Abstract
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.
Highlights
Multimodal neuronal sensors in the carotid bodies signal a host of autonomic reflexes [1]
LPA receptors (LPAr)’s 1, 2, 4 and 6 Messenger RNA (mRNA) are expressed within the carotid body of naïve Brown Norway (BN) rats, and the mRNA of all four receptors are upregulated in sensitised ovalbumin sensitised and challenged (OVA) BN rats (Fig. 3a)
LPAr 1, 2, 4, 5, 6 and Transient receptor potential vanilloid subtype 1 channel (TRPV1) mRNA are expressed in the petrosal ganglia of naïve animals; asthma causes upregulation of carotid body and petrosal LPAr mRNA (1>4>2>5>6), but the level of Protein kinase c epsilon (PKCε) and TRPV1 mRNA expression is unchanged (Fig. 3b)
Summary
Multimodal neuronal sensors in the carotid bodies signal a host of autonomic reflexes [1]. Known for their oxygen sensitivity [2], growing evidence demonstrates their immune sensing capability and coordination during bacterial infection [3,4,5,6]. We showed that the carotid bodies were sufficient to produce bronchoconstriction by stimulating efferent parasympathetic activity. This bronchoconstriction was instigated, in part, by increased plasma
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
