IndraLab
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"Our results show that the simultaneous addition of interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) elicited a marked (13-fold) increase of NGF protein released by cultured rat glomerular mesangial cells within 24 h, whereas IL-1 alpha in combination with TNF-alpha, as well as the cytokines alone, did not promote the synthesis of NGF."
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"Previous work has shown TNFα upregulates NGF in NP and AF cells in vitro, so annular puncture with intradiscal injections of TNFα or PBS may facilitate nerve ingrowth and upregulation of neurotropic factors including NGF and VEGF, while anti-TNFα injection mitigates nerve ingrowth and expression of these neurotropic factors."
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"The first involves the nonneuronal events: the resident and migratory immune cells produce a vast number of hypernociceptive inflammatory mediators including pronociceptive cytokines TNF-α, IL-1β, and chemokines, nerve growth factor, and kinins, which trigger the release of directly acting hyperalgesic mediators (Verri et al. 2006)."
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"Recent preliminary evidence suggests that the pro inflammatory cytokine tumour necrosis factor alpha (TNFalpha) and growth factor withdrawal can both activate a common apoptotic pathway in nerve growth factor (NGF)-responsive PC12 cells involving caspase 3, albeit through very distinct upstream pathways : the former through active signalling and the latter through passive or lack of survival signalling."
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"TNF-α stimulates the activity of monocytes and macrophages, enhances their cytotoxicity and activates the production of several proteins (IL-1, IL-6, granulocyte colony stimulating factor 3 (G-CSF), granulocyte macrophage colony-stimulating factor (GM-CSF), nerve growth factor (NGF), platelet-derived growth factor (PDGF) and epidermal growth factor (EGF)) [18]."
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"Thus, NGF production during inflammation might be involved in the modulation rather than in the induction of the joint inflammatory response.The findings of the present study suggest that the elevated production of TNF-α and IL-6 in the acute phase after MIA injection may have induced elevated production of NGF and that these elevated proinflammatory cytokines are involved in the modulation of joint inflammation."