1977
DOI: 10.1007/bf01951305
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Prostaglandin production by human polymorphonuclear leucocytes during phagocytosis in vitro

Abstract: Human polymorphonuclear leukocytes were found to be able to synthetize and release substantial amounts of PGE2' when stimulated by a phagocytic stimulus such as zymosan particles coated with complement. Hydrocortisone, at a concentration of 10(-5) M, which proved to be effective in other biological systems, failed to inhibit phagocytosis and PG release.

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Cited by 23 publications
(9 citation statements)
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“…In view of its multifaceted roles in airway inflammation, future studies will examine the impact of tulathromycin on PGE 2 production and the consequence of this effect on airway inflam- mation. Using the experimental protocol described here, zymosan was found to significantly increase PGE 2 production 24 h postchallenge, consistent with previous studies using other models in vivo (43)(44)(45) or in vitro (46), an effect that was blocked by tulathromycin. Another immunomodulating antibiotic for cattle and pigs, tilmicosin, also blocks PGE 2 production in LPS-stimulated bovine alveolar macrophages via a decrease in COX-2 expression and/or partial inhibition of secretory phospholipase A 2 activity (47,48).…”
Section: Fig 3 Tulathromycin Reduces Levels Of Prostaglandin E 2 In Csupporting
confidence: 90%
“…In view of its multifaceted roles in airway inflammation, future studies will examine the impact of tulathromycin on PGE 2 production and the consequence of this effect on airway inflam- mation. Using the experimental protocol described here, zymosan was found to significantly increase PGE 2 production 24 h postchallenge, consistent with previous studies using other models in vivo (43)(44)(45) or in vitro (46), an effect that was blocked by tulathromycin. Another immunomodulating antibiotic for cattle and pigs, tilmicosin, also blocks PGE 2 production in LPS-stimulated bovine alveolar macrophages via a decrease in COX-2 expression and/or partial inhibition of secretory phospholipase A 2 activity (47,48).…”
Section: Fig 3 Tulathromycin Reduces Levels Of Prostaglandin E 2 In Csupporting
confidence: 90%
“…These findings were forgotten in the literature until recently, when it was demonstrated that inhibition of neutrophil migration prevented the hypernociception induced by allergic stimuli in rats [24]. Considering that activated neutrophils produce and release proinflammatory cytokines, including TNF-␣, IL-1␤, and CINC-1/CXCL1 and mediators such as PGs [25][26][27][28][29], which are essential to the development of inflammatory hypernociception, it is conceivable to suggest that neutrophils could be a relevant source of hypernociceptive cytokines or alternatively, of the direct-acting hypernociceptive mediators, such as PGs. In the present study, we investigated whether neutrophils played a relevant role in the genesis of inflammatory hypernociception induced by carrageenan and whether neutrophils were a relevant source of hypernociceptive cytokines or direct-acting hypernociceptive mediators.…”
Section: Introductionmentioning
confidence: 98%
“…In all of these studies it seems likely that most of the bone resorbing activity was formed after the removal of the tissue. Prostaglandins can be produced in vitro by bone in the presence of complement [6], by various other tissues including rheumatoid synovia [7] and dental cysts [8], and by inflammatory cells such as macrophages [9] and polymorphonuclear leukocytes [10].…”
Section: Introductionmentioning
confidence: 99%