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Chemokines form nanoparticles with DNA and can superinduce TLR-driven immune inflammation

ABSTRACT: Chemokines form nanoparticles with DNA and can superinduce TLR-driven immune inflammation

PROVIDER: PRJNA835473 | ENA |

REPOSITORIES: ENA

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Chemokines form nanoparticles with DNA and can superinduce TLR-driven immune inflammation

Project description:Chemokines are chemotactic cytokines that control the migratory patterns and positioning of immune cells. Many chemokines have been associated with systemic autoimmune diseases that have chronic IFN signature. We now describe that a series of chemokines, including CXCL4, CXCL10, CXCL12 and CCL5, can superinduce type I IFN (IFN-I) by TLR9-activated plasmacytoid DCs (pDCs), independently of their respective known chemokine receptors. Mechanistically, we show that chemokines such as CXCL4 mediate transcriptional and epigenetic changes in pDCs, mostly targeted to the IFN-I pathways. We also describe that chemokines physically interact with DNA to form nanoparticles which promote clathrin-mediated cellular uptake and delivery of DNA in the early endosomes of pDCs. Using two mouse models of skin inflammation, we observed the presence of CXCL4 associated with DNA in vivo. These data thus reveal a non-canonical role for chemokines to modulate TLR signaling, and extend our understanding on the mechanism associated with the chronic expression of IFN-I by pDCs in autoimmune diseases.

2022-05-24 | GSE202333 | GEO

Chemokines and galectins form heterodimers to modulate inflammation.

Project description:Chemokines and galectins are simultaneously upregulated and mediate leukocyte recruitment during inflammation. Until now, these effector molecules have been considered to function independently. Here, we tested the hypothesis that they form molecular hybrids. By systematically screening chemokines for their ability to bind galectin-1 and galectin-3, we identified several interacting pairs, such as CXCL12 and galectin-3. Based on NMR and MD studies of the CXCL12/galectin-3 heterodimer, we identified contact sites between CXCL12 ?-strand 1 and Gal-3 F-face residues. Mutagenesis of galectin-3 residues involved in heterodimer formation resulted in reduced binding to CXCL12, enabling testing of functional activity comparatively. Galectin-3, but not its mutants, inhibited CXCL12-induced chemotaxis of leukocytes and their recruitment into the mouse peritoneum. Moreover, galectin-3 attenuated CXCL12-stimulated signaling via its receptor CXCR4 in a ternary complex with the chemokine and receptor, consistent with our structural model. This first report of heterodimerization between chemokines and galectins reveals a new type of interaction between inflammatory mediators that can underlie a novel immunoregulatory mechanism in inflammation. Thus, further exploration of the chemokine/galectin interactome is warranted.

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Human keratinocytes exposed to tungsten carbide and tungsten carbide cobalt nanoparticles and cobalt chloride

Project description:Comparison of transcriptional profiles after exposure of HaCaT cells to WC or WC-Co nanoparticles and respective amount of free cobalt in form of CoCl2 after 3 hours and 3 days of exposure. Genes responding especially to nanoparticles or leached cobalt ions should be determined.

2010-02-01 | GSE16727 | GEO

miRNA Expression analysis from genomic form of Rhodopsin DNA Nanoparticles treated P23H Knock-in Heterozygous Mouse (P23H+/-)

Project description:Expression of miRNA analysis in mouse retinocytes was analysed using Next-generation sequencing (NGS) method in Rhodopsin DNA Nanoparticles treated P23H Knock-in Heterozygous Mouse (P23H+/-).

2020-06-24 | GSE153053 | GEO

Nanoparticles

Project description:Dietary silver nanoparticles can disturb the gut microbiota in mice

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miRNA Expression analysis from genomic form of Rhodopsin DNA Nanoparticles treated P23H Knock-in Heterozygous Mouse (P23H+/-)

Project description:miRNA Expression analysis from genomic form of Rhodopsin DNA Nanoparticles treated P23H Knock-in Heterozygous Mouse (P23H+/-)

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Chemokines profiling in tumors treated with UNC1999

Project description:Increased expression of chemokines in UNC1999-treated tumor tissues were successfully checked out through chemokines profiles screening of a total 25 different mouse chemokines using control and UNC1999-treated tumor tissues.

2022-08-25 | GSE211880 | GEO

Notch and TLR signaling coordinate monocyte cell fate and inflammation

Project description:Notch and TLR signaling coordinate monocyte cell fate and inflammation

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Application of Carbon Nanoparticles in Laparoscopic Colorectal Surgery

Project description:The project aims to evaluate the safety, effectiveness, accuracy and economy efficiency of the application of carbon nanoparticles for tumor localization and lymph nodes mapping in the laparoscopic coloectal surgery.

| 2259563 | ecrin-mdr-crc

Notch and TLR signaling coordinate monocyte cell fate and inflammation

Project description:We studied the role of Notch2 signaling in Ly6Chi monocyte cell fate during TLR7-induced acute inflammation. To characterize the gene expression changes involved in monocyte differentiation, we subjected monocyte subsets from peripheral blood of wt and myeloid Notch2 mutant mice after Sham or IMQ treatment to RNA-sequencing and gene expression analysis. We found that Cell-intrinsic Notch2 and TLR7-Myd88 pathways independently and synergistically promote Ly6Clo patrolling monocyte development from Ly6Chi monocytes under inflammatory conditions. At the same time TLR7 stimulation in the absence of functional Notch2 signaling promotes resident tissue macrophage gene expression signatures in monocytes and ectopic differentiation of Ly6Chi monocytes into macrophages and dendritic cells. Thus, Notch2 is a master regulator of Ly6Chi monocyte cell fate and inflammation in response to TLR signaling.

2020-08-04 | GSE147492 | GEO

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