The carotid bodies are multimodal sensors that regulate various autonomic reflexes. Recent evidence demonstrates their role in immune reflex regulation. Our previous studies using the allergen (ovalbumin) sensitised and exposed Brown Norway rat model of asthma suggest that carotid bodies mediate asthmatic bronchoconstriction through a lysophosphatidic acid (LPA) receptor (LPAr)-protein kinase C epsilon (PKCε)-transient receptor potential vanilloid one channel (TRPV1) pathway. Whilst naïve carotid bodies respond to LPA, whether their response to LPA is enhanced in asthma is unknown. Here, we show that asthmatic sensitisation of Brown Norway rats involving repeated aerosolised allergen challenges over 6 days, results in an augmentation of the carotid bodies’ acute sensitivity to LPA. Increased expression of LPAr in the carotid bodies and petrosal ganglia likely contributed to this sensitivity. Importantly, allergen sensitisation of the carotid bodies to LPA did not alter their hypoxic response, nor did hypoxia augment LPA sensitivity acutely. Our data demonstrate the ability of allergens to sensitise the carotid bodies, highlighting the likely role of the carotid bodies and blood-borne inflammatory mediators in asthma.

中文翻译：

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吸入哮喘过敏原使颈动脉体对溶血磷脂酸敏感

颈动脉体是调节各种自主反射的多模式传感器。最近的证据表明它们在免疫反射调节中的作用。我们之前使用过敏原（卵白蛋白）致敏和暴露的布朗挪威大鼠哮喘模型的研究表明，颈动脉体通过溶血磷脂酸（LPA）受体（LPAr）-蛋白激酶 C ε（PKCε）-瞬时受体电位香草素一介导哮喘支气管收缩通道 (TRPV1) 通路。虽然幼稚的颈动脉体对 LPA 有反应，但它们对 LPA 的反应是否在哮喘中增强是未知的。在这里，我们表明，在 6 天内反复雾化过敏原挑战的 Brown Norway 大鼠的哮喘致敏导致颈动脉体对 LPA 的急性敏感性增加。颈动脉体和岩神经节中 LPar 表达的增加可能导致了这种敏感性。重要的是，颈动脉体对 LPA 的过敏原致敏并没有改变它们的缺氧反应，缺氧也不会急剧增加 LPA 的敏感性。我们的数据证明了过敏原使颈动脉体敏感的能力，突出了颈动脉体和血源性炎症介质在哮喘中的可能作用。