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Sensory Neurons Promote Immune Homeostasis in the Lung

ABSTRACT: Sensory Neurons Promote Immune Homeostasis in the Lung

PROVIDER: PRJNA910080 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22574319_1.fastq.gz	Fastqsanger.gz
	SRR22574319_2.fastq.gz	Fastqsanger.gz
	SRR22574320_1.fastq.gz	Fastqsanger.gz
	SRR22574320_2.fastq.gz	Fastqsanger.gz
	SRR22574321_1.fastq.gz	Fastqsanger.gz

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Sensory Neurons Promote Immune Homeostasis in the Lung

Project description:Cytokines employ downstream Janus kinases (JAKs) to promote many chronic inflammatory disorders. JAK1-dependent type 2 cytokines drive allergic inflammation and patients with JAK1 gain-of-function (GOF) variants develop atopic dermatitis (AD) and asthma. To explore the tissue-specific role of JAK1, we inserted a human JAK1 GOF variant into mice and observed the spontaneous development of AD-like skin inflammation but unexpected resistance to allergic lung inflammation when JAK1 GOF expression was restricted to the stroma. Further, we identified the chemical denervation of both vagal and spinal visceral afferents exacerbated allergic lung inflammation, though selective denervation of spinal visceral afferent did not change the disease severity compared to control groups. Collectively, we suggested that neuron-intrinsic JAK1 in the vagal afferents protect against allergic lung inflammation.

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Immunity to the microbiota promotes sensory neurons regeneration via IL-17A

Project description:Tissue physiology and responses to injury can be controlled by the cross-talk between all physiological systems including the nervous and immune system. How the microbiota influences this dialogue remains unclear. Here, we show that adaptive responses to the microbiota directly promote sensory neuron regeneration. At homeostasis, commensal-specific Th17 co-localize with sensory neurons within the dermis and display a transcriptional profile associated with tissue and nerve repair. Following injury, commensal-specific Th17 cells promote axon growth and local nerve regeneration. Mechanistically, our data support the idea that IL17-A produced by commensal-specific T cells directly signal sensory neurons via IL17RA, the transcription of which is specifically upregulated in injured neurons. Collectively our work reveals that microbiota-specific T cells can bridge biological systems by directly promoting neuronal repair and identify IL17-A as a major determinant of this fundamental process.

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Project description:We report that molecularly distinct populations of vagal sensory neurons would play a role in causing differences in metabolic homeostasis between the sexes.

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Project description:Sensory neurons are nerve cells that are activated by sensory input such as heat, light and convey information to the brain. Although a key cell type in complex organisms, human sensory neurons are challenging to study because they are impossible to obtain from living donors. We have collaborated with the Neucentis Pharmaceutical Research Unit to differentiate sensory neuron like cells from human induced pluripotent stem cells derived as part of the Human Induced Pluripotent Stem Cells Initiative. We will sequence RNA from 100 IPS lines derived from healthy individuals and perform RNA-seq on the differentiated cells to identify noncoding variants that alter gene expression in human sensory neurons.

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Project description:PNS injuries initiate transcriptional changes in glial cells and sensory neurons that promote axonal regeneration. While the factors that initiate the transcriptional changes in glial cells are well characterized, the full range of stimuli that initiate the response of sensory neurons remain elusive. Here, using a genetic model of glial cell ablation, we find that glial cell loss results in transient PNS demyelination without overt axonal loss. By profiling sensory ganglia at single-cell resolution we show that glial cell loss induces a transcriptional injury response preferentially in proprioceptive and Aβ RA-LTMR neurons. The transcriptional response of sensory neurons to mechanical injury has been assumed to be a cell autonomous response. By identifying a similar response in non-injured, demyelinated neurons, our study suggests that this represents a non-cell autonomous transcriptional response of sensory neurons to the loss of axon-glial cell interactions.

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