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YKL-40 is up-regulated in mild and moderate/severe persistent allergic rhinitis, and its expression can be regulated differentially by different cytokines, possibly contributing to the remodeling of nasal mucosa in allergic rhinitis.

Objectives/Hypothesis: Hydrogen sulfide (H2S), the third endogenous gaseous transmitter, may be a crucial mediator in airway hyper‐responsiveness and airway inflammation, including asthma. To elucidate the role of H2S in allergic rhinitis, the present study was undertaken to determine the level of expression of H2S in healthy nasal mucosa and mild and moderate/severe persistent allergic nasal mucosa as well as peripheral blood obtained from each patient. The expression and distribution pattern of the H2S‐synthesizing enzymes cystathione γ‐lyase (CSE) and cystathione β‐synthase (CBS) were investigated in healthy and allergic nasal mucosa. Study Design: Controlled, prospective study. Methods: The concentration of H2S in nasal mucosa and plasma was determined by zinc trap spectrophotometry. The expression levels and patterns of distribution of CSE and CBS mRNA and proteins were evaluated using real time polymerase chain reaction, Western blot, and immunohistochemistry. Results: The levels of expression of H2S in nasal mucosa and plasma were increased in patients with mild and moderate/severe persistent allergic rhinitis compared with healthy controls. CSE was localized in vascular endothelium and surrounding muscles, and submucosal glands, whereas CBS was exclusively distributed in the superficial epithelium and submucosal glands. Their expression levels were increased in mild and moderate/severe persistent allergic rhinitis. Conclusions: The current findings indicate that, in parallel with increased expression levels of CSE and CBS, H2S is upregulated in nasal mucosa and plasma of allergic patients. Based on localization of CSE and CBS, H2S may play multiple functions in human nasal mucosa, contributing to the development of allergic symptoms such as rhinorrhea, sneezing, and nasal stuffiness. Laryngoscope, 2013

These results indicate that the localized anti-inflammatory effects of glucocorticoids are regulated by inflammatory cytokines, which can modulate the expression of 11β-HSD1, 11β-HSD2, and CYP11B1, and by the intracellular concentrations of bioactive glucocorticoids.

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