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However, some possibilities may be extrapolated from other literature indicating that they mediate inflammatory processes (Bind et al. 2012).
Increased sympathetic nervous system activation in response to stress has been suggested to mediate inflammatory processes [ 45].
In contrast, because nucleated cells rapidly regenerate this enzyme, a shorter dosing interval is required to persistently impact COX activity in cells that mediate inflammatory processes.
Although our classical perception of platelets is that of key players in haemostasis and thrombosis, several lines of evidence suggest that platelets also mediate inflammatory processes [ 1– 3].
In particular, emerging evidence suggests that dietary flavonoids may exert neuroprotective effects by suppressing the activation of microglia, which mediate inflammatory processes in the CNS (see the earlier section).
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Several genes mediating inflammatory processes were also highly up-regulated, such as the chemokine receptor CCR5, and the glycoprotein CD74.
A chronic, T cell mediated inflammatory process determines the growth and development of atherosclerotic lesions [1] [3].
IL-6 mediates inflammatory process by stimulating B cell activation, B cell differentiation, differentiation of T cell and macrophages and NK cell activation [ 37].
It is likely that the effects of APC on inflammation are mediated by EPCR, which may mediate downstream inflammatory processes [ 45].
Support for the notion that APC has anti-inflammatory properties comes from in vitro findings, demonstrating an APC-binding site on monocytes that may mediate downstream inflammatory processes [ 40, 41].
Next, we hypothesized that the attenuation of post-infarct remodeling might be mediated by inflammatory processes.
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