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. 2009 Feb 13;156(5):818–825. doi: 10.1111/j.1476-5381.2008.00094.x

Figure 4.

Figure 4

Systemic effect of NOS inhibition in the neutrophil influx in zymosan-induced arthritis and peritonitis in β2-integrin (β2−/−) and ICAM-1 (ICAM-1−/−) genetically deficient mice. Wild-type (WT) mice received 30 mg·kg−1 LN i.p. or s.c. 30 min prior to i.art. or i.p. zymosan (30–100 µg) respectively. Non-treated (-, =) animals were given only saline i.p. or s.c. prior to zymosan. Naïve animals received only saline; (A,C) and (B,D) represent data from arthritis and peritonitis respectively. β2−/− and ICAM-1−/− mice received 30 mg·kg−1 LN i.p. or s.c. 30 min prior to i.art. or i.p. zymosan (30µg) respectively. Results are expressed as the mean ± SEM of number of cells for each group of six animals. *P < 0.05 compared with non-treated (-); #P < 0.05 compared with non-treated (=).i.art., intra-articular; ICAM-1, intercellular adhesion molecule-1; ICAM-1−/−, mice genetically deficient for ICAM-1; LN, NG-nitro-L-arginine methyl ester; NOS, nitric oxide synthase.