Search

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.

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.Controlled, prospective study.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.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.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.

Objectives/Hypothesis: Acidic mammalian chitinase (AMCase) has emerged as an important mediator of allergic asthma in both animal models and in humans. Recently, chitotriosidase has been suggested to play a role in innate immunity because of its phagocytic-specific expression. Thus, AMCase and chitotriosidase may play a role in the pathogenesis of allergic nasal mucosa. The expression and pattern of distribution of AMCase and chitotriosidase were, therefore, determined in normal and allergic nasal mucosa. Study Design: Controlled, prospective study. Methods: Normal inferior turbinate mucosa was obtained in patients who were admitted for augmentation rhinoplasty. Allergic turbinate mucosa was obtained from patients who had perennial allergic rhinitis during septo-turbinate surgery. Reverse transcriptase-polymerase chain reaction (RT-PCR), immunohistochemistry, and Western blotting were applied to the normal and allergic nasal mucosa. Results: The expression of AMCase and chitotriosidase mRNAs and proteins analyzed by RT-PCR and Western blot were detected in all normal and allergic turbinate mucosa tested. The levels of expression of AMCase and chitotriosidase mRNAs and proteins were increased in allergic turbinate mucosa compared with normal turbinate mucosa. In both normal and allergic turbinate mucosa, AMCase and chitotriosidase were detected in the epithelium, inflammatory cells, and submucosal glands. The staining intensity for AMCase and chitotriosidase was stronger in allergic nasal mucosa than normal nasal mucosa. Conclusions: AMCase and chitotriosidase are constitutively expressed in normal turbinate mucosa, suggesting involvement in defense against chitin-containing pathogens. Upregulation of these chitinases in allergic condition suggests that they may play a role in the nasal allergic reaction like other inflammatory mediators in allergic rhinitis. Laryngoscope, 2010

Objective: The lymphatic system plays an important role in the maintenance of tissue fluid homeostasis, which facilitates interstitial protein transport. Until recently, the lymphatic system of the sinonasal mucosa has been relatively poorly studied. The authors aimed to investigate the distributional and quantitative changes of the lymphatic vessels in inflammatory sinus mucosa and nasal polyps in comparison with healthy sinus mucosa using D2-40 antibody. Methods: Immunohistochemistry and Western blotting with D2-40 antibody were applied to normal and edematous ethmoid sinus mucosa and nasal polyps. The number, size, and length densities of lymphatic vessels were evaluated using tissue sections and whole mount preparations. Results: Most lymphatic vessels in normal and edematous ethmoid sinus mucosa were distributed in the subepithelial layer. Some of these vessels were dilated, whereas others were compressed and had a slit-like lumen. No D2-40 positive vessels were found in samples of nasal polyps. Lymphatic vessels showed no statistically significant difference in their number, size, or length density between normal and edematous ethmoid sinus mucosa. Western blot also showed no differences in their expression levels. Conclusion: These findings indicate that lymphangiogenesis does not occur in edematous ethmoid sinus mucosa, which may not reuptake interstitial fluid efficiently in inflammatory conditions, resulting in the formation of mucosal edema in chronic inflammation.