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Bi-directional neuro-immune communication regulates host defense against helminth infection

ABSTRACT: Bi-directional neuro-immune communication regulates host defense against helminth infection

PROVIDER: PRJNA1082736 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28198166_1.fastq.gz	Fastqsanger.gz
	SRR28198166_2.fastq.gz	Fastqsanger.gz
	SRR28198167_1.fastq.gz	Fastqsanger.gz
	SRR28198167_2.fastq.gz	Fastqsanger.gz
	SRR28198168_1.fastq.gz	Fastqsanger.gz

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Bi-directional neuro-immune communication regulates host defense against helminth infection

Project description:Emerging studies reveal that neuropeptides play critical role in regulating anti-helminth immune responses, hinting at the potential of intrinsic enteric neurons (iENs) in orchestrating intestinal immunity. However, whether and how the iENs get activated during infection, and whether they engage in a bi-directional communication with the immune cells, remain poorly defined. Here we show that iENs became activated in response to helminth infection. Single-nucleus RNA sequencing of the iENs revealed significant alterations in gene expression in IL-13R+ intrinsic primary afferent neurons (IPANs), including the upregulation of the neuropeptide -CGRP. Using genetic mouse models, we demonstrated that both group 2 innate lymphoid cells (ILC2s) and neuronal IL-13R signaling are indispensable for optimal iEN activation, which subsequently inhibit ILC2 responses and anti-helminth immunity. Together, these results reveal a previously unrecognized bi-directional neuro-immune crosstalk in the intestine.

2025-01-31 | GSE260708 | GEO

Directional endothelial communication by polarized extracellular vesicle release

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Bi-directional interactions of omental adipocytes and SKOV3ip1 cells

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Bi-directional regulation between circadian rhythm and neurodegeneration-associated FUS

Project description:Circadian rhythms are daily physiological and behavioral changes governed by an internal molecular clock, and dysfunctions in circadian rhythms have long been associated with various neurodegenerative diseases. Abnormal sleep-wake cycle often precedes the onset of cognitive and motor symptoms in patients, while the pathological changes may further exacerbate the disturbance in circadian cycle. It is unclear whether dysregulated circadian rhythm is a consequence of, or a contributing factor for, neurodegeneration. In addition, the evidence directly connecting the neurodegeneration-associated proteins to core circadian clock gene expression remains sparse. Here we show that FUS, a RNA-binding protein implicated in the pathogenesis of ALS and frontotemporal dementia, exhibits a bi-directional regulation with circadian rhythm. Our meta-analysis of RNAseq datasets and subsequent biochemical analysis revealed FUS as a gene regulated by circadian oscillation. Furthermore, NR1D1 binds the FUS promoter and regulates the amplitude of FUS oscillation. Meanwhile, FUS is recruited by transcriptional co-repressor PSF, and is found in the same complex as Bmal-Clock to repress Per2 expression. More strikingly, in cells and brain tissues from homozygous knock-in rats, the pathogenic R521C mutant FUS significantly alters the oscillation patterns of core circadian genes even at young age. Therefore, our results have revealed a novel bi-directional mechanism whereby dysregulated circadian clock and FUS expression may exacerbate neurodegeneration via mutual influence.

2017-04-12 | GSE77572 | GEO

Bi-directional epithelial-mesenchymal crosstalk provides self-sustaining pro-fibrotic signals in pulmonary fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is the prototypic progressive fibrotic lung disease with a median survival of 2-4 years. Injury to and/or dysfunction of alveolar epithelium are strongly implicated in IPF disease initiation, but what factors determine why fibrosis progresses rather than normal tissue repair occurs remain poorly understood. We previously demonstrated that ZEB1-mediated epithelial-mesenchymal transition (EMT) in human alveolar epithelial type II (ATII) cells augments TGF-β-induced profibrogenic responses in underlying lung fibroblasts by paracrine signalling. Here we investigated bi-directional epithelial-mesenchymal crosstalk and its potential to drive fibrosis progression. RNA sequencing (RNA-seq) of lung fibroblasts exposed to conditioned media from ATII cells undergoing RAS-induced EMT identified many differentially expressed genes including those involved in cell migration and extracellular matrix (ECM) regulation. We confirmed that paracrine signalling between AS-activated ATII cells and fibroblasts augmented fibroblast recruitment and demonstrated that this involved a ZEB1-tissue plasminogen activator (tPA) axis. In a reciprocal fashion, paracrine signalling from TGF-β-activated lung fibroblasts or IPF fibroblasts induced RAS activation in ATII cells, at least partially via the secreted protein, SPARC. Together these data identify that aberrant bi-directional epithelial-mesenchymal crosstalk in IPF drives a chronic feedback loop that maintains a wound-healing phenotype and provides self-sustaining pro-fibrotic signals.

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Bi-directional ribosome scanning controls the stringency of start codon selection

Project description:The fidelity of start codon recognition by ribosomes is paramount during protein synthesis. The textbook knowledge of eukaryotic translation initiation depicts 5’→3’ unidirectional migration of the pre-initiation complex (PIC) along the 5’UTR. In probing translation initiation from ultra-short 5’UTR, we report that an AUG triplet near the 5’ end can be selected via PIC backsliding. The bi-directional ribosome scanning is supported by competitive selection of closely spaced AUG codons and recognition of two initiation sites flanking an internal ribosome entry site. Transcriptome-wide PIC profiling reveals footprints with an oscillation pattern near the 5’ end and start codons. Depleting the RNA helicase eIF4A leads to reduced PIC oscillations and impaired selection of 5’ end start codons. Enhancing the ATPase activity of eIF4A promotes nonlinear PIC scanning and stimulates upstream translation initiation. The helicase-mediated PIC conformational switch may provide an operational mechanism that unifies ribosome recruitment, scanning, and start codon selection.

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