Articles tagged with Chronic Inflammation
Researchers at the University of Copenhagen have discovered a new type of regulatory blood cell that can fight hyperactive T-cells causing chronic inflammation in multiple sclerosis. The cells express FoxA1, which suppresses inflammation and degeneration of the brain.
Researchers have identified a key protein called TL1A that drives chronic inflammation, leading to diseases like arthritis. The discovery provides hope for developing targeted biological medicines to halt disease progression and alleviate symptoms.
A new study by University of Iowa researchers found that staph bacteria superantigens trigger pro-inflammatory molecules in fat cells, amplifying inflammation and potentially leading to diabetes. Chronic exposure to these toxins creates a 'perfect storm' for inflammation, worsening the risk of developing diabetes.
A study of 3044 civil servants found that chronic exposure to high interleukin-6 levels was associated with a lower likelihood of healthy aging, including impaired musculoskeletal functioning and diabetes. Maintaining low interleukin-6 levels may facilitate successful aging by reducing the risk of these age-related diseases.
Research finds that socioeconomic status is strongly associated with an increased risk of developing type 2 diabetes, with chronic inflammation being a key mediator. The study analyzed data from the Whitehall II cohort study, which followed over 10,000 British civil servants since the mid-1980s.
Researchers discovered a common biochemical thread to multiple diseases and found that CD36 draws soluble particles inside cells, triggering an inflammatory response. Blocking the CD36 receptor reduces inflammation and improves symptoms in mice with atherosclerosis.
A team of Caltech biologists found that microRNA-146a acts as a critical regulator and protector of blood-forming stem cells during chronic inflammation. Mice lacking miR-146a showed a decline in HSCs, while normal mice maintained their levels despite long-term inflammation.
Researchers at the Hebrew University of Jerusalem discovered that TNF-a plays a critical role in inducing immune suppression during chronic inflammation. They found that TNF-a directly affects myeloid-derived suppressor cells, leading to impaired host immune responses.
Researchers have identified telomerase as a cause of chronic inflammation in human cancers, a key underlying factor for many diseases. Developing drugs to target this enzyme may lead to novel treatments that alleviate common ailments such as cancer and diabetes.
A study found that inactivating the epidermal growth factor receptor increases colorectal tumors, while promoting its activity reduces inflammation and tumor development. This suggests that increasing epidermal growth factor activity in IBD patients may lower their long-term cancer risk.
A Northwestern University study found that early exposure to microbes reduces the risk of chronic inflammation related to diseases like cardiovascular disease, diabetes, and dementia. Adults in Ecuador showed no signs of chronic inflammation, unlike many US adults with chronically elevated C-reactive protein levels.
A team led by Caroline Genco is studying the cellular mechanisms responsible for immune system activation and its link to chronic inflammation caused by persistent bacteria. The study focuses on two pathogens, Chlamydophila pneumoniae and Porphyromanas gingivalis, which can lead to atherosclerosis and other systemic diseases.
Researchers from BUSM have identified a key role for monocytes in maintaining pro-inflammatory T cells, promoting chronic inflammation associated with Type 2 diabetes. The study suggests that restoring balance among immune system cells could be a novel treatment approach.
A new study published in the Journal of Leukocyte Biology suggests that our innate immune systems are a major contributor to chronic lung diseases like silicosis. Researchers found that mice with an inactive adaptive immune system developed more severe silicosis, highlighting the importance of reducing chronic inflammation.
Researchers at the University of Montreal identified a novel molecular mechanism that prevents cancer by regulating the p53 gene. The SOCS1 molecule plays a crucial role in suppressing cancer-causing cytokine activity, offering potential new treatments for chronic inflammatory diseases and cancer prevention strategies.
Researchers found that consumption of red meat introduces a non-human glycan molecule, promoting chronic inflammation and tumor growth. Anti-inflammatory treatment reduced tumor size in mice, suggesting a potential link between red meat and cancer risk.
Researchers found that inducible nitric oxide synthase (iNOS) activation promotes mutagenic changes in DNA, leading to biliary carcinogenesis. NO generation was increased by inflammatory cytokines and suppressed by an iNOS inhibitor.
Researchers found that acute colitis was associated with decreased body weight, food intake, and fat content, while chronic colitis led to reduced bone mineral density and lower energy expenditure. Chronic inflammation also altered metabolism, reducing the use of nutrients as an energy source.
A mouse model study reveals B cell activation is essential for early epithelial neoplastic development. Transfer of B cells restores chronic inflammation and tumorigenesis mechanisms, supporting the interaction between adaptive and innate immune systems in cancer development.