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It seems probable that both leukocyte adhesion and circulating mediators play a role in mediating endothelial barrier dysfunction in sepsis, possibly with a different time course.
These inflammatory mediators play a role in increased vascular permeability and local oedema [11, 12].
It is known that excessive inflammatory mediators play a central role in the development of endotoxin-induced DIC.
Increased proinflammatory cytokines are found in intestinal samples from NEC cases, suggesting that these mediators play a role in the development of NEC [3] [8].
Furthermore, locally produced mediators play a major role in systemic inflammatory syndromes.
Inflammatory mediators play a fundamental role in the initiation, progression, and eventual rupture of atherosclerotic plaques.
Similar(38)
The lipid mediators play an important role in the resolution and repair of corneal injuries [7, 12, 13].
Cellular innate immune receptors and mediators play an important role in defence against UTIs but the role of humoral innate immunity has not been explored.
Lipid mediators play an important role in causing inflammation and pain.
Increasing evidence suggests that intrarenal inflammatory mediators play an important role in the pathogenesis of kidney injury[ 11- 14].
Such inflammatory mediators play an important role in fatal cases with fulminant progression and in the development of shock [ 5].
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