OBJECTIVE The discovery of carbon monoxide (CO) and hydrogen sulfide (H2S) as pathogenic signaling molecules in airway-related diseases has led to significant insights into the pathophysiologic mechanisms underlying the development of allergic rhinitis (AR). The potential crosstalk between CO and H2S signaling pathways in AR has not been adequately investigated. This study was performed to elucidate the mechanistic relationship between CO and H2S in AR. STUDY DESIGN Experimental prospective animal study. SETTING Animal laboratory of Tongji Hospital, Tongji University, Shanghai, China. SUBJECTS AND METHODS A well-established model of AR was used whereby guinea pigs (N=24) were randomly divided into 4 treatment groups (n=6 for each group): The first group received ovalbumin only; the second group was administered exogenous hemin, a CO-binding metalloporphyrin; the third group received zinc protoporphyrin, an inhibitor of heme oxygenase-1. A control group was challenged using only saline. Symptoms of AR were recorded, and quantitation of plasma CO and H2S levels was performed. Expression of heme oxygenase-1 and H2S-generating enzyme cystathionine-γ-lyase (CSE) were measured from nasal mucosa. RESULTS Plasma CO and heme oxygenase-1 expression levels of nasal mucosa were significantly increased in the AR group compared to controls, whereas H2S concentrations were significantly decreased. Exogenous administration of CO exacerbated allergic symptoms, resulting in higher levels of both CO and heme oxygenase-1 expression, and a further reduction in H2S levels and CSE expression. Zinc protoporphyrin decreased CO concentrations and increased levels of both H2S and CSE expression. CONCLUSIONS Results indicated an inverse relationship between H2S levels and CO in the pathogenesis of AR.

中文翻译：

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一氧化碳/血红素加氧酶对豚鼠变应性鼻炎发病机理中硫化氢/半胱氨酸-γ-裂合酶途径的影响。

目的一氧化碳（CO）和硫化氢（H2S）作为气道相关疾病中的致病性信号分子的发现，导致人们对变应性鼻炎（AR）发病的病理生理机制有了重要的认识。尚未充分研究AR中CO和H2S信号通路之间的潜在串扰。进行这项研究是为了阐明AR中CO和H2S之间的机制关系。研究设计实验性前瞻性动物研究。地点，上海同济大学同济医院动物实验室。受试者和方法使用建立良好的AR模型，将豚鼠（N = 24）随机分为4个治疗组（每组n = 6）：第一组仅接受卵清蛋白；第二组仅接受卵清蛋白。第二组给予外源性血红素，与CO结合的金属卟啉; 第三组接受血红素加氧酶-1抑制剂锌原卟啉锌。对照组仅使用盐水攻击。记录AR的症状，并进行血浆CO和H 2 S水平的定量。从鼻粘膜测量血红素加氧酶-1和生成H2S的酶胱硫醚-γ-裂合酶（CSE）的表达。结果与对照组相比，AR组的鼻粘膜血浆CO和血红素加氧酶-1表达水平显着升高，而H2S浓度则显着降低。外源施用CO加剧了过敏症状，导致CO和血红素加氧酶-1的表达均较高，并且H2S水平和CSE表达进一步降低。锌原卟啉降低了CO浓度，并增加了H2S和CSE表达水平。