Articles tagged with Macrophages
Researchers at KU Leuven and Seoul National University create method to stimulate immune system cells to repair damaged tissues, offering new potential treatment for inflammatory bowel disease. The technique involves targeting specific macrophage cells with liposomes containing a substance that triggers tissue regeneration.
Researchers identified GAPLINC, a long noncoding RNA that regulates inflammatory gene expression and protects mice from septic shock. The study found that reducing GAPLINC levels enhanced inflammatory responses, but unexpectedly, this effect also protected mice from endotoxic shock.
A Stanford study reveals that chronic inflammation driven by myeloid cells is the main driver of brain aging. The researchers found that blocking a specific hormone-receptor interaction in these cells can restore youthful metabolism and calm down inflammation, potentially reversing age-related cognitive decline.
The EGR1 transcription factor inhibits expression of pro-inflammatory genes in macrophages, blunting their activation and the immune response. This discovery sheds light on the fundamental process of macrophage maturation, which is critical for inflammation.
Research reveals that macrophages, key immune cells, respond to pathogens and stress through circadian-controlled metabolism. The study showed an incredible amount of circadian timing in macrophage behavior, but the clock regulated immunity in unexpected ways.
New research from Karolinska Institutet reveals the development of lung macrophages, immune cells that can protect or harm lungs. Classical monocytes migrate into airways and lung tissue, becoming protective macrophages, while non-classical monocytes develop into pro-inflammatory macrophages.
A recent study found that macrophages play a crucial role in suppressing the effectiveness of PARP inhibitor therapy in breast cancer patients. The researchers identified CSF-1R-positive macrophages as the key suppressive cells, which can be targeted to enhance anti-tumor responses.
Researchers identified MAARS, a lncRNA expressed specifically in macrophages of atherosclerotic plaques, contributing to disease progression. Targeted interruption of MAARS's function reduced atherosclerotic lesion formation by 52%.
Researchers have identified a potential therapeutic strategy for obesity by discovering the signalling pathways responsible for the development of adipose tissue macrophages (ATMs) in obesity. ATMs play a key role in preventing lipotoxicity, where fat molecules are deposited in non-adipose tissues.
Researchers at the Buck Institute have identified chronic inflammation as a driver of NAD+ decline, a key metabolite central to an efficient and healthy metabolism. Senescent cells activate CD38, which degrades NAD+, leading to age-related diseases. Blocking CD38 activity may offer a new target for therapeutic interventions.
A study by Cincinnati Children's Hospital Medical Center found that targeting the BCAP protein could help control overactive immune responses and promote tissue repair in inflammatory diseases. The researchers suggest that modulating BCAP activity could be used to dampen inflammation and accelerate response against tumors.
Researchers at Ludwig-Maximilians-Universität München identified a mechanosensitive ion channel in an endolysosomal system of macrophages. This channel is activated by mechanical stimuli and alterations in osmolarity, regulating the secretion of signaling molecules that control the immune system.
A label-free imaging technique has been developed to examine immune cells called macrophages in the retina of healthy humans and patients with glaucoma. Cell density decreased with age in healthy participants, while cell processes moved more quickly and covered a smaller area in patients.
A new study reveals that macrophages play a complex role in cancer spread, with two types - M1 and M2 - exhibiting different behaviors. The research uses advanced technologies to identify a distinct population of macrophage cells that migrate towards cancer cells, promoting tumor growth.
Macrophages, such as M1 and M2 cells, play a crucial role in the immune response. Researchers have developed a method using gold nanorod scattering to identify these cells from tissue fluids or blood samples. This technique has the potential to predict disease stages, including cancer, atherosclerosis, and fibrosis.
Researchers at University of California San Diego School of Medicine discovered a molecule called Girdin (GIV) that acts as a brake on macrophages. The GIV-mimic peptide can shut down immune cells' overreaction, supporting a mechanism critical for survival in mouse models of sepsis and colitis.
Researchers at CNIC have discovered a mechanism explaining how macrophages regulate obesity and related diseases like fatty liver disease and type 2 diabetes. The study shows that oxidative stress leads to mitochondrial metabolism changes in macrophages, fostering inflammation and obesity.
A study published in Cell reveals a previously unknown mechanism for the heart's waste removal, highlighting the critical role of macrophages in maintaining cardiac health. The discovery suggests that cardiac dysfunction may arise from defects in immune cells rather than cardiomyocytes.
Researchers have found pro-inflammatory lipids that precede Type 1 diabetes onset in a mouse model and high-risk children. The findings suggest that these lipids may serve as biomarkers for the disease and offer a therapeutic target to prevent its development.
Macrophage activation syndrome plays a key role in COVID-19's cytokine storm, which causes systemic hyperinflammation. Researchers found that therapies targeting IL-6 and TNFα show promise in reducing severity of the disease.
Researchers at the University of Bonn identify a disease mechanism where fat crystals cause immune system hyperreaction, leading to chronic inflammation. The study reveals that deoxysphingolipid crystals disrupt mitochondrial function and activate an inflammatory response in immune cells.
Researchers at UIC have discovered that blood vessel cells play a crucial role in programming macrophages to reduce inflammation and promote tissue repair. The study found that Rspondin3, a protein released by blood vessels, helps guide the programming of macrophages.
The study found that macrophages play a critical role in muscle inflammation, fibrosis, and regeneration. Researchers believe that therapeutic manipulations of these cells hold promise for promoting muscle injury repair and improving outcomes for individuals with muscular dystrophy.
Scientists discovered that identifying tumor-associated macrophage patterns in lung tumor tissue enables the prediction of disease progression. The study found that a higher number of tumor-promoting macrophages near the invasive margin is associated with lower patient survival rates.
A team of researchers has developed a potential approach to overcome anti-VEGF resistance in patients with age-related macular degeneration. By combining apolipoprotein A-I binding protein (AIBP) with anti-VEGF, the strategy effectively suppresses choroidal neovascularization (CNV) and reduces drug resistance.
New research from Saarland University suggests that low levels of the stress hormone cortisol and protein GILZ can trigger chronic inflammatory responses in the body. This leads to macrophage ageing, which impairs immune cells' ability to control inflammation, resulting in increased pro-inflammatory signalling molecules.
Researchers developed a new method to apply anti-inflammatory substances to implants to reduce undesirable inflammatory reactions. The coatings contain heparin and hyaluronic acid, which inhibit the immune system's response to the implant.
Researchers at UC San Diego School of Medicine discovered a new way to treat cancer by manipulating macrophages, immune cells found in tumor tissues. IRE1α, a molecule regulating the unfolded protein response, was shown to boost PD-L1 levels on macrophages, allowing tumors to evade the immune system.
A study reveals that smooth muscle cells near necrotic cores of atherosclerotic plaques produce complement protein C3, stimulating macrophage activation and driving clonal expansion. The cells' ability to evade immune surveillance is restored by inhibiting CD47, suggesting these cells as viable therapeutic targets.
Researchers discovered that M2-type macrophages are more susceptible to ferroptosis and may exacerbate chronic inflammation. A mathematical model was developed to describe the stability of macrophages under different conditions.
Researchers at the University at Buffalo have discovered that hematopoietic stem cell transplantation improves Krabbe disease outcomes through a mechanism independent of cross-correction. The study found that macrophages expressing GALC enzyme aid in myelin debris degradation, leading to better patient outcomes.
Researchers at University of Nottingham have developed biomaterials that can control the body's immune response, potentially reducing implant rejection rates. The new materials use surface shape and chemical composition to influence macrophage attachment and behavior.
Researchers at Harvard's Wyss Institute have created disc-shaped particles that control macrophage behavior to slow tumor growth and metastasis in mice. The 'backpacks' keep macrophages in their tumor-killing state for up to five days, reducing the size of tumors and metastatic nodules.
Researchers have found that elevated ferritin concentrations are associated with increased production of special signalling molecules, leading to complications and death in COVID-19 patients. Marker CD163 is also an important indicator of macrophage activation and high risk of complications.
A new study at CNIC discovers a molecular mechanism regulating macrophages, key immune sentinels. The research may lead to cancer treatments and tissue repair by targeting these cells.
Researchers develop new type of immunotherapy targeting macrophages in omental fat, which appears to reduce ovarian cancer spread and tumour growth. The study shows promise for improving treatment outcomes, but further testing is needed.
Researchers identified 497 genes expressed in resistant mice and 22 genes in susceptible mice, showing the development of disease depends on host genetics. The study aims to develop biomarkers for diagnosis and treatment of leishmaniasis.
Scientists have successfully engineered CAR macrophages to target and kill solid tumors, using a novel approach that could lead to more effective cancer treatments. The discovery centers around harnessing the immune-boosting properties of macrophages, which are often co-opted by tumors.
Researchers have found a new mechanism for long-lasting pain relief through the production of endogenous opioids by immune cells. The discovery uses cytokine interleukin-4 to induce M2 macrophages, which produce opioids and reduce pain, offering potential alternative pain management options.
Research suggests that beta cells produce signals that aid their own demise in Type 1 diabetes, leading to increased inflammation and damage. The study found that the absence of a specific enzyme enhances anti-inflammatory responses, while its overexpression promotes inflammatory ones.
Researchers discovered that shortly after a stroke, macrophages from the blood attack dead and adjacent healthy brain tissue. This process was hindered by inactivating the Cxcr4 gene, which acts like an antenna for inflammatory processes in the brain.
Researchers have discovered that heterotopic ossification, a painful complication of trauma, is caused by macrophages sending errant signals to bone-forming stem cells. A new study suggests that targeting TGF-beta expressing macrophages may prevent this abnormal bone formation
A new biochemical switch involved in M2 macrophage polarization and proliferation has been identified, which can be targeted to inhibit cancer growth. The discovery was made by a research team from the University of Vienna and could lead to novel therapies against systemic diseases and cancer.
Scientists at DESY used an advanced X-ray combination technique to trace nanocarriers for tuberculosis drugs within cells with high precision. The method also revealed the calcium content in human bone, benefiting osteoporosis research.
Researchers at Columbia University Irving Medical Center found putrescine, a compound responsible for the foul smell of decomposing flesh, may help treat atherosclerosis. The study suggests putrescine's role in removing dead cells through efferocytosis could improve plaques and prevent chronic inflammation.
Researchers found that microglia, immune cells in the brain and central nervous system, encase macrophages, preventing them from dispersing into areas they shouldn't be. This discovery may lead to new treatments for conditions like multiple sclerosis and Alzheimer's disease.
Researchers at University of Oxford have identified a new target for repairing the heart after a heart attack by modulating the immune response. Macrophages play a key role in forming cardiac scars, and modifying their behavior could lead to more efficient repair and potentially avoid heart failure.
Researchers at Tokyo University of Science discovered a novel anti-cancer strategy targeting tumor-associated macrophages (TAMs) by regulating FROUNT protein. Disulfiram, an alcoholism treatment, was found to inhibit cancer cell growth and suppress TAM movement in animal experiments.
Researchers have invented a Trojan Horse nanoparticle that selectively targets and eats away at plaque-causing cells, reducing plaque size and stabilizing it. This approach shows promise as a potential treatment for atherosclerosis, the leading cause of death in the US.
Researchers have discovered a rare African-specific variant of the TP53 gene that causes iron accumulation in macrophages, leading to poorer responses to bacterial infections. However, this variant also improves response to malaria toxin, potentially offering protection against severe inflammation and disease severity.
Toxoplasma gondii injects proteins into host macrophages, altering their behavior and suppressing the immune response. This manipulation leads to the creation of M2 macrophages, which reduce inflammation and allow the parasite to evade elimination by T cells.
A new study reveals that high-protein diets can lead to increased plaque buildup in arteries, particularly unstable plaque prone to rupture. This can increase the risk of heart attacks. Researchers found that excess amino acids from a high-protein diet activate macrophages, leading to cell death and worsening plaque complexity.
A recent study published in PNAS reveals that extracellular matrix protein-1 (ECM1) plays a crucial role in the pathogenesis of ulcerative colitis, a type of inflammatory bowel disease. The researchers found that ECM1 is highly expressed in macrophages and regulates their polarization through the GM-CSF/STAT5 signaling pathway.
Researchers study how gut infections damage the nervous system, leading to chronic inflammation and conditions like IBS. They find that specific genes contribute to cell death and propose potential treatments by boosting polyamine production or restoring gut microbial communities.
Researchers have found that deleting the BMAL1 clock gene makes immune cells more effective at fighting off pneumonia-causing bacteria. The study reveals that strengthening the actin skeleton of these cells is key to their increased effectiveness.
Scientists at Ohio State University have created a treatment for late-stage sepsis using nanotechnology to transform donated immune cells into a powerful antibacterial drug. The therapy demonstrated significant improvements in survival rates and bacteria clearance in mouse models of sepsis.
Macrophages change their metabolism drastically after coming into contact with bacteria, triggering an inflammatory response. This process involves the activation of Toll-like receptors, which leads to histone acetylation and changes in gene expression.
Researchers discovered that Crohn's disease-associated bacteria can switch between replicating and non-growing states within macrophages to tolerate antibiotics. This stress response allows a reservoir of antibiotic-tolerant bacteria to survive in the host and cause long-term inflammation and irritation.
A study suggests that monocyte-derived macrophages can induce lung fibrosis without prior alveolar epithelial cell injury. The research found increased flux through the mevalonate pathway in bronchoalveolar cells from IPF patients, which exacerbates fibrosis.
A new method has been developed to identify aggressive breast cancer by analyzing tumor tissue signatures, showing a correlation with poor outcome in patients. The study used mouse models and bioinformatics expert to isolate macrophages from mice affected by breast cancer and compared them with those from healthy breast tissue.