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.
Subject(s)
Nodose Ganglion/drug effects , Pneumonia/genetics , Receptor, Cholecystokinin B/genetics , Sensory Receptor Cells/drug effects , Transcriptome , Vagus Nerve Injuries/genetics , Animals , Ganglia, Spinal/drug effects , Ganglia, Spinal/immunology , Ganglia, Spinal/pathology , Gene Expression Profiling , Intracellular Signaling Peptides and Proteins/genetics , Intracellular Signaling Peptides and Proteins/immunology , Lipopolysaccharides/pharmacology , Lung/drug effects , Lung/immunology , Lung/pathology , Membrane Proteins/genetics , Membrane Proteins/immunology , Mice , Mice, Inbred C57BL , Nodose Ganglion/immunology , Nodose Ganglion/pathology , Peptide Hormones/genetics , Peptide Hormones/immunology , Pneumonia/chemically induced , Pneumonia/immunology , Pneumonia/pathology , Receptor, Cholecystokinin B/immunology , Receptors, G-Protein-Coupled/genetics , Receptors, G-Protein-Coupled/immunology , Sensory Receptor Cells/immunology , Sensory Receptor Cells/pathology , Sequence Analysis, RNA , Trigeminal Ganglion/drug effects , Trigeminal Ganglion/immunology , Trigeminal Ganglion/pathology , Vagus Nerve Injuries/chemically induced , Vagus Nerve Injuries/immunology , Vagus Nerve Injuries/pathologyABSTRACT
We herein report the first case of glossopharyngeal nerve and vagus nerve palsies that appeared after an influenza vaccination. A 15-year-old boy developed dysphagia and dysarthria seven days after receiving an inoculation of the inactivated influenza vaccine. Massive intravenous immunoglobulin (IVIg) treatment was applied, as the patient's symptoms were considered to be immunological adverse effects of the influenza vaccine. He responded well to IVIg, and the symptoms immediately diminished. The mechanisms underlying the development of neurologic symptoms following vaccination are difficult to determine; however, providing immediate immunological treatment, such as IVIg, is effective and beneficial in countering these symptoms.