ArticleJournal of neuroinflammation2021
Asthmatic allergen inhalation sensitises carotid bodies to lysophosphatidic acid.
Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Basophils activate oncostatin M receptor-expressing vagal sensory neurons.The Journal of allergy and clinical immunology · 2026Article
- Chemoreflex function in pulmonary diseases - A review.The Journal of physiology · 2025Review
- Modulating TRPV1 and TRPA1 channels: a viable strategy for treating asthma using Chinese herbal medicines.Frontiers in pharmacology · 2025Review
- BASOPHILS ACTIVATE PRURICEPTOR-LIKE VAGAL SENSORY NEURONS.bioRxiv : the preprint server for biology · 2024Article
- Commonalities and differences in carotid body dysfunction in hypertension and heart failure.The Journal of physiology · 2023Article
- Pathogen recognition by sensory neurons: hypotheses on the specificity of sensory neuron signaling.Frontiers in immunology · 2023Article
- TRPM7 channels regulate breathing during sleep in obesity by acting peripherally in the carotid bodies.The Journal of physiology · 2022Article
- Cellular basis of learning and memory in the carotid body.Frontiers in synaptic neuroscience · 2022Review
Corrections and comments
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Authors and funding
3 authors.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.