Monocytes of allergics and non-allergics produce, store and release the neurotrophins NGF, BDNF and NT-3

Rost, Bettina; Hanf, Gerald; Ohnemus, Ulrich; Otto-Knapp, Ralf; Groneberg, David A.; Kunkel, G.; Noga, Oliver

doi:10.1016/j.regpep.2004.06.024

Cited by 70 publications

(53 citation statements)

References 36 publications

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“…be due to the monocytes secreting protective substances, such as neurotrophins, to protect the cells. The idea that monocytes may be a possible source of local and circulating neurotrophins, specifically NT3, has been demonstrated (Rost et al 2005). Therefore, conditions with increased neuronal survival correlating to increased OTK18 expression in U937 cells may stimulate these cells to produce more neurotrophins to sustain neuronal life.…”

Section: Discussionmentioning

confidence: 99%

The effect of OTK18 upregulation in U937 cells on neuronal survival

Gilling

Carlson

2009

In Vitro Cell.Dev.Biol.-Animal

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The intent of this study was to characterize the effect OTK18 upregulation in monocytic cells had on neuronal survival. The human monocytic cell line, U937, was differentiated into macrophages or left as an undifferentiated monocyte. These cells were transfected with a plasmid containing the enhanced green fluorescent protein and OTK18 (pEGFP-OTK18) or an empty control vector (pEGFP-N3). The supernatants from the transfected U937 cells were used to culture rat neuronal cells (PC12). A live/dead assay was performed to determine the effect of culturing on cell survival. The protein levels of the neurotoxin, tumor necrosis factor alpha (TNF-alpha), and the neurotrophin, neurotrophin three (NT3), were determined by enzyme linked immunosorbent assay. The results of the live/dead assay showed differential cell survival between conditions with pEGFP-OTK18 when compared to the control empty vector. Quantitative real-time polymerase chain reaction assays demonstrated that OTK18 had an increased expression level when compared to the control. Lastly, NT3 protein levels were upregulated in treated cells with increased OTK18 expression, suggesting that OTK18 may play a role in neurotrophin production and consequently support neuronal survival.

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Section: Discussionmentioning

confidence: 99%

The effect of OTK18 upregulation in U937 cells on neuronal survival

Gilling

Carlson

2009

In Vitro Cell.Dev.Biol.-Animal

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“…2). BDNF is also released in other tissues; salivary glands, stomach, duodenum, ileum, colon, lung, heart, liver, pancreas, kidney, bladder, uterus, oviduct, monocytes and eosinophils [57][58][59]. BDNF regulates functions of the gut and pancreatic beta islet activity in response to plasma levels of glucose, protein, fatty acids, insulin, and leptin in which hypothalamus plays a critical role.…”

Section: Bdnf Obesity and Insulin Resistancementioning

confidence: 99%

Effect of Brain Derived Neurotrophic Factor, In Relation to Diet and Lifestyle Factors, for Prevention of Neuropsychiatric and Vascular Diseases and Diabetes

Singh¹,

Takahashi²,

Tokunaga³

et al. 2014

TONUTRAJ

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Abstract:Background: Brain-derived neurotrophic factor (BDNF) is a major neurotrophin which may have promise to be a nutraceutical of this decade. It has a documented role in neurogenesis, angiogenesis, and neuronal survival. BDNF can have beneficial effects on several cardio-metabolic and neuro-psychiatric disorders, indicating that it is important in brainbody interactions. Diet and lifestyle factors may also have an influence on BDNF levels. In this review, we examine the beneficial role of BDNF on risk factors of vascular diseases, type 2 diabetes mellitus and anxiety disorders. Methods: Internet search and discussion with peer colleagues. Results: Majority of the BDNF (70-80%) is derived from dendrite of neurons but it is also present in other body tissues. BDNF controls the food intake and appetite as well as lipid and glucose metabolism. Sedentary behavior and tobacco intake may be associated with BDNF deficiency. Lower serum concentration of BDNF and higher vascular endothelial growth factor (VEGF) concentrations were associated with increased risk of incident stroke/TIA. BDNF may serve as an intermediate biomarker for subclinical vascular disease and may also have biological potential to serve as a therapeutic target for primary and secondary prevention of vascular diseases, as well as clinical and subclinical vascular brain disease. BDNF deficiency has been observed in association with anxiety, depression, insomnia, dementia, insulin resistance, type 2 diabetes and vascular diseases. The phenotypes associated with insulin resistance are at increased risk for developing cognitive decline and neuro-degeneration resulting in vascular dementia, and depression as well as diabetes mellitus and metabolic syndrome, which are risk factors for CVDs. BDNF may be administered as nutraceutical due to its protective influence on BDNF concentrations, insulin receptors and hypothalamic dysfunction leading to beneficial effects on cardiovascular risk and neuropsychological dysfunction. It is proposed that omega-3 fatty acids and moderate physical activity may enhance BDNF release. Conclusions: It is possible that circulating BDNF deficiency is a risk factor for obesity, CVDs and diabetes as well as risk factor for neuropsychiatric diseases. BDNF administration may modify the risk of clinical and subclinical stroke, depression, and dementia as well as of obesity and type 2 diabetes.

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“…The first immune cell shown to associate with NGF was the mast cell, and its close localization to the nerve cells suggests the functional interaction between the nervous system and the immune system. Exogenous NGF was shown to activate mast cells in some peripheral tissues and to increase their number, size and degranulation [26,27]. In addition to mast cells, NGF receptors are expressed in T and B lymphocytes, monocytes, macrophages, and granulocytes.…”

Section: Ngf and Inflammationmentioning

confidence: 99%

“…In addition to mast cells, NGF receptors are expressed in T and B lymphocytes, monocytes, macrophages, and granulocytes. Studies have shown that NGF is not only synthesized in immune cells, but also interacts with them [22,24,26].…”

Section: Ngf and Inflammationmentioning

confidence: 99%