ArticleAmerican journal of physiology. Lung cellular and molecular physiology2020
Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide-induced lung inflammation.
Article in American journal of physiology. Lung cellular and molecular physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Phosgene inhalation injury in mice: Modeling human pathophysiology, biomarker discovery, and therapeutic target identification.Toxicology and applied pharmacology · 2026Article
- Vagal neuropathies: An underrecognized potential driver of physical, mental, and immune symptoms.Brain, behavior, & immunity - health · 2026Review
- Neural Circuits between Nodose Ganglion and Pulmonary Neuroendocrine Cells Regulate Lung Inflammatory Responses.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Orphan Receptor GPR151: Discovery, Expression, and Emerging Biological Significance.ACS chemical neuroscience · 2025Review
- Novel Porcine Model Reveals Two Distinct LGR5 Cell Types during Lung Development and Homeostasis.American journal of respiratory cell and molecular biology · 2025Article
- Sensory neurons on guard: roles in pathogen defense and host immunity.Current opinion in immunology · 2025Review
- The peripheral neuroimmune system.Journal of leukocyte biology · 2024Review
- Cytokines reprogram airway sensory neurons in asthma.bioRxiv : the preprint server for biology · 2024Article
- Cerebellar ataxia, neuropathy and vestibular areflexia syndrome: a neurogenic cough prototype.ERJ open research · 2024Article
- Netazepide, an Antagonist of Cholecystokinin Type 2 Receptor, Prevents Vincristine-Induced Sensory Neuropathy in Mice.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Brain circuits for retching-like behavior.National science review · 2024Article
- Prdm12 represses the expression of the visceral neuron determinants Phox2a/b in developing somatosensory ganglia.iScience · 2023Article
- Infectious and Inflammatory Pathways to Cough.Annual review of physiology · 2023Review
- Cough hypersensitivity and chronic cough.Nature reviews. Disease primers · 2022Review
- Anatomical differences in nociceptor neurons sensitivity.Bioelectronic medicine · 2022Article
- The Cholecystokinin Type 2 Receptor, a Pharmacological Target for Pain Management.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Transcriptome Analysis of Selenium-Treated Porcine Alveolar Macrophages Against Lipopolysaccharide Infection.Frontiers in genetics · 2021Article
- A pharmacological interactome between COVID-19 patient samples and human sensory neurons reveals potential drivers of neurogenic pulmonary dysfunction.Brain, behavior, and immunity · 2020Article
- Peripheral and central mechanisms of cough hypersensitivity.Journal of thoracic disease · 2020Review
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The lungs and the immune and nervous systems functionally interact to respond to respiratory environmental exposures and infections. The lungs are innervated by vagal sensory neurons of the jugular and nodose ganglia, fused together in smaller mammals as the jugular-nodose complex (JNC). Whereas the JNC shares properties with the other sensory ganglia, the trigeminal (TG) and dorsal root ganglia (DRG), these sensory structures express differential sets of genes that reflect their unique functionalities. Here, we used RNA sequencing (RNA-seq) in mice to identify the differential transcriptomes of the three sensory ganglia types. Using a fluorescent retrograde tracer and fluorescence-activated cell sorting, we isolated a defined population of airway-innervating JNC neurons and determined their differential transcriptional map after pulmonary exposure to lipopolysaccharide (LPS), a major mediator of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) after infection with gram-negative bacteria or inhalation of organic dust. JNC neurons activated an injury response program, leading to increased expression of gene products such as the G protein-coupled receptor Cckbr, inducing functional changes in neuronal sensitivity to peptides, and Gpr151, also rapidly induced upon neuropathic nerve injury in pain models. Unique JNC-specific transcripts, present at only minimal levels in TG, DRG, and other organs, were identified. These included TMC3, encoding for a putative mechanosensor, and urotensin 2B, a hypertensive peptide. These findings highlight the unique properties of the JNC and reveal that ALI/ARDS rapidly induces a nerve injury-related state, changing vagal excitability.
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Registered trials
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