macrophage
Pathways
Studies (19)
Niacin ameliorates ulcerative colitis via prostaglandin D2‐mediated D prostanoid receptor 1 activation
Out of 26 patients with moderate ulcerative colitis (inflammation of the colon) who were unresponsive to conventional treatments, 92.3% responded positively and 88.5% went into remission after receiving a daily niacin enema treatment for 6 weeks. The had no serious side effects, showed notable improvements in intestinal healing, reduced symptoms like rectal bleeding and stool frequency. Niacin is a promising, well-tolerated alternative for inducing clinical remission of ulcerative colitis.
Acne Vulgaris Is a Special Clinical Type of Pellagra
People with acne often have abnormal lipid profiles and elevated oily secretion on their skin. Foam cells are an important pathological change in acne lesions. Acne is not a skin disease induced by infection, because no bacteria, fungi or parasites can be seen in early phase of acne lesion. The foam cells in acne lesions are white blood cells that have ingested large amounts of lipids. Niacin is the only vitamin that promotes the ability of HDL to scoop up cholesterol particles from plaques in the heart's blood vessels and move those particles to the liver for disposal, which prevents foam cell formation. Foam cells in acne lesions suggest that patients with acne are deficient in niacin and that acne can be considered a type of pellagra (niacin deficiency).
Emerging roles of GPR109A in regulation of neuroinflammation in neurological diseases and pain
Summary of GPR109A (niacin receptor) role in inflammation of the nervous system, especially the brain, and how activation of GPR109A plays a role in healing may conditions such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, stroke, and pathological pain.
The β-hydroxybutyrate receptor HCA2 activates a neuroprotective subset of macrophages
Nicotinic acid mimics the effect of a ketogenic diet in activating HCA2, which induces a neuroprotective phenotype in bone marrow-derived macrophages that infiltrate the brain and that this results in an improved outcome in a mouse model of stroke.
Plasma acetylcholine and nicotinic acid are correlated with focused preference for photographed females in depressed males: an economic game study
This study showed depressed males have a narrower preference for female photographs (only preferring good looking ones) which is a marker for lower cognitive flexibility. The less nicotinic acid in their body, the narrower their preference. This indicates nicotinic acid may regulate human social decision-making (especially preference-related behaviors) by acting on the HCAR2 in microglia (the resident immune cells of the brain and spinal cord which constantly patrol the cerebral microenvironment to respond to pathogens and damage).
Inflammation stimulates niacin receptor (GPR109A/HCA2) expression in adipose tissue and macrophages
Many of the beneficial and adverse effects of niacin are mediated via GPR109, which is highly expressed in adipose tissue and macrophages. Multiple infectious and inflammatory stimuli stimulate GPR109A expression in adipose tissue and in macrophages.
Activation of Gpr109a, Receptor for Niacin and the Commensal Metabolite Butyrate, Suppresses Colonic Inflammation and Carcinogenesis
GPR109A expressed in immune cells as well as in colonic tissue is necessary for protection against colitis and colon carcinogenesis. Niacin suppresses colitis and colon cancer in a GPR109A-dependent manner. GPR109A is key in mediating the beneficial effects of gut microbiota and dietary fiber in colon. Niacin suppresses atherosclerosis by activating GPR109A in immune cells. GPR109A mediates butyrate effects in colon and is a critical molecular link between colonic bacteria and dietary fiber and the host.
Niacin Reverses Migratory Macrophage Foam Cell Arrest Mediated by oxLDL In Vitro
Oxidized Low Density Cholesterol, oxLDL induced inhibition of macrophage migration may be reversed by Niacin, which explains part of Niacin's atheroprotective effects on cardiovascular disease independent of its effects on plasma lipids. Macrophage foam cells are a type of macrophage that localize to fatty deposits on blood vessel walls. Niacin also inhibited the formation of peroxynitrite (which is a powerful oxidant exhibiting a wide array of tissue damaging effects)
Anti-inflammatory effects of nicotinic acid
Niacin has multi-faceted anti inflammatory properties that act in both localized and systemic ways. A major area of its activity is in tissue related to fat storage via the GPR109A receptor. Dosing cells with TNF-alpha ( an inflammatory substance ) showed that niacin treated cells increased the atheroprotective hormone adiponectin and reduced macrophage chemotaxis
Niacin attenuates the production of pro-inflammatory cytokines in LPS-induced mouse alveolar macrophages by HCA2 dependent mechanisms
Explores protective effect of niacin on lung tissue by dosing mouse lung white blood cells with niacin and exposing them to inflammatory toxins (Lipopolysaccharides). This demonstrated strong anti-inflammatory effects of niacin ( reduced levels of TNF-α, IL-6 and IL-1β) and that the protective effect depends on expression of GPR109A.
Niacin attenuates lung inflammation and improves survival during sepsis by downregulating the nuclear factor-κB pathway
Rats injected with e coli bacteria to induce lung inflammation survived better with high dose (~1% of diet) niacin supplementation. The reduced lung inflammation and damage was associated with downregulation of the NF-κB (Nuclear Factor Kappa B) pathway.
Niacin-mediated rejuvenation of macrophage/microglia enhances remyelination of the aging central nervous system
Niacin via its ability to enhance macrophage and microglia is great for repairing (myelin) sheaths that protect nerve fibers, which deteriorate in diseases like multiple sclerosis.
Anti-inflammatory effects of nicotinic acid in adipocytes demonstrated by suppression of fractalkine, RANTES, and MCP-1 and upregulation of adiponectin
Adipose tissue (body tissue used for the storage of fat) is major site of action for niacin. When adding a white blood cell attractant to adipose tissue, niacin suppresses the pro-atherogenic (plaque inducing) chemokines and upregulates the atheroprotective (protective against plaque and improves metabolism of sugar) adiponectin.
Niacin Attenuates Pulmonary Hypertension Through H-PGDS in Macrophages
When mice are induced with pulmonary hypertension via drugs and low oxygen, those on niacin have less severe outcomes, due to enhanced macrophage activity and release of PGD2.
Network Pharmacology and bioinformatics analyses identify intersection genes of niacin and COVID-19 as potential therapeutic targets
Computer modeling shows niacin a key to therapy for covid via enhancing the immune system, inhibiting inflammation and regulating cellular microenvironment.
Control of brain tumor growth by reactivating myeloid cells with niacin
Niacin treatment of mice bearing intracranial brain tumor initiative cells increased macrophage representation within the tumor, reduced tumor size, and prolonged survival.
Activated niacin receptor HCA2 inhibits chemoattractant-mediated macrophage migration via Gβγ/PKC/ERK1/2 pathway and heterologous receptor desensitization
GPR109A (aka HCA2) is highly expressed in immune cells and together with niacin seems to inhibit proinflammatory aspects of immune cell activity.
Periodontitis and intake of thiamine, riboflavin and niacin among Korean adults
Low niacin in diet leads to higher (~125%) rates of severe gum infection.
Niacin and its metabolites as master regulators of macrophage activation
The focus is on how niacin and its metabolites enable white blood cells to react to a changing microenvironment (macrophage plasticity). It also discusses the anti-oxidant and anti-inflammatory aspects of niacin.