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Carbon nanotubes (CNTs) may elicit inflammatory responses following pulmonary exposure.
In addition, they may elicit inflammatory processes that induce irreversible tissue damage to the respiratory system and the lungs, possibly resulting in fibrosis [33, 34].
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There is some evidence that PLGA microsphere degradation products alone may elicit an inflammatory cellular response [ 42].
Metal prosthesis may elicit an inflammatory response whereby macrophages accumulate at the site of injury (Black and Hastings, 1998).
Injured RPE cells activate and recruit choroidal dendritic cells that may elicit an inflammatory or complement-mediated response (Hageman et al. 2001).
This suggests that SDC porridge does not contribute to elicit inflammatory reactions.
As a mechanism of MOF, it has been hypothesized that ventilator-induced lung inflammation may elicit release of inflammatory mediators into the circulation, thereby amplifying a pro-inflammatory systemic environment and eventually leading to detrimental effects in distal organs [ 17- 19].
The resultant competitive inhibition of AA oxidation represents the primary theory by which n-3 fatty acids may elicit therapeutic anti-inflammatory effects [ 23].
On the other hand, in vivo, CS given orally prevents hepatic NF-κB nuclear translocation, suggesting that systemic CS may elicit an anti-inflammatory effect in many tissues besides the joint [ 14].
Telomere erosion in neutrophils and lymphocytes, cells critical to the inflammatory response, may elicit an abnormal, sustained profibrotic response.
Both constitutive and ligand-activated AhR may elicit a weak to moderate pro-inflammatory signal, but seems to restrict activation of p65 upon encounters with strong activators of the classical NF-κB pathway, such as Poly I C or TNF-α.
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