[The expression and DNA sequence of recombination activating gene-1 in nasal membrane of allergic rhinitis].
OBJECTIVE
To study the mechanism of recombination activating gene-1 in pathogenesis of allergic rhinitis and its relation to interleukin-4 (IL-4), interleukin-10 (IL-10) and immunoglobin E (IgE).


METHODS
Three groups of allergic rats models were established with ovalbumin (OVA) and intervened with Dexamethasone (DEX). The times of sneeze were recorded, the cutaneous reaction of rats to the passive cutaneous allergen access (PCA) were investigated and the expression and DNA sequence of recombination activating gene-1 were examined and tested with reverse transcription-polymerase chain reaction (RT-PCR) and DNA analysator. The serum levels of IL-4, IL-10 and IgE were examined and tested with enzyme linked immunosorbent assay (ELISA) method in comparison with the controls.


RESULTS
RAG-1 mRNA expression was not found in normal nasal membrane. Both in AR group and DEX intervention group were seen different expressions; DNA sequence determination didn't find mutation of RG1 genes. The serum level of IL-4[(106.31 +/- 12.90) ng/L] and IgE[(38.67 +/- 4.13) ng/L] in AR group were significantly higher than those in normal control [(93.65 +/- 7.78) ng/L, (23.27 +/- 1.36) ng/L respectively] (P < 0.05), but the IL-10 level [(38.15 +/- 4.89) ng/L] in AR group was significantly lower than those in normal control [(48.74 +/- 3.49) ng/L] (P < 0.05). After DEX intervention, the serum level of IL-4[(92.67 +/- 16.40) ng/L] and IgE[(24.23 +/- 4.38) ng/L] significantly dropped as compared with AR group (P < 0.05) while IL-10[(46.18 +/- 5.01) ng/L] significantly rose (P < 0.05).


CONCLUSIONS
It proves that the high expression of recombination activating genes is closely related to the pathogenesis of allergic rhinitis, which leads to the secretion of IL-4 and inhibits that of IL-10 and whose sequence is conservative in the nasal mucosa of AR. As glucocorticoid does not affect the expression of RAG-1 genes, it suggests that RAG-1 may be an immunomodulator on a higher level in the pathogenesis of AR.
Zhang
Ruxin
R
Department of Otolaryngology, Changhai Hospital, the Second Military Medical University, Shanghai, 200433, China. rxzhang@X263.com
Wu
Geping
G
Wen
Wu
W
Liu
Guojun
G
Yan
Zhiqiang
Z
Yu
Shaoqing
S
Sun
Wei
W
D000818:Animals; D005260:Female; D015870:Gene Expression; D018398:Homeodomain Proteins / Q000235:genetics*; D007073:Immunoglobulin E / Q000276:immunology; D016753:Interleukin-10 / Q000276:immunology; D015847:Interleukin-4 / Q000276:immunology; D008297:Male; D009297:Nasal Mucosa / Q000276:immunology / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012221:Rhinitis, Allergic, Perennial / Q000235:genetics* / Q000276:immunology / Q000378:metabolism*; D017422:Sequence Analysis, DNA
D018398:Homeodomain Proteins; C064658:RAG-1 protein; D016753:Interleukin-10; D015847:Interleukin-4; D007073:Immunoglobulin E