A study by DGIST researchers found that brain inflammation leads to overactivity in NMDA glutamate receptors, causing repetitive behaviors in autism spectrum disorder (ASD) and obsessive-compulsive disorder (OCD). Administering memantine, a treatment for Alzheimer's disease, reduced symptoms and restored normal activity.
Researchers at KAIST have identified a key mechanism behind neuroinflammatory responses in Parkinson's disease, which is regulated by an RNA editing enzyme called ADAR1. This discovery suggests that targeting this enzyme could serve as a novel therapeutic strategy for treating the disease.
Scientists from DZNE found that preventing brain inflammation may help treat Alzheimer's disease. The study, published in Immunity, suggests that inhibiting the NLRP3 inflammasome can reduce neuroinflammation and help microglia clear harmful amyloid-beta deposits.
Researchers will showcase results of a randomized clinical trial demonstrating Biovanta's efficacy in reducing common cold symptoms by strengthening the respiratory barrier and controlling inflammation. The presentation will also include preclinical data on antiviral formulas targeting rhinovirus and influenza.
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Scientists at Duke-NUS Medical School have identified how mast cells release bioactive chemicals after encountering allergens, a critical step in anaphylactic shock. The discovery could lead to the development of drugs to prevent severe reactions and offers new hope for millions with asthma and food allergies.
Researchers discovered that fasting raises arachidonic acid levels, which inhibit the NLRP3 inflammasome and reduce chronic inflammation. This finding may explain how calorie restriction protects against diseases linked to Western diets.
A team of researchers discovered a multiprotein complex involving NLRP3, AIM2, NLRC4, and Pyrin that drives PANoptosis, a type of programmed inflammatory cell death. The findings have implications for understanding inflammasome biology and identifying potential therapeutic targets.
Research suggests visfatin stimulates membrane raft clustering, leading to NLRP3 inflammasome activation and podocyte injury. The study highlights the role of membrane raft redox signaling in visfatin-induced inflammation and kidney damage.
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Researchers found that inhibiting NLRP3 signaling reduces podocyte senescence, improves lifespan, and slows down healthy podocyte aging in mice. This discovery holds promise for treating age-related kidney diseases.
Researchers discovered that nickel-cobalt alloy nanocrystals inhibit the activation of three inflammasomes, including NLRP3, NLRC4, and AIM2, in primary macrophages. The study found that these nanocrystals effectively treated colitis and acute peritonitis by reducing disease symptoms.
A new study reveals a previously unknown way the immune system detects certain viruses, including SARS-Cov-2, using the inflammasome protein CARD8. Researchers found that CARD8 functions differently among various species and even varies between individuals in the human population.
A study published in PLOS Biology found that the CARD8 inflammasome sensor is essential for detecting coronavirus infections, but may detect different viruses in different people. The researchers also discovered that genetic variation among humans and across species affects the sensor's ability to detect viral enzymes.
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Researchers at USP in Brazil discovered that Leishmania parasites manipulate the protein gasdermin-D to prevent the immune system from killing them. This allows the parasite to continue replicating and causing disease. The findings offer hope for developing novel treatments for leishmaniasis, a disease affecting 30,000 people annually.
Scientists at Duke-NUS Medical School have discovered a protein called ASC2 that inhibits inflammasomes, thereby limiting inflammation in bats. This discovery could lead to the development of new anti-inflammatory drugs for human diseases, including those caused by viral infections and ageing.
Human macrophages use Siglec-14 receptors to recognize and engulf carbon nanotubes, leading to inflammation. The discovery could pave the way for developing safer carbon nanotubes and therapies to prevent inflammatory diseases.
Researchers have discovered how TKI cancer drugs cause inflammation, linking it to mitochondrial dysfunction and the NLRP3 inflammasome. The study found that all tested TKIs share a common off-target activity against mitochondrial SFKs.
Researchers discovered a previously unknown property of certain immune cells called Th17 cells, which produce the pro-inflammatory cytokine IL-1α. This finding sheds light on autoimmune diseases like rheumatoid arthritis in children and provides new insights into the defense against fungal infections.
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Researchers at the University of Bonn have identified a new signaling pathway that triggers inflammatory responses in the skin after UV damage. This pathway involves the activation of p38 molecularly modifying NLRP1, a critical switch for inflammation, and initiates the assembly of inflammasomes.
Researchers found that immune checkpoint blockade therapy may be beneficial for certain cases of severe COVID-19. In pre-clinical trials, treatment with a PD-1 inhibitor restored T cell functionality and reduced inflammation in mice infected by MHV-A59, another betacoronavirus.
A new study suggests that niclosamide, an anthelmintic drug, shows promise in combating exaggerated inflammation associated with severe COVID-19. The drug's anti-inflammatory effects are attributed to its inhibition of the inflammasome mechanism, a protein complex present in defense cells.
Researchers have identified two NLRP sensors, NLRP1 and CARD8, as key players in Coxsackievirus B3-induced heart inflammation. Targeting CARD8 may prevent CVB3 infections from progressing to heart failure. The study provides new insights into the inflammatory response triggered by this common viral cause of viral myocarditis.
A new study suggests that supplementing a diet with Ascidiacea, also known as sea squirts, reverses some main signs of aging in animal models. The researchers found that plasmalogens, vital to body processes, decrease with age and contribute to neurodegenerative diseases like Alzheimer's and Parkinson's.
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Researchers found that Rivaroxaban reduces atherosclerosis progression by inhibiting factor Xa-PAR2 mediated macrophage autophagy and inflammasome activity. The study suggests RIV as a potential anti-atherosclerotic drug, offering hope for treating this fatal disease.
Research in mice suggests that first-responder cells launching repair after a heart attack promote more inflammation than necessary, threatening optimum healing of the heart.
Researchers at the University of Maryland discovered a gene in tuberculosis that inhibits the inflammasome, a signaling system that helps defend against pathogens. The finding may lead to effective gene-based treatments or preventative therapies for tuberculosis.
Researchers discovered that cannabidiol accelerates oral ulcer healing by inactivating the CMPK2-mediated NLRP3 inflammasome. This mechanism may lead to the development of new treatments for oral ulcers.
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The study found that AIM2 inflammasome is at the intersection of COPD and lung cancer, with higher expression correlating to lower survival rates in smoking COPD adenocarcinoma patients. This suggests that the AIM2 inflammasome may be a potential target for developing novel treatments for COPD patients who develop lung cancer.
Researchers from Kanazawa University found that gasdermin D forms pores in the cell membrane, allowing factors to flow in and activating IL-1® maturation. This study provides insight into the essential functions of the human immune system and the regulation of immune function.
Researchers found that metformin prevents pulmonary inflammation, a major factor in COVID-19 severity and mortality, by inhibiting inflammasome activation and reducing IL-1β production. Metformin may have therapeutic potential for treating severe COVID-19 and other forms of acute respiratory distress syndrome.
Research finds inflammasomes play a role in inflammation and intestinal barrier integrity. Obesity-associated colon cancer is linked to increased gene expression levels of certain proteins, including NLRP3 and IL1B.
A study published in International Immunology found that a tropical ginger-derived compound, ACA, attenuates mitochondrial damage and reduces inflammation by blocking the activation of the NLRP3 inflammasome. This suggests ACA may be a promising therapeutic strategy for diseases such as rheumatoid arthritis.
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Researchers found that anti-inflammatory therapies could be effective in preventing heart disease in people with clonal hematopoiesis, a common age-related blood condition. The study suggests that targeting the inflammasome may reduce cardiovascular risk and improve plaque stability.
Researchers led by Olaf Groß will test the effectiveness of their IMMUNOSTIM compounds in boosting cancer treatment and vaccine efficacy. The team aims to develop a new class of immune-activating drugs that can enhance the body's natural defense against infectious diseases.
Researchers at University of Pennsylvania School of Veterinary Medicine discovered that gut cells lining intestines send warning signals to the immune system upon parasite invasion. The discovery sheds light on early stages of pathogen recognition and response.
Researchers find that inhibiting pro-IL-1α helps modulate NLRP3 inflammasome activation, reducing damage to mitochondria and alleviating inflammation. This discovery offers potential therapeutic applications for treating various diseases, including atherosclerosis, arthritis, and Alzheimer's disease.
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Researchers identified two inflammatory pathways involving complement and the inflammasome that promote abnormal blood vessel formation in wet AMD. Blocking these pathways, including essential proteins of the inflammasome, may lead to improved therapies for this common blinding disease.
Research reveals Aspergillus fumigatus activates inflammasome through galactosaminogalactan, increasing inflammation. The fungal pathogen's GAG is essential for NLRP3 inflammasome activation.
Researchers found that inflammasomes, a type of immune cell complex, are activated in response to SARS-CoV-2 infection, leading to excessive inflammation and potentially life-threatening complications. The study provides new insights into the disease's progression and suggests potential therapeutic targets.
A new study by the University of Bonn reveals that platelets exacerbate immune responses by activating inflammasomes and increasing IL-1 production. This finding has significant implications for treating autoimmune diseases such as rheumatism and diabetes.
Researchers are working on developing drugs that inhibit the function of NLRP3, an inflammatory protein involved in various diseases such as atherosclerosis, cancer, Alzheimer's, Parkinson's, and arthritis. Several NLRP3 inhibitors are currently in preclinical trials with varying mechanisms.
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Scientists at UC Berkeley have identified a molecular 'switch' that controls chronic inflammation, which can contribute to devastating diseases. Removing a small bit of molecular matter through deacetylation switches off the immune machinery, potentially reversing age-related conditions.
Researchers at Cincinnati Children's Hospital Medical Center discovered a new molecular process in mice that triggers T cell-driven inflammation and causes autoimmune diseases. The study found that interactions between myeloid cells and CD4-positive T cells produce excessive IL-1b, leading to auto-inflammatory diseases.
A Brazilian team at FAPESP-supported Center for Research on Inflammatory Diseases identified the strategy used by immune cells to combat the pathogen Mayaro virus. The study provides a basis for the development of drugs against this disease, targeting the NLRP3 inflammasome and its role in producing proinflammatory molecules.
Researchers found that inflammatory processes triggered by the NLRP3 inflammasome play a key role in emerging tau pathology, a hallmark of neurodegenerative diseases like Alzheimer's. The study suggests that modulating the immune response could be a promising approach for treating these conditions.
A study published in Mucosal Immunology reveals that ASC and NLRP3 are key players in maintaining innate immune homeostasis in the airway, independent of caspase-1. This alternative mechanism may provide a new understanding of different possible mechanisms involved in airway protection against microbial infections.
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Scientists at St. Jude Children's Research Hospital have identified DDX3X as a crucial molecule in determining the fate of stressed cells. The molecule plays a pivotal role in regulating the innate immune response and helps cells interpret and respond to various stressors with measures meant to ensure cell survival or death. This findi...
Researchers at Umea University found that bacteria release hydrogen peroxide to inactivate inflammasomes, a key component of the immune system. Vitamins like Vitamin C may boost anti-bacterial immunity by neutralizing hydrogen peroxide.
Researchers at University of Queensland discover a way to stop inflammation by inhibiting the inflammasome protein complex. This breakthrough could lead to the design of new anti-inflammatory drugs, informing treatment for chronic inflammatory diseases such as Parkinson's and Alzheimer's.
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Scientists have discovered that bacterial proteins and endotoxin activate the inflammasome, leading to pyroptosis and the release of tissue factor, which initiates blood clotting. This understanding may lead to new treatments for sepsis by targeting inflammatory responses.
A team of researchers from Trinity College Dublin has discovered that SARM plays an important role in the immune response and regulates inflammation. The study suggests that targeting SARM could provide a new option for treating diseases such as diabetes, cancer, and Alzheimer
Researchers developed a new method to alleviate chronic inflammatory disease by inducing mitophagy and removing damaged mitochondria. The treatment with choline kinase inhibitors reduced NLRP3 inflammasome activation and prevented inflammation in mice with genetic diseases such as Muckle-Well Syndrome.
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A new study found that the mutated MLX gene impairs the immune system by promoting inflammasome activation, leading to chronic inflammation and arterial disease. The discovery provides potential treatments, such as tocilizumab, which has shown efficacy in other inflammatory diseases.
Scientists have identified a previously unknown structural change within cells that triggers the activation of the inflammasome, a multiprotein complex involved in inflammation. This finding provides a new avenue for developing therapeutics to target the NLRP3 pathway for inflammatory diseases.
Researchers at the University of California San Diego School of Medicine have identified a signaling pathway that activates the NLRP3 inflammasome implicated in several severe chronic inflammatory disorders. Blocking the CMPK2 enzyme may result in new treatments for osteoarthritis, Alzheimer's disease, and lung cancer.
Researchers found that activating inflammatory signaling in heart cells can lead to abnormal electrical patterns similar to those observed in atrial fibrillation. This suggests a potential new target for therapies aiming to treat the condition.
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A team of researchers has created a mouse model exhibiting diabetic retinopathy symptoms, paving the way for future translational research studies. The study also reveals that the NLRP3 inflammasome plays a key role in the development of diabetic retinopathy.
Researchers have uncovered how an inflammation process automatically switches off in healthy cells, a discovery that could lead to stopping damage caused by uncontrolled inflammation. The study focuses on inflammasomes, which are machine-like protein complexes at the heart of inflammation and disease.
Researchers use cryo-EM to visualize the molecular interface between flagellin and NAIP5, revealing how bacteria are recognized by the immune system. The study found that flagellin is in contact with six different parts of NAIP5, providing new insights into potential strategies for protection from pathogens.
Researchers at LMU's Gene Center found that human cells use a different mechanism to recognize misplaced DNA than mouse cells. The inflammasome complex is activated via the cGAS-STING recognition mechanism, triggering both an antiviral response and a classical inflammatory reaction.
A team of researchers discovered a way to treat severe inflammation from mosquito-borne diseases like Chikungunya and Ross River virus. They developed an NLRP3 inhibitor drug MCC950, which provided significant relief from inflammation and disease in infected mice.
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