The Laryngoscope · 2013
Expression levels of endogenous hydrogen sulfide are altered in patients with allergic rhinitis.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Park Se Jin, Kim Tae Hoon, Lee Seung Hoon, Ryu Hyei Yul, Hong Ki Hong, Jung Jong Yoon, Hwang Gyu Ho, Lee Sang Hag
Аннотация
OBJECTIVES/HYPOTHESIS: Hydrogen sulfide (H(2) S), the third endogenous gaseous transmitter, may be a crucial mediator in airway hyper-responsiveness and airway inflammation, including asthma. To elucidate the role of H(2) S in allergic rhinitis, the present study was undertaken to determine the level of expression of H(2) S 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 H(2) S-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 H(2) S 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 H(2) S 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, H(2) S is upregulated in nasal mucosa and plasma of allergic patients. Based on localization of CSE and CBS, H(2) S may play multiple functions in human nasal mucosa, contributing to the development of allergic symptoms such as rhinorrhea, sneezing, and nasal stuffiness.
STUDY DESIGN: Controlled, prospective study.
METHODS: The concentration of H(2) S 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 H(2) S 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, H(2) S is upregulated in nasal mucosa and plasma of allergic patients. Based on localization of CSE and CBS, H(2) S may play multiple functions in human nasal mucosa, contributing to the development of allergic symptoms such as rhinorrhea, sneezing, and nasal stuffiness.