A new Yale-led study finds that older adults are more susceptible to flu due to a reduced antiviral response, leading to increased inflammation and damage. Researchers propose targeting inflammation to combat flu in vulnerable patients.
Researchers found that SLE neutrophils release oxidized mitochondrial DNA, stimulating type I interferon production and contributing to disease pathogenesis. Targeting pathways for oxidized DNA degradation may offer new treatment options for chronic autoimmune disease.
Monophosphoryl lipid A (MPLA) has shown protective effects in mice with burn injuries, stimulating G-CSF production to bolster immune cells' ability to fight bacteria. Increased neutrophil levels mediate this protection.
Researchers found that pyruvate kinase M2 (PKM2) aids wound healing by promoting the development of new blood vessels at the wound site. PKM2 treatment aided early wound closure and promoted higher levels of vessel growth, suggesting its functional role in the wound healing process.
Researchers discovered that neutrophils can internalize C. neoformans in the brain vasculature and circulate them back into the bloodstream for removal. This process enables the prevention of cryptococcal meningoencephalitis, a deadly brain infection.
Researchers have discovered that neutrophils promote cardiac repair by producing a factor that stimulates the differentiation of macrophages, which accelerate tissue repair. This finding challenges previous views on neutrophils' role in inflammation and suggests a potential therapeutic approach to boost repair processes.
CNIC researchers have identified a new target for the treatment of fatty liver disease, p38 gamma and p38 delta proteins. Inhibition of these proteins with specific inhibitors has shown potential as a treatment for fatty liver disease, potentially preventing inflammation, liver damage, and diabetes linked to obesity.
Researchers discovered that mitochondrial reactive oxygen species induce cell death by NETosis in a process dependent on RNA-protein immune complexes found in lupus patients. The extracellular release of oxidized mitochondrial DNA promotes an inflammatory reaction, and scavengers that clean up the overflow can reduce type I interferon ...
A study reveals how CARD9 specifically protects the mammalian central nervous system (CNS) from fungal infections. Researchers found that mice and humans lacking functional CARD9 cannot recruit neutrophils to control Candida infection in the CNS, highlighting the critical role of CARD9 in promoting antifungal immunity.
A study reveals that Aspergillus fumigatus uses its sugar galactosaminogalactan to evade the immune system, making it more resistant to neutrophil killing and increasing its virulence. This finding suggests targeting GAG as a potential antifungal approach for human patients.
Researchers found that tamoxifen enhances clearance of antibiotic-resistant bacterial pathogen MRSA and reduces mortality in mice. The study suggests that tamoxifen's immune-boosting effect could aid the immune system in cases where traditional antibiotics have failed.
Research found that depleting the microbiome with antibiotics can reduce neutrophil activity in sickle cell disease, preventing acute crises and reducing organ damage. The study also suggests antibiotics may help treat septic shock by eliminating pro-inflammatory neutrophils.
The study found that immune cell-mediated thrombotic processes are a realistic target for novel therapies to prevent stent thrombosis. Leukocyte infiltrations were hallmarks of both early and late ST, with neutrophils being the most prominent subset.
Researchers at UTMB discovered a key mechanism behind developing allergic asthma and seasonal nasal allergies after exposure to airborne pollens like ragweed. The study found that neutrophils, white blood cells, attract in response to allergens, trigger inflammation and oxidative stress in the airways.
Researchers identified neutrophils as the bloody culprit behind immune cell-induced bleeding. Blocking neutrophil passage could prevent complications in transplant and chemotherapy patients.
Researchers found that neutrophils divert to nearby precancerous skin cells, causing rapid cell division and potentially leading to melanoma. The study suggests a physical link between wound-associated inflammation and skin cancer progression.
In a study published in Nature Medicine, researchers found that disabling the production of NETs (neutrophil extracellular traps) can speed up wound healing in diabetic mice. By preventing neutrophils from producing NETs, wounds healed more quickly and tissue repair was improved.
Researchers from Boston Children's Hospital discovered that body's own immune cells produce bacteria-trapping NETs, which slow healing in diabetic mice. Methods to prevent NET production or cleave them might alleviate wound healing problems in people with diabetes.
Researchers found that MET inhibitors can have a double-edged effect on tumors, promoting cell-cycle arrest or death in cancer cells while blunting pro-inflammatory reactions in neutrophils. This discovery could lead to optimizing cancer treatment by stratifying patients based on MET expression and dependency.
Researchers found that neutrophils can travel to lymph nodes within 8 hours of infection and prime other immune cells for attack. This collaboration between innate and adaptive arms may improve anti-microbial responses and prevent microbial spread.
Scientists at Helmholtz Zentrum München have identified a new isoform of neutrophil elastase involved in the pathogenesis of pulmonary emphysema. The cleaved form of the enzyme is particularly aggressive and resistant to inhibitors, leading to increased tissue damage.
Breast tumors trick immune cells to produce neutrophils that block T-cell action, allowing cancer to spread. Anti-IL17 drugs already exist for inflammatory diseases, offering potential treatment for metastatic breast cancer.
Research shows that different neutrophil subtypes exist, with some anti-tumor properties while others promote tumor progression. The study highlights the importance of targeting specific neutrophil populations to develop effective new therapies for cancer.
Enzymes linked to diabetes and obesity play key roles in arthritis and leukemia, potentially opening new avenues for treating these diseases. Targeting ether lipids may reduce neutrophil levels, allowing the immune system to return to normal.
Researchers developed a new technique to study neutrophil motion in confined spaces, revealing a second mode of motion that doesn't rely on integrins. The findings suggest that physical confinement is key to reproducing this motion and may lead to the development of new drugs to optimize neutrophil movement in specific tissue types.
Researchers at Massachusetts General Hospital have identified a potential biomarker for sepsis in patients with major burns. By analyzing the movement of white blood cells called neutrophils, they found that changes in their motility patterns may predict the development of sepsis, which is a leading cause of death among burn patients.
A new study reveals that macrophages induce neutrophil reverse migration to resolve inflammation in wounds. Without macrophages, neutrophils remain in wounds longer, leading to recurring infections and exaggerated inflammation.
The study found that younger people have a more robust immune response to grief, while elderly people are more likely to experience reduced immune function. The researchers suggest that hormonal supplements could be used to help individuals at risk of stress, but highlight the importance of a strong support network in managing grief.
Researchers at Kansas State University have discovered a family of proteins in Staphylococcus aureus that prevent neutrophils from functioning, leading to potential new treatments for staph infections and inflammatory diseases such as emphysema. The study sheds light on how the bacteria evade the immune system.
Research reveals Salmonella Typhi uses Vi capsular polysaccharide to evade neutrophil recognition, allowing it to disseminate throughout the body. The 'cloaking device' makes S. Typhi practically invisible to neutrophils.
Researchers discover periodontal bacteria selectively disarm immune system, promoting dysbiosis and bone loss. The study reveals a two-pronged mechanism involving protein receptors C5aR and TLR2, which protects 'bystander' gum bacteria from clearance.
Researchers found that inhibiting COX-2, an immune protein causing inflammation, eliminated recurrent urinary tract infections in mice. This suggests that over-the-counter painkillers like ibuprofen may reduce susceptibility to recurring UTIs by targeting the underlying inflammatory response.
Scientists found that inhibiting COX-2, an immune protein causing inflammation, eliminated recurrent urinary tract infections in mice. COX-2 inhibitors, such as ibuprofen, showed promise in reducing susceptibility to repeat infections without increasing future risk.
A team of University of Wisconsin-Madison researchers has developed a faster, cheaper and more accurate tool for diagnosing even mild cases of asthma. The handheld technology uses neutrophil cell function in a single drop of blood to diagnose asthma.
A new study led by Penn Dental Medicine researchers has reversed bone loss and inflammation in patients with leukocyte adhesion deficiency, a rare immune disorder. The breakthrough discovery identifies IL-17 as the key driver of periodontitis and bone loss in these patients.
Researchers at Case Western Reserve University have found a novel population of neutrophils that produce Interleukin 17 (IL-17) and exhibit enhanced microbial killing activity. These cells may contribute to both controlling infection and causing tissue damage, highlighting the need for further regulation.
Scientists created nanoparticles that selectively bind to abnormal immune cells causing inflammation, allowing anti-inflammatory drugs to reach them while leaving healthy ones untouched. This targeted approach shows promise for treating inflammatory diseases with fewer side effects.
Researchers at the University of Bonn have decoded a new immunoregulatory mechanism controlling defense in urinary tract infections. The mechanism involves two types of macrophages regulating neutrophils, with sentinel macrophages triggering an alarm and helper macrophages providing a safety mechanism to prevent collateral damage.
Scientists at Helmholtz Centre for Infection Research find that interferon-beta inhibits neutrophil migration into tumors, reducing new blood vessel formation and tumor growth. This discovery could improve treatment options for certain cancers.
Researchers discovered that despite apparent signs of improvement, GCA patients' neutrophils become severely altered after steroid therapy, potentially leading to stroke or blindness. This finding could lead to better clinical insight into disease progression and therapeutic control for GCA patients.
Researchers found that oxygen levels alter the effectiveness of anti-inflammatory glucocorticoid drugs in neutrophil lifespans. This discovery may help tailor anti-inflammatory agents to specific diseases, improving treatment outcomes for patients with severe asthma, COPD, and other inflammatory conditions.
Researchers from the University of Missouri School of Medicine found a more accurate way to screen for bacterial meningococcal infection in its early stages. They discovered that abnormalities in neutrophil counts can indicate a serious infection, including meningococcal disease.
Researchers have identified Human Neutrophil Peptide-1 (HNP-1) as a potential treatment for leishmaniasis, a vector-borne disease affecting young individuals worldwide. HNP-1 has been shown to directly kill Leishmania parasites and increase the lifespan of neutrophils, reducing their susceptibility to infection.
Researchers at UT Southwestern Medical Center have identified neutrophils, white blood cells, as a major source of interferon-gamma, a protein that stimulates the immune system to fight viruses and other pathogens. The discovery challenges long-held beliefs about the role of neutrophils in immunity.
A novel treatment using resolvins has restored appropriate neutrophil motion in burn-injured rats, significantly improving survival rates. The treatment may help determine risk of septic complications in patients and prevent associated deaths.
Researchers discovered that severe trauma injuries or burns lead to defective neutrophils, which contribute to septic complications. Measuring neutrophil motility could become a biomarker for predicting risk of septic complications and personalizing treatments.
Researchers discovered that discarded immune cells stimulate the release of hematopoietic stem cells from the bone marrow into the bloodstream. This process is regulated by the daily elimination of neutrophils and follows a circadian cycle, which could have implications for cardiovascular health.
Researchers found that hyperglycemia promotes the production of inflammatory cells, which contribute to plaque build-up in blood vessels. Treating diabetic mice with a drug that lowers blood sugar levels reduced circulating monocyte and neutrophil numbers and allowed plaques to heal.
Researchers at Sanford-Burnham discovered an imbalance between neutrophil elastase and its inhibitor causes inflammation, obesity, insulin resistance, and fatty liver disease. In mouse models and human studies, reversing this imbalance protected against weight gain, metabolic problems, and inflammation.
Researchers discovered that neutrophil membrane tethers act like slings to anchor the cell and maintain control during high-speed blood flow. This unique structure enables neutrophils to navigate through narrow venules without being swept away, allowing them to effectively present their antigen-sensing ligands at the infection site.
New study finds that blocking leukotriene B4 production reduces allergic skin inflammation in mice with eczema. Neutrophil recruitment to the skin is essential for the disease's development.
A new model developed by Weizmann Institute mathematicians and physicians proposes a more individualized approach to chemotherapy by considering not only the quantity but also the quality of blood cells. This could lead to better precautions for high-risk patients and spare unnecessary preventive treatments for those at low risk.
Researchers found that neutrophil elastase impairs insulin signaling and boosts resistance. Deletion of NE in obese mice improved insulin sensitivity. Neutrophils may hold the key to developing treatments for insulin resistance and diabetes.
Mount Sinai researchers found that neutrophils boost antibody production and reprogram B-cells to create a potent immune response. This discovery has significant promise for developing vaccines against blood-borne infections and HIV.
Researchers have discovered a human peptide that effectively blocks HIV entry into cells by targeting specific targets on both the virus and the cells. The peptide, human neutrophil peptide 1, prevents early and late stages of HIV-cell fusion and inhibits viral uptake without compromising cell function.
Researchers found that miR-122 modulates fat and cholesterol metabolism and has a tumor suppressive function in hepatocytes. A mouse model with MiR-122 loss of function also promoted breast tumor growth by differentially regulating ERα and ERβ.
Researchers use intravital two-photon imaging to track individual immune cells as they swarm into the heart muscle, causing inflammation and tissue damage. The technique allows for real-time observation of inflammation in the heart, paving the way for new therapeutic targets.
La Jolla Institute scientist Klaus Ley reveals a novel mechanism played a major role in inflammation. Neutrophils use sling-like membrane tethers to latch on to blood vessel walls during high blood flow, providing new insights into critical biological mechanisms underlying heart disease and other disorders.
Studies found that DNA damage activates NF-κB, a transcription factor driving cellular aging. Inflammation was also linked to oxidative stress, senescence, and degenerative changes caused by aging. Meanwhile, social isolation disrupted neurotransmission in young rodents, affecting AMPA receptor delivery and synaptic function.
Scientists at Max Planck Institute of Neurobiology have discovered a new serine protease, neutrophil serine protease 4 (NSP4), which forms part of the antibacterial defense arsenal of neutrophil granulocytes. NSP4 could provide a new target for treating diseases involving an overactive immune system.