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Inflammation mediators can induce tubular cell dysfunction with conformational changes of tubule Na+/H+ exchanger, urea, or chloride channels that will influence urine composition independently of any structural damage [14, 64, 65].
That proinflammatory mediators can induce TRP receptor function has been demonstrated in primary human lung cell culture [ 21].
It was recently demonstrated that uterine epithelial cells secrete soluble mediators to the stroma and that these mediators can induce a tolerogenic phenotype in local dendritic cell populations.
Mast cell mediators can induce angiogenesis through their action at different stages of angiogenesis, that is, degradation of the ECM, migration and proliferation of endothelial cells, formation and distribution of new vessels, synthesis of ECM, and pericyte mobilization [ 10, 90].
Inflammation mediators can induce tubular cell dysfunction with conformational changes of tubule Na+/H+ exchanger, urea, or chloride channels that will influence urine composition independently of any structural damage [ 14, 64, 65].
Though essential for the elimination of invasive antigens, chronic expression of the above mediators can induce a variety of inflammatory disorders, including RA and many other autoimmune diseases [ 2].
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We also showed that the ectopic production of nerve growth factor (NGF) in the melanoma tumor tissue as a tumor-released mediator can induce expression of the TF Egr-1 in the salivary gland.
Several immune mediators that can induce cross-protection have been described, such as CD4 T-cells, CD8 T-cells and antibodies, including IgA.
As a biologically active pro-inflammatory mediator, AA can induce apoptosis through its effects on mitochondria (e.g. calcium uptake into mitochondria, or production of ceramide) [ 1, 2].
Overexpression of inflammatory mediators by microglia can induce several neurological diseases.
The knowledge of how mediators of inflammation can induce disease would contribute for the design of affordable therapeutic strategies, as well as to the diagnosis of virus not detected and viral meningoencephalitis.
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