MK was critical for leukocyte adhesion and extravasation in inflamed cremaster muscle venules. (A-C) Intravital microscopy of cremaster muscle postcapillary venules in MK^+/+ and MK^−/− mice 2 hours after intrascrotal administration of TNF-α (500 ng). (A) Number of rolling leukocytes; n = 21 venules from 5 MK^+/+ mice, n = 24 venules from 5 MK^−/− mice. (B) Leukocyte rolling velocity was analyzed offline; accumulated frequency of rolling velocity includes 224 cells from 5 MK^+/+ mice and 221 cells from 5 MK^−/− mice. (C) Number of adherent leukocytes as analyzed by intravital microscopy; n = 21 venules from 5 MK^+/+ mice, n = 24 venules from 5 MK^−/− mice. (D) Differential cell counts of perivascular leukocytes as assessed in cremaster muscle whole mounts were determined morphologically. (E) Analysis of leukocyte adhesion in cremaster muscle venules of MK^+/+ or MK^−/− mice during trauma-induced inflammation before (no treatment) and 10 minutes after systemic application of rMK using intravital microscopy. For MK^+/+ mice, no treatment: n = 24 venules from 6 mice; rMK: n = 9 venules from 3 mice; for MK^−/− mice, no treatment: n = 21 venules from 6 mice; rMK: n = 10 venules from 3 mice. (F) Flow cytometric analysis of cell surface expression of Gr-1, as well as expression of CD11a, CD11b, or CD18 in unstimulated (w/o) or TNF-α (100 ng/ml) treated PMNs from MK^+/+ or MK^−/− mice following 20 minutes incubation at 37°C. Histograms are representative of 3 independent experiments. (A-E) Show mean ± SEM. *P < .05; ***P < .001. Eos, eosinophils; Others, lymphocytes and basophils; n.s., not significant.