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Although the molecular mechanisms that attenuate the extent of LPS-induced production of lipid mediators are not well discerned, a growing body of evidence suggests that the initial event in the generation of proinflammatory lipids is the liberation of arachidonic acid from membrane phospholipids by activation of cytosolic phospholipase [A.
If the tubes contain significant amounts of endotoxin, then monocytes will be stimulated to produce proinflammatory cytokines, and the plasma or serum will contain high cytokine concentrations.
11-18) In patients with allergic rhinitis, increased iNOS expression caused by the release of proinflammatory cytokines in the upper and lower respiratory tract mucosae has emerged as a possible cause of increased NO levels.
This patent pertains to the discovery that the functional polymorphism (Ser/Gly248) in the cytoplasmic domain of Fc alpha receptor (FcAR) determines the proinflammatory potential of serum IgA autoantibodies through cell signaling and production of cytokines such as TNF-alpha, IL-6, and IL-1 in an allele-dependent manner.
sup][1],[2] Although increased evidence have implicated that asthma is a Th2-type inflammatory disorder,[sup][1],[2] other mediators including proinflammatory cytokines interleukin-1 (IL-1), IL-6, IL-17, and tumor necrosis factor-alpha (TNF-a) and various chemokines such as CXC and CC chemokines CXCL8, CXCL10, CCL2, CCL4, CCL11, and others may also participate in the pathogenesis of asthma, through acting directly or indirectly on the target cells.
Moreover, it increased oxidative stress (decreased antioxidant enzyme activities and GSH/GSSG ratio, increased xanthine oxidase enzyme activity, lipid peroxidation, protein carbonylation and ROS generation) and enhanced the proinflammatory cytokines levels, activity of myeloperoxidase and nuclear translocation of NF[kappaB in the cardiac tissue of the experimental animals.
Neurologists, cardiologists, and pulmonologists from the US, Europe, and Israel focus on sleep apnea as they discuss oxidative stress, proinflammatory vascular risk factors, and endothelial disease; autonomic dysfunction and vascular diseases; hypertension; stroke risk factors and the arousal response; atrial fibrillation; patent foramen ovale and the association with ischemic stroke; the pathogenesis of cerebral small-vessel disease; acute stroke deterioration; the effect of continuous positive airway pressure on stroke risk factors and stroke; rehabilitation of stroke; and restless legs syndrome, periodic limb movements, and vascular risk factors.
Activation of microglia and astrocytes also increases proinflammatory agents, including TNF[alpha], that alter the transmission of nerve signals (i.
Conclusions: In recent years controversial data concerning the activity of triterpene acids on proinflammatory mediators have been published.
Mechanistic studies suggested that DE interacts with ongoing inflammation to amplify the proinflammatory response, which may be neurotoxic.