Figure 3.
Aspirin, sodium salicylate, and sulfasalazine, unlike dexamethasone, are no less antiinflammatory in p105 (NFκB) knockout mice than in wild-type mice. Breeding pairs of NFκB (p105; −/−) knockout mice (B6; 129–Nfkb1fm1Bal) and wild-type controls (+/+; C57BL/6; 129) were obtained from The Jackson Laboratory and bred in the New York University Medical Center animal facility. Air pouches were formed, and the animals were treated with aspirin or sodium salicylate before induction of inflammation and quantitation of leukocytes, as described in Methods and Results. Animals treated with dexamethasone were given a single i.p. dose of dexamethasone (1.5 mg/kg) 1 h before induction of inflammation in the air pouch, and animals treated with sulfasalazine were given sulfasalazine (100 mg/kg) by gastric gavage for 3 days before and on the day of the induction of inflammation. The inhibition of leukocyte accumulation differed significantly between aspirin-treated and dexamethasone-treated knockout and wild-type mice (P < 0.02 for both; Student’s t test). The data are presented as the mean percentages ± SEM of inhibition of leukocyte accumulation in 6–10 mice per group, studied on at least two separate occasions.