Articles tagged with Neutrophils
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Research reveals that IL-26 is increased among chronic smokers with lung disease, mobilizing neutrophils and exacerbating bacterial infections. The study provides new insights into the pathogenic mechanisms behind COPD and chronic bronchitis, suggesting IL-26 as a promising molecular target for therapy.
Researchers at Boston Children's Hospital describe an innovative approach that boosts neutrophil strength and kills bacteria more effectively, while minimizing lung tissue damage. By inhibiting IP6K, a key enzyme, the immune system produces 'super' neutrophils that actively kill bacteria without causing excessive inflammation.
Researchers at Massachusetts General Hospital developed a microfluidic device that measures neutrophil motility to accurately diagnose sepsis. The device achieved more than 95% accuracy in distinguishing patients with sepsis from those without, offering a promising new approach to timely treatment.
Studies using mouse models of lung cancer found that neutrophils help tumors hide from T cells and promote their own growth through the production of Snail protein. This 'vicious cycle' between neutrophils and tumor cells hinders immunotherapy's effectiveness in up to two-thirds of patients.
Researchers have identified a communication network between lung tumors and bone marrow that contributes to tumor progression. Tumors activate osteoblasts in the bone marrow, leading to the production of immune cells that promote cancer growth.
Researchers found that cell cycle proteins are crucial for releasing neutrophil extracellular traps (NETs) in immune cells. This process helps to contain and eliminate fungal infections in mice and human cells.
Scientists at the University of Michigan found that injecting nanoparticles can redirect neutrophil immune cells away from an injury site, reducing inflammation. This discovery could lead to new treatments for acute lung injuries, sepsis, and atherosclerosis.
Researchers found that elevated blood eosinophil and neutrophil concentrations were associated with accelerated lung function decline and airflow obstruction. These biomarkers may serve as an early warning system for 9/11 firefighters at risk of developing severe lung problems.
A study published in the Journal of Neuroscience reveals that neutrophils, a type of immune cell, play a significant role in clearing debris from damaged nerves. Without this cellular clearance mechanism, nerves cannot properly regenerate after injury.
Researchers found that neutrophils can inhibit T lymphocyte activity, weakening the effect of cancer immunotherapy. This mechanism, triggered by soluble mediators released by cancer tissues, can cause an 'evil alter ego' in neutrophils, making them less effective at fighting cancer cells.
Researchers found that injecting interleukin-27 (IL-27) into mice after a hemorrhagic stroke helped them recover and had less brain damage. IL-27 may play a critical role in protecting the brain from stroke-induced damage, offering new avenues for stroke treatment strategies.
Neutrophils, white blood cells that can cause damage after a hemorrhagic stroke, can be trained to release beneficial molecules like lactoferrin. This could lead to a new therapeutic approach for reducing brain damage after the injury.
Researchers discovered etosis in human blood monocytes, a type of immune cell that can project DNA outside the cell. This process has implications for understanding inflammation and potentially developing new diagnostic tools and therapeutic targets.
Staphylococcus aureus, a common bacteria causing severe infections, has developed mechanisms to evade the human immune system. Researchers have identified various tactics used by S. aureus to slow down neutrophil migration, impede priming, and even kill neutrophils. Understanding these strategies can lead to new therapeutic approaches.
Researchers found that neutrophils lose oxygen-sensing protein, leading to overactive response to infection and chronic inflammation. Studying glucose regulation in neutrophils may lead to new treatments for patients with low oxygen levels and lung disease.
Researchers at NYU Dentistry aim to understand how immune cells contribute to sex differences in oral cancer pain. The study will determine if neutrophil infiltration affects pain levels in patients and explore a potential mechanism for improving pain management.
Scientists discovered that nonclassical monocytes play a key role in driving primary graft dysfunction after lung transplantation. Targeting these cells could lead to novel treatments and potentially prevent death.
Researchers have discovered a way to quickly calm activated neutrophils, which can get stuck in the lungs' tiny capillaries, leading to life-threatening problems. The breakthrough, developed by a Creighton University physics professor, could lead to new treatments for acute respiratory distress syndrome (ARDS) and acute lung injury (ALI).
A recent study has shown that a gene variant in Duffy-negative individuals leads to a relative paucity of circulating neutrophils. This phenomenon may provide a selective advantage against infections such as malaria. Researchers believe that the specific properties of these neutrophils have a positive impact on innate immune responses.
A new study links HMGB1 protein to post-sepsis immunosuppression and neutrophil dysfunction. Researchers found that neutralizing HMGB1 restores neutrophil function, offering a potential therapeutic approach for sepsis recovery.
Researchers discovered a chemical signal linked to life-threatening lung inflammation, pointing towards new therapies. Blocking molecular signalling mechanisms in patients with Acute Respiratory Distress Syndrome (ARDS) alleviated lung inflammation.
A new study published in Oncoimmunology suggests that kidney dysfunction in cancer patients can be triggered by the immune system's response to the tumor. Researchers identified neutrophils as a key player in this process, which can lead to impaired blood flow and inflammation in organs like the kidneys.
Researchers at CNIC identified metoprolol's mechanism of action, which protects the heart from inflammation caused by neutrophils. The study opens up new applications for the cheap and safe drug, published in Nature Communications.
Researchers at Osaka University have found that the breakdown of SEMA4D protein causes inflammation and disease in AAV patients. The study suggests that SEMA4D could be used as a new clinical marker to improve diagnosis accuracy.
Researchers found that H. pylori bacteria can alter the structure of white blood cells, known as neutrophils, allowing them to survive within the human body. This change enables the bacteria to evade the immune system, but also shares characteristics with tumor-associated neutrophils that may limit cancer growth.
Researchers used imaging technology to track immune cells in living animals and identified a molecule required for their entry into the joint, which sets off inflammation. This discovery could lead to new treatments for inflammatory arthritis.
Researchers have identified an endogenous peptide that reduces cholesterol levels in mice, inhibiting the development of atherosclerosis. The protein, human neutrophil peptide 1 (HNP1), binds to LDL in the bloodstream and induces rapid uptake by the liver, reducing hypercholesterolemia.
Researchers at Vanderbilt University Medical Center have made a groundbreaking discovery about the human immune system's response to the bird flu vaccine. They found that neutrophils, a type of white blood cell, play a previously unobserved role in vaccine response and may function as antigen-presenting cells.
A high-fiber diet triggers microorganisms in the gut to produce short-chain fatty acids, which induce neutrophil apoptosis and resolution of inflammation. This finding has important implications for treating gout and possibly other inflammatory diseases.
Early research led by Queen Mary University of London found that neutrophils play a role in promoting blood vessel growth and normal placental development. Treating pre-eclamptic neutrophils with hormone therapy may help improve fetal growth, according to the study.
A research team at the University of Georgia has discovered that a pathogen's ability to move through the body triggers an immune response. The study found that bacterial motility induces the formation of neutrophil extracellular traps, which are web-like structures of DNA associated with antimicrobial molecules.
A team of Japanese researchers revealed the mechanism for fever and bone pain caused by G-CSF, which is essential for treating hematological malignancies. The study found that PGE2 produced by neutrophils governed by sympathetic nervous system is behind the unpleasant symptoms caused by G-CSF.
A team of scientists at Brown University has made key discoveries about the body's natural immune response to fungal infections. They found that specific receptors on white blood cells signal the cells to take action against the fungus, and manipulating these receptors may help develop new therapies to combat growing drug resistance.
A study published in PLOS Pathogens found that flagellar motility of P. aeruginosa is the main factor required to induce neutrophil extracellular traps (NETs). The researchers developed an assay to quantify the levels of P. aeruginosa flagellin and found that immotile strains failed to stimulate NET formation.
Researchers found that nicotine activates neutrophils, leading to the release of inflammatory molecules and increased inflammation throughout the body. This discovery has implications for tobacco-related diseases and may suggest alternative forms of nicotine inhalation have detrimental effects.
Researchers discovered that neutrophils, common white blood cells, can be hijacked by cancer cells to promote metastasis. A potential treatment using DNAse, an enzyme that degrades NETs, has shown promise in mice models of triple-negative breast cancer.
Neutrophils, the body's immune superheroes, switch from migrating to murdering invaders when exposed to reactive oxygen species. A receptor called TRPM2 senses ROS levels and triggers a shutdown of migration, allowing neutrophils to focus on killing bacteria and other pathogens.
A study reveals that nicotine triggers the release of neutrophil extracellular traps (NETs), which can harm tissue and contribute to conditions like COPD. The discovery provides a new link between nicotine consumption and inflammation, emphasizing the importance of quitting tobacco products.
Researchers at La Jolla Institute for Immunology discovered a novel mechanism by which neutrophil receptors latch onto vessel walls, dampening inflammation. Integrins assume an unorthodox shape that exposes the high affinity patch but maintains a bent conformation, preventing it from binding to ICAM-1 expressed on blood vessel cells.
Researchers have identified a marker for myeloid-derived suppressor cells (MDSCs) that distinguish them from normal neutrophils. Higher numbers of these cells are associated with larger tumor sizes, suggesting the marker could help predict disease severity and outcome.
A team of researchers found that a subset of macrophage cells in the heart produce molecules attracting neutrophils. Loss of these macrophages or blocking their production reduces neutrophil migration to the injured area. The study suggests resident macrophages provide signals calling neutrophils to the site.
Researchers at Université de Genève discovered that a protein called CCN1 produced by platelets and blood vessels is essential for the recruitment of immune cells during viral infections. Without CCN1, the immune response is impaired, highlighting a new potential target for antiviral treatments.
Researchers have visualized how immune cells create networks of DNA traps called NETs to capture and destroy microbes. The process, known as NETosis, involves the transformation of histones and release of digestive enzymes into the extracellular space.
Researchers at University of Birmingham develop test to predict sepsis in burn victims using biomarkers of neutrophil function. The test shows promise in identifying patients at risk of developing sepsis, a life-threatening condition that can be fatal if left untreated.
A worldwide competition of engineered cells through microfluidic mazes revealed that neutrophil-like cells must balance speed against chemotactic accuracy. An adapted version of the amoeba Dicty with increased activity of a particular protein, Ric8, emerged as the most successful strategy.
Researchers found that circadian rhythms influence the influx of immune cells into damaged tissue, worsening heart attack outcomes. The study showed that neutrophil recruitment is correlated with CXCR2 expression and peaking in early morning hours, leading to increased inflammation and scar formation.
A team of researchers has developed an all-on-chip method for testing neutrophil chemotaxis directly from whole blood using a microfluidic system. The method enables rapid and accurate analysis of neutrophil migration in under 25 minutes, overcoming labor-intensive traditional cell preparation methods.
Researchers discovered that NETs are strongly correlated with airway infection and disease severity in COPD patients, suggesting a potential biomarker for identifying those at risk of progression. This finding may lead to the development of new treatments targeting NET formation.
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.