来自原核生物粘附素的肽在体外和体内均可阻止白细胞迁移。

Peptide from a prokaryotic adhesin blocks leukocyte migration in vitro and in vivo.

作者信息

Rozdzinski E, Spellerberg B, van der Flier M, Bhattacharyya C, Hoepelman A I, Moran M A, Jarpe A, Putney S D, Starzyk R M, Tuomanen E

机构信息

Laboratory of Molecular Infectious Diseases, Rockefeller University, New York, New York 10021, USA.

出版信息

J Infect Dis. 1995 Sep;172(3):785-93. doi: 10.1093/infdis/172.3.785.

DOI:10.1093/infdis/172.3.785

PMID:7544820

Abstract

The integrin CD11b/CD18 promotes leukocyte extravasation during inflammation. Filamentous hemagglutinin (FHA) of Bordetella pertussis binds to CD11b/CD18, raising the possibility that peptides derived from FHA might inhibit leukocyte migration. The Arg-Gly-Asp (RGD) sequence of FHA has been suggested to modulate binding of ligands to CD11b/CD18. Peptides derived from this region inhibited adherence and transendothelial migration of neutrophils in vitro and prevented recruitment of leukocytes into the cerebrospinal fluid in an experimental model of meningitis in rabbits. The mechanism of the antiinflammatory effect may involve modulation of the activity of CD11b/CD18 through peptide interaction with the leukocyte response integrin/integrin-associated protein complex.

摘要

整合素CD11b/CD18在炎症过程中促进白细胞外渗。百日咳博德特氏菌的丝状血凝素（FHA）与CD11b/CD18结合，这增加了源自FHA的肽可能抑制白细胞迁移的可能性。FHA的精氨酸-甘氨酸-天冬氨酸（RGD）序列已被认为可调节配体与CD11b/CD18的结合。源自该区域的肽在体外抑制中性粒细胞的黏附和跨内皮迁移，并在兔脑膜炎实验模型中阻止白细胞募集到脑脊液中。抗炎作用的机制可能涉及通过肽与白细胞反应整合素/整合素相关蛋白复合物的相互作用来调节CD11b/CD18的活性。