Increased expression of arginase I and II in allergic nasal mucosa.

OBJECTIVES/HYPOTHESIS: It is known that arginase may be a regulator of diverse pathways, including production of nitric oxide (NO). Increased expression of arginase has been reported in several inflammatory lung diseases, including allergic asthma, suggesting that this may be a common feature underlying the pathophysiology of airway hyperreactivity. Thus, arginase I and II may play a role in the pathogenesis of allergic rhinitis. The distribution pattern and level of expression of arginase I and II were therefore determined in normal and allergic nasal mucosa. STUDY DESIGN: Controlled, prospective study. METHODS: The distribution pattern and level of expression of arginase I and II in normal and allergic nasal mucosa were evaluated using RT-PCR, immunohistochemistry, and Western blotting. RESULTS: The level of expression of arginase I and II mRNA was increased in allergic nasal mucosa in comparison with normal nasal mucosa. In normal nasal mucosa, arginase I and II were expressed in the surface epithelium, submucosal glands, vascular endothelium, and fibroblasts. In allergic nasal mucosa, both enzymes were also localized to similar sites, in addition to inflammatory cells, and the level of expression were greatly increased compared with normal nasal mucosa. These findings were verified by Western blotting. CONCLUSIONS: These results indicate that arginase I and II may play a role in the pathophysiology of allergic rhinitis, and suggest the possible role of the L-arginine metabolic pathway through modulation of L-arginine availability as a substrate for nitric oxide synthase (NOS) and arginase in the pathogenesis of allergic rhinitis.

The expression of adiponectin receptor is altered in mild and moderate/severe persistent allergic nasal mucosa.

BACKGROUND: Adiponectin, one of the adipokines, has been implicated in the inflammatory process in patients with allergic rhinitis. The level of adiponectin is affected by immunotherapy. Considering the fact that adiponectin receptors (AdipoRs) mediate intracellular signaling events in response to the binding of adiponectin, the role of AdipoRs in healthy and allergic nasal mucosa should be determined. This study investigates the level of expression and distribution pattern of AdipoR1 and AdipoR2 in healthy, mild, and moderate/severe persistent allergic nasal mucosa to understand the role of adiponectin in allergic rhinitis. METHODS: The level of expression and distribution pattern of AdipoR1 and AdipoR2 were evaluated in healthy, mild, and moderate/severe persistent allergic nasal mucosa, using semiquantitative reverse-transcriptase-polymerase chain reaction (RT-PCR), immunohistochemistry, and Western blot analysis. RESULTS: AdipoR1 was expressed in healthy, mild, and moderate/severe persistent allergic nasal mucosa where it was commonly localized to the vascular endothelium. However, AdipoR2 was not expressed in any samples of nasal mucosa tested in the present study. Semiquantitative RT-PCR and Western blot analysis showed that the level of expression of AdipoR1 mRNA and protein was decreased in mild and moderate/severe persistent allergic nasal mucosa in comparison with healthy nasal mucosa, but not significantly different between mild and moderate/severe persistent allergic nasal mucosa. CONCLUSION: These results indicate that AdipoR1 may play an important role in the pathogenesis of allergic nasal mucosa, suggesting a role for AdipoR1 in vascular dysfunction in mild and moderate/severe persistent allergic nasal mucosa.