Tissue-specific expression of Sema7A controls neutrophil migration in response to inflammation. Intravital microscopic analysis of murine cremaster tissue after IV. LPS stimulation shows the role of Sema7A expression in different cells during inflammation. (A) Representative video images of the microvasculature of LysMCre⁺Sema7A^loxP/loxP mice and littermate controls exposed to LPS for 15 minutes compared with the baseline control (0 min; scale bar, 50 μm). (B) Cell speed, transmigration, transmigration distance, and stationary PMNs in LysMCre⁺Sema7A^loxP/loxP and littermate controls were analyzed by intravital microscopy after exposure to LPS for 15 minutes and compared with the baseline control (0 min). (C) Representative video images of the microvasculature of PF4Cre⁺Sema7A^loxP/loxP mice and littermate controls exposed to LPS for 15 minutes compared with the baseline control (0 min; scale bar, 50 μm). (D) Cell speed, transmigration, transmigration distance, and stationary PMNs of PF4Cre⁺Sema7A^loxP/loxP mice and littermate controls were analyzed by intravital microscopy after exposure to LPS for 15 minutes and compared with the baseline control (0 min; scale bar, 50 μm). (E) Representative video images of the microvasculature of Tie2Cre⁺Sema7A^loxP/loxP mice and littermate controls exposed to LPS for 15 minutes and compared with the baseline control (0 min). (F) Cell speed, transmigration, transmigration distance, and stationary PMNs in Tie2Cre⁺Sema7A^loxP/loxP and littermate controls were analyzed by intravital microscopy after exposure to LPS for 15 minutes and compared with the baseline control (0 min). Triplicate experiments were performed, and multiple cells were tracked for 15 to 20 minutes after LPS incubation over periods of 10 seconds at 90 fps. From the acquired videos, cells were tracked manually, and relevant group comparisons were performed by unpaired 2-tailed Student t tests (the data are the mean ± SD). ∗P < .05; ∗∗P < .01; ∗∗∗P < .001 as indicated, (arrows mark PNCs).