Non-prostaglandin effects of aspirin III and salicylate: inhibition of integrin-dependent human neutrophil aggregation and inflammation in COX 2- and NF kappa B (P105)-knockout mice.

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Weissmann G, Montesinos MC, Pillinger M, Cronstein BN

Non-prostaglandin effects of aspirin III and salicylate: inhibition of integrin-dependent human neutrophil aggregation and inflammation in COX 2- and NF kappa B (P105)-knockout mice.

Adv Exp Med Biol. 2002;507:571-7.

PubMed ID

12664642 [ View in PubMed

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Abstract

Two, non-prostaglandin effects of antiinflammatory levels of salicylates (i.e. aspirin III) are shown here: 1) Exposure of neutrophils to aspirin or sodium salicylate inhibited Erk activity and integrin-dependent aggregation of neutrophils, consistent with antiinflammation but not COX inhibition. Inhibition of Mek (proximal activator of Erk) also blocked stimulation of Erk and neutrophil aggregation by FMLP and arachidonic acid. Thus, the antiinflammatory effects of salicylates may be mediated by inhibition of Erk signaling required for integrin-mediated responses. 2) Acute inflammation was induced in murine air-pouches of wild-type mice and mice rendered deficient in either COX-2 or p105, the precursor of p50 of NF kappa B. The antiinflammatory effects of aspirin and sodium salicylate were independent of the presence of COX-2 or p105 component of NF kappa B or the levels of prostaglandins at the inflammatory site. In contrast, glucocorticoid action depended on the p105.

DrugBank Data that Cites this Article

Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Acetylsalicylic acid	Extracellular signal-regulated kinase (ERK) (Protein Group)	Protein group	Humans	Unknown	Not Available	Details