Immune cell recruitment to inflammatory loci is impaired in mice deficient in basement membrane protein laminin α4

Journal of Leukocyte Biology

Ellinor Kenne²  Pierre Rotzius²  Oliver Soehnlein²  Lennart Lindbom²  Guillem Genové¹  Einar E. Eriksson² 

[1] Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden;Departments of Physiology and Pharmacology and Departments of Physiology and Pharmacology and Departments of Physiology and Pharmacology and

关键词: inflammation;    leukocyte recruitment;   

DOI  :  10.1189/jlb.0110043

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

For leukocytes to penetrate the vessel wall, they need to interact sequentially with the endothelial lining and the perivascular BM. The matrix protein laminin-411 is a major constituent of the vascular BM. The laminin α4 chain is a component of laminin-411 and has structural and signaling functions. Here, we addressed the role of BM laminin α4 in leukocyte recruitment to inflammatory loci. We used several recruitment models in Lam4−/− and WT mice to determine whether lack of laminin-411 in the perivascular BM influences extravasation of inflammatory cells. Recruitment of all major leukocyte subsets (neutrophils, monocytes, and lymphocytes) was reduced in Lam4−/− mice compared with WT. With the use of intravital microscopy, we concluded that this decrease was a result of impaired diapedesis through the vessel wall, as neither leukocyte adhesion to the endothelial lining nor migration in extravascular tissue was hampered in Lam4−/− mice. Collectively, our data suggest a reduced ability of immune cells to penetrate the vessel wall in mice deficient in laminin α4.

【 授权许可】

Unknown