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Litomosoides sigmodontis microfilariae-induced eosinophil ETosis is dependent on the canonical inflammasome pathway.
Cell Rep
January 2025
Institute for Medical Microbiology, Immunology and Parasitology, University Hospital Bonn, 53127 Bonn, Germany; German Center for Infection Research (DZIF), Partner Site Bonn-Cologne, Bonn, Germany.
Granulocytes exert several effector mechanisms, including the release of DNA traps during ETosis. While bacteria-induced ETosis has been linked to the non-canonical inflammasome pathway, the role of the inflammasome activation during ETosis in response to extracellular pathogens has not been investigated. The current study demonstrates that microfilariae (MF) of the rodent filarial nematode Litomosoides sigmodontis induce eosinophil ETosis via the canonical inflammasome pathway.
View Article and Find Full Text PDFDHX15 and Rig-I Coordinate Apoptosis and Innate Immune Signaling by Antiviral RNase L.
Viruses
December 2024
Department of Biological Sciences, University of Toledo, 2801 West Bancroft Street, Toledo, OH 43606, USA.
During virus infection, the activation of the antiviral endoribonuclease, ribonuclease L (RNase L), by a unique ligand 2'-5'-oilgoadenylate (2-5A) causes the cleavage of single-stranded viral and cellular RNA targets, restricting protein synthesis, activating stress response pathways, and promoting cell death to establish broad antiviral effects. The immunostimulatory dsRNA cleavage products of RNase L activity (RL RNAs) recruit diverse dsRNA sensors to activate signaling pathways to amplify interferon (IFN) production and activate inflammasome, but the sensors that promote cell death are not known. In this study, we found that DEAH-box polypeptide 15 (DHX15) and retinoic acid-inducible gene I (Rig-I) are essential for apoptosis induced by RL RNAs and require mitochondrial antiviral signaling (MAVS), c-Jun amino terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK) for caspase-3-mediated intrinsic apoptosis.
View Article and Find Full Text PDFAnalysis of regulatory patterns of NLRP3 corpuscles and related genes and the role of macrophage polarization in atherosclerosis based on online database.
Mol Genet Genomics
December 2024
Department of Cardiovascular Medicne, The Second Affiliated Hospital of Nanchang University, No.1 Minde Road, Nanchang, 330006, P.R. China.
Our study examined the relationships and interactions among 30 genes related to the NOD-like receptor protein 3 (NLRP3) inflammasome. We identified 368 interconnections between these 30 genes, with NLRP3 participating in 38 interactions. The potential roles of these genes in atherosclerosis were evaluated based on protein-protein interaction networks and coexpression analysis.
View Article and Find Full Text PDFAntimicrobial Peptide CATH-2 Attenuates Avian Pathogenic -Induced Inflammatory Response via NF-κB/NLRP3/MAPK Pathway and Lysosomal Dysfunction in Macrophages.
Int J Mol Sci
November 2024
Joint International Research Laboratory of Animal Health and Animal Food Safety, College of Veterinary Medicine, Southwest University, Chongqing 400715, China.
Cathelicidins have anti-inflammatory activity and chicken cathelicidin-2 (CATH-2) has shown to modulate immune response, but the underlying mechanism of its anti-inflammation is still unclear. Therefore, in this study, we investigated the anti-inflammatory activity of CATH-2 on murine peritoneal macrophages during avian pathogenic (APEC) infection. The results showed that CATH-2 priming significantly reduced the production of IL-1β, IL-6, IL-1α, and IL-12.
View Article and Find Full Text PDFCrosstalk between SIRT1/Nrf2 signaling and NLRP3 inflammasome/pyroptosis as a mechanistic approach for the neuroprotective effect of linagliptin in Parkinson's disease.
Int Immunopharmacol
January 2025
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, 11562, Egypt. Electronic address:
In recent years, special attention has been paid to highlighting the antiparkinsonian effect of linagliptin. However, the mechanism of its action has not yet been well investigated. The present study aimed to verify the neuroprotective effect of linagliptin in the rotenone model of Parkinson's disease (PD) and further explore its potential molecular mechanisms.
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