Inflammasomes are multiprotein complexes that serve as signaling platforms initiating innate immune responses. These structures are assembled upon a large array of stimuli, sensing both microbial products and endogenous signals indicating loss of cellular homeostasis. As such, inflammasomes are regarded as sensors of cellular integrity and tissue health, which, upon disruption of homeostasis, provoke an inflammatory response by the release of potent cytokines. Recent evidence suggests that in addition to sensing cellular integrity, inflammasomes are involved in the homeostatic mutualism between the host and its indigenous microbiota. Here, we summarize the involvement of various inflammasomes in host-microbiota interactions and focus on the role of commensal as well as pathogenic bacteria in inflammasome signaling.
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http://dx.doi.org/10.1007/s00281-014-0451-7 | DOI Listing |
Adv Sci (Weinh)
January 2025
Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Ischemic stroke is the most common cerebrovascular disease and the leading cause of permanent disability worldwide. Recent studies have shown that stroke development and prognosis are closely related to abnormal tryptophan metabolism. Here, significant downregulation of 3-hydroxy-kynurenamine (3-HKA) in stroke patients and animal models is identified.
View Article and Find Full Text PDFMucosal Immunol
January 2025
Institute for Laboratory Animal Science, Hannover Medical School, Hannover, Germany.
Intestinal immune homeostasis relies on intestinal epithelial cells (IECs), which provide an efficient barrier, and warrant a state of tolerance between the microbiome and the mucosal immune system. Thus, proper epithelial microbial sensing and handling of microbes is key to preventing excessive immunity, such as seen in patients with inflammatory bowel disease (IBD). To date, the molecular underpinnings of these processes remain incompletely understood.
View Article and Find Full Text PDFBiochem Soc Trans
January 2025
School of Biosciences, University of Sheffield, Western Bank, Sheffield, S10 2TN, United Kingdom.
NLRP3 is an inflammasome seeding pattern recognition receptor that initiates a pro-inflammatory signalling cascade in response to changes in intracellular homeostasis that are indicative of bacterial infection or tissue damage. Several types of post-translational modification (PTM) have been identified that are added to NLRP3 to regulate its activity. Recent progress has revealed that NLRP3 is subject to a further type of PTM, S-acylation (or palmitoylation), which involves the reversible addition of long-chain fatty acids to target cysteine residues by opposing sets of enzymes.
View Article and Find Full Text PDFJ Neurosci
January 2025
Department of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire 03766, USA.
Microglia respond to cytotoxic protein aggregates associated with the progression of neurodegenerative disease. Pathological protein aggregates activate the microglial NLRP3 inflammasome resulting in proinflammatory signaling, secretion, and potentially pyroptotic cell death. We characterized mixed sex primary mouse microglia exposed to microbial stressors and alpha synuclein preformed fibrils (αsyn PFFs) to identify cellular mechanisms related to Parkinson's disease.
View Article and Find Full Text PDFACS Appl Mater Interfaces
January 2025
Molecular Diagnostic Center, Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, Hangzhou First People's Hospital, Hangzhou 310006, China.
The designability and high reactivity of nanotechnology provide strategies for antitumor therapy by regulating the redox state in tumor cells. Here, we synthesize a kind of vanadium dioxide nanoparticle encapsulated in bovine serum albumin and containing disulfide bonds (VSB NPs) for photothermal-enhanced ferroptosis and pyroptosis effects. Mechanism studies show that disulfide bonds can effectively consume overexpressed glutathione (GSH) in the tumor microenvironment, leading to a decrease in glutathione peroxidase 4 (GPX4) activity.
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