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Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide induced lung inflammation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE141400 | GEO | 2020/03/15

REPOSITORIES: GEO

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Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide-induced lung inflammation.

Project description: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.

| S-EPMC7272742 | biostudies-literature

Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide induced lung inflammation III

Project description:While the inflammatory immune response of the lung to allergens and pathogens has been extensively studied, little is known about how sensory nerves change in response to an inflammatory insult within the organ they innervate. In our study we describe the collection of vagal sensory neurons innervating the mouse lung, labelled with a retrograde fluorescent tracer instilled into the airways, and the analysis of their transcriptomes by RNAseq. We also determined transcriptomes of the complete sensory ganglia (vagal, trigeminal, DRG) for comparison. We identified transcripts of genes exclusively expressed in vagal nerves, and not in any other sensory nerve type or any other organ. These include unique ion channels, G-protein coupled receptors and several transcripts of unknown function.

2020-03-15 | GSE141399 | GEO

Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide induced lung inflammation II

2020-03-15 | GSE141395 | GEO

Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide induced lung inflammation I

2020-03-15 | GSE141268 | GEO

Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide induced lung inflammation

Project description:Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide induced lung inflammation

| PRJNA593269 | ENA

Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide induced lung inflammation III

Project description:Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide induced lung inflammation III

| PRJNA593271 | ENA

Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide induced lung inflammation I

Project description:Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide induced lung inflammation I

| PRJNA592995 | ENA

Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide induced lung inflammation II

Project description:Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide induced lung inflammation II

| PRJNA593272 | ENA

Acute inflammation sensitizes knee-innervating sensory neurons and decreases mouse digging behavior in a TRPV1-dependent manner.

Project description:Ongoing, spontaneous pain is characteristic of inflammatory joint pain and reduces an individual's quality of life. To understand the neural basis of inflammatory joint pain, we made a unilateral knee injection of complete Freund's adjuvant (CFA) in mice, which reduced their natural digging behavior. We hypothesized that sensitization of knee-innervating dorsal root ganglion (DRG) neurons underlies this altered behavior. To test this hypothesis, we performed electrophysiological recordings on retrograde labeled knee-innervating primary DRG neuron cultures and measured their responses to a number of electrical and chemical stimuli. We found that 24-h after CFA-induced knee inflammation, knee neurons show a decreased action potential generation threshold, as well as increased GABA and capsaicin sensitivity, but have unaltered acid sensitivity. The inflammation-induced sensitization of knee neurons persisted for 24-h in culture, but was not observed after 48-h in culture. Through immunohistochemistry, we showed that the increased knee neuron capsaicin sensitivity correlated with enhanced expression of the capsaicin receptor, transient receptor potential vanilloid 1 (TRPV1) in knee-innervating neurons of the CFA-injected side. We also observed an increase in the co-expression of TRPV1 with tropomyosin receptor kinase A (TrkA), which is the receptor for nerve growth factor (NGF), suggesting that NGF partially induces the increased TRPV1 expression. Lastly, we found that systemic administration of the TRPV1 antagonist, A-425619, reversed the decrease in digging behavior induced by CFA injection, further confirming the role of TRPV1, expressed by knee neurons, in acute inflammatory joint pain.

| S-EPMC6277850 | biostudies-literature

G9a participates in nerve injury-induced Kcna2 downregulation in primary sensory neurons.

Project description:Nerve injury-induced downregulation of voltage-gated potassium channel subunit Kcna2 in the dorsal root ganglion (DRG) is critical for DRG neuronal excitability and neuropathic pain genesis. However, how nerve injury causes this downregulation is still elusive. Euchromatic histone-lysine N-methyltransferase 2, also known as G9a, methylates histone H3 on lysine residue 9 to predominantly produce a dynamic histone dimethylation, resulting in condensed chromatin and gene transcriptional repression. We showed here that blocking nerve injury-induced increase in G9a rescued Kcna2 mRNA and protein expression in the axotomized DRG and attenuated the development of nerve injury-induced pain hypersensitivity. Mimicking this increase decreased Kcna2 mRNA and protein expression, reduced Kv current, and increased excitability in the DRG neurons and led to spinal cord central sensitization and neuropathic pain-like symptoms. G9a mRNA is co-localized with Kcna2 mRNA in the DRG neurons. These findings indicate that G9a contributes to neuropathic pain development through epigenetic silencing of Kcna2 in the axotomized DRG.

| S-EPMC5118693 | biostudies-literature

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