COX-2 expression and inflammatory effects by diesel exhaust particles in vitro and in vivo

Involvement of mitogen-activated protein kinases and nuclear factor kappa B pathways in signaling COX-2 expression in chronic rhinosinusitis

“…In some cell types, including human airway epithelia cell, LPS stimulation has been proven to increase COX-2 expression as well as PGE 2 accumulation [8,9]. Recent studies suggested that altered regulation of COX-2 might play an important role in the development of airway inflammation [10,11]. However, the expression and localization of COX-2 in the normal and inflamed human nasal mucosa have not been fully identified and the mechanisms of altered COX-2 expression during inflammation in human nasal epithelia (HNE) cells and the signal molecules involved remain to be elucidated.…”

Diesel exhaust modulates ozone-induced lung function decrements in healthy human volunteers

“…A possible mechanism involved with the augmented FEV1 change to O 3 on Day 2 in this study may involve, at least in part, altered production of prostaglandins E 2 (PGE 2 ) and F 2α (PGF 2α ) which have been associated with O 3 -induced lung function decrements [33]. Both prostaglandins can alter lung C-fiber activity directly inducing discharge and/or altering the threshold for discharge to an agonist [34] The possible altered AA metabolism in response to sequential DE and O 3 exposures (i.e., increased AA release, decreased re-uptake, and COX-2 protein for increased conversion of AA to PGE 2 and F 2α ), based upon in vivo and in vitro findings [35]–[39], may explain, at least in part, the observed greater FEV1 decrement. It should be noted that an adequate duration of time is needed for COX-2 protein to be upregulated [40].…”

Effect of maternal exposure to ozone on reproductive outcome and immune, inflammatory, and allergic responses in the offspring

“…One possible mechanism by which this may occur is through the action of arachidonic acid metabolites that are known to be immunosuppressive particularly during pregnancy (Papadogiannakis et al, 1985;Parhar et al, 1989). Both O 3 and diesel exposures increase prostaglandin E 2 (PGE 2 ) levels in the lung fluid of mice (Canning et al, 1991;Ahn et al, 2008), and blocking this activity with indomethacin in the case of O 3 has reversed health effects such as reduced phagocytosis (Canning et al, 1991) and increased susceptibility to infection (Gilmour et al, 1993). However, maternal exposure to cigarette smoke components by inhalation increases allergic sensitization in both experimental animals (Penn et al, 2007;Wu et al, 2009) and in humans (Strachan and Cook, 1998;Gilliland et al, 2006), and this may be due to a different profile of mediators produced in the lung.…”