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. 2009 Mar 16;206(3):577–593. doi: 10.1084/jem.20081859

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© 2009 Jakus et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 6. — Leukocyte–endothelial interaction in fMLP-treated cremaster muscle venules in vivo. (A and B) Intravital microscopy of postcapillary cremaster muscle venules superfused with 1 µM fMLP. (A) Leukocyte adhesion in postcapillary venules of WT and PLCγ2^−/− (PLCγ2 KO) bone marrow chimeras before (pre) and at the indicated time points during superfusion with fMLP. (B) Leukocyte spreading in fMLP-superfused cremaster muscle venules. The rate of spreading is expressed as the percent decrease in cell diameter perpendicular to the vessel wall. Mean and SEM of data obtained from four WT and five PLCγ2 KO chimeras are shown. (C and D) Leukocyte adhesion (C) and extravasation (D) assessed by histological analysis of whole mount preparations of cremaster muscles of WT or PLCγ2 KO bone marrow chimeras superfused for 15 min in the presence or absence of 1 µM fMLP. The mean and SEM are shown of the number of intravascular (C) and perivascular (D) leukocytes in 29–41 individual vessels per group from four WT and five PLCγ2 KO chimeras, each tested independently during the same day.