemokines and their receptors in the pathogenesis of allergic rhinitis by observing the complementary DNA (cDNA) expression of the chemokines and their receptors in the nasal mucosa of patients with and without allergic rhinitis, using gene chips. METHODS: The total RNAs were isolated from the nasal mucosa of 20 allergic rhinitispatients and purified to messenger RNAs, and then reversely transcribed to cDNAs and incorporated with samples of fluorescence-labeled with Cy5-dUPT (rhinitispatient samples) or Cy3-dUTP (control samples of nonallergic nasal mucosa). Thirty-nine cDNAs of chemokines and their receptors were latticed into expression profile chips, which were hybridized with probes and then scanned with the computer to study gene expression according to the different fluorescence intensities. RESULTS: The cDNAs of the following chemokines were upregulated: CCL1, CCL2, CCL5, CCL7, CCL8, CCL11, CCL13, CCL14, CCL17, CCL18, CCL19, CCL24, and CX3CL1 in most of the allergic rhinitis sample chips. CCR2, CCR3, CCR4, CCR5, CCR8 and CX3CR1 were the highly expressed receptor genes. Low expression of CXCL4 was found in these tissues. CONCLUSION: The T helper cell (T(H)) immune system is not well regulated in allergic rhinitis. Most of the upregulated genes we identified are of chemokines and their receptors that play important roles in T(H)2 response, and some are involved in the induction of allergic reaction, accumulation of inflammatory cells, and degranulation of sensitized cells. These findings can point to new strategies for allergic rhinitis immunotherapy.