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PECAM‐1 & JAM‐A mediate leukocyte transmigration in a stimulus‐specific manner: Is this phenomenon governed by the strain of mice investigated?
Author(s) -
Woodfin Abigail,
Larbi Karen,
Krombach Fritz,
Dejana Elisabetta,
Nourshargh Sussan
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a127-b
Subject(s) - microbiology and biotechnology , in vivo , cremaster muscle , knockout mouse , chemistry , ratón , biology , leukocyte trafficking , immunology , inflammation , chemokine , gene , genetics , biochemistry
We have shown that the ability of PECAM‐1 & JAM‐A to mediate leukocyte transmigration in vivo is stimulus‐specific, eg both molecules mediate leukocyte transmigration through cremasteric venules of C57BL/6 mice as elicited by IL‐1β but not TNFα. As it has been suggested that in contrast to some other laboratory mouse strains, C57BL/6 mice can compensate for PECAM‐1 blockade/deletion (Schenkel et al., 2004), we sought to investigate whether the stimulus‐specific roles of PECAM‐1/JAM‐A in the cremaster muscle model are governed by the strain of mice used. In line with the findings of Schenkel et al., the anti‐PECAM‐1 blocking mAb Mec 13.3 suppressed thioglycollate‐induced leukocyte migration into the peritoneum of SJL but not C57BL/6 mice. In contrast, in the cremaster muscle model whilst IL‐1β‐induced leukocyte transmigration (as observed by IVM) was inhibited by Mec 13.3 in the mouse strains C57BL/6, FVB and SJL (84 %, 93% and 100% inhibition, respectively), no inhibition of TNFα‐induced transmigration was noted in these mouse strains. In addition, the anti‐JAM‐A mAb BV‐11, blocked IL‐1β‐induced, but not TNFα‐induced, leukocyte transmigration in both C57BL/6 and FVB mice. The results suggest that the stimulus‐specific roles of PECAM‐1 & JAM‐A in different mouse strains may be governed by the inflammatory model employed. Supported by EU Network of Excellence ‘MAIN’(LSHG‐CT‐2003‐502935)