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Role of mechanical signal in regulating neutrophil function

ABSTRACT: Role of mechanical signal in regulating neutrophil function

PROVIDER: PRJNA863667 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20717459_1.fastq.gz	Fastqsanger.gz
	SRR20717459_2.fastq.gz	Fastqsanger.gz
	SRR20717460_1.fastq.gz	Fastqsanger.gz
	SRR20717460_2.fastq.gz	Fastqsanger.gz
	SRR20717461_1.fastq.gz	Fastqsanger.gz

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Role of mechanical signal in regulating neutrophil function

Project description:It is not understood, how mechanical signals influence the behavior and action of circulating cells in our body. Previous studies showed that the process of migration through narrow slits might enhance lifespan of polymorpho-nuclear cells (PMN / neutrophil). But it is unknown, how the mechanical signal is received, relayed, and translated into specific phenotype shift in PMN. Here we investigated whether compressional force affects defense system of circulating lymphocytes by increasing their killing ability during migration through narrow endothelial junctions. To decipher the receiving and transducing components of this mechanical signal relay process, we performed gene expression analysis between transmigrated and non-transmigrated neutrophils. Comparison of early gene-expression pattern of transmigrated and non-transmigrated neutrophils revealed a huge change in gene expression profile. Molecular and genetic analysis of the proteins revealed from gene-expression analysis led us to understand the mechanism of mechanical signal relay from the neutrophil membrane to bacterial-killing machinery. As neutrophils are most abundant and immediate-responding circulating immune cells in our body, our study advances the path for understanding the general process of mechano-transduction, and mechano-modulatory applications with mechanically enhanced neutrophils.

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Study on the mechanisms of Piezo1-lars2 signal path mediating the mechanical loading on endochondral ossification process of fracture healing

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Neutrophil trapping and nexocytosis are mast cell processes for inflammatory signal relay

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MicroRNA-183 cluster continuously scales mechanical pain sensitivity by regulating basal and neuropathic pain gene pathways.

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WFA+ Mac-2 binding protein (M2BPGi) regulating signal in the HCC cells

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Transcriptome analysis of CD16/CD62L neutrophil subsets during human experimental endotoxemia

Project description:During systemic inflammation, different neutrophil subsets are mobilized to the blood circulation. These neutrophil subsets can be distinguished from normal circulating neutrophils (CD16bright/CD62Lbright) based on either an immature CD16dim/CD62Lbright or a CD16bright/CD62Ldim phenotype. Interestingly, the latter neutrophil subset is known to suppress lymphocyte proliferation ex vivo, but the underlying mechanism is largely unknown. We performed transcriptome analysis on the different neutrophil subsets to identify changes that are relevant for their functions. Neutrophil subsets were isolated by FACS sorting from the blood of healthy volunteers who were administered a single dose of lipopolysaccharide (LPS). The transcriptome was determined by microarray. The mobilized neutrophil subsets were characterized by specific transcriptome profiles reflecting their phase in neutrophil lifespan. Interestingly, the CD16bright/CD62Ldim suppressive neutrophils showed an interferon-induced transcriptome profile. This was confirmed by stimulation of peripheral neutrophils with IFNgamma. These cells acquired the capacity to suppress lymphocyte proliferation through the expression of programmed death ligand 1 (PD-L1). These data demonstrate that the suppressive phenotype of the neutrophil subset is induced by IFNgamma. Specific stimulation of neutrophils might have a pivotal role in regulating lymphocyte-mediated inflammation and autoimmune disease. After LPS infusion, blood was taken at t=0 and t=4 hours. Neutrophils were FACS sorted based on CD16 and CD62L expression. Gene expression of neutrophil subsets was assessed relative to t=0 as control.

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