Interactions of C-Reactive Protein and Serum Amyloid P Component with Interleukin-8 and Their Role in Regulation of Neutrophil Functions

Autor: Elena V., Galkina, Peter G., Nazarov, Alexander V., Polevschikov, Larissa K., Berestovaya, Vitold E., Galkin, Natalia V., Bychkova
Rok vydání: 2003
Zdroj: Russian journal of immunology : RJI : official journal of Russian Society of Immunology. 5(4)
ISSN: 1028-7221
Popis: C-reactive protein (CRP) and serum amyloid P component (SAP) are acute phase proteins, whose concentrations increase within 24 h of inflammation along with concentration of IL-8. Polymorphonuclear neutrophil leukocytes (PMNs) form the earliest barrier protecting an injured organ during acute phase response. The aim of present work was to study interactions between CRP, SAP and IL-8, and to estimate the role of these interactions in regulation of neutrophil transendothelial migration. The results have shown that IL-8 binds to immobilized but not to free CRP. Binding of IL-8 to immobilized SAP was less strong. SAP like IL-8 increased CD11/CD18 integrin expression. IL-8 did not abolish the effect of SAP, and the mixture of IL-8 and SAP has stimulated CD11/CD18 expression. CRP upregulated CD18 but not CD11b expression. Under simultaneous action of CRP and IL-8, the stimulatory effect on CD11b and CD18 was abolished. The expression of fibronectin receptor was reduced by either IL-8 or CRP but increased by SAP. Effect of each protein was downregulated after following preincubations: CRP+SAP, CRP+IL-8 or SAP+IL-8. The mixtures of CRP with SAP, CRP with IL-8 or SAP with IL-8 showed no chemotactic activity, although each of the proteins was chemoattractive. Thus, acute phase proteins and IL-8 can act as anti-inflammatory factors upon binding each other. In summary, CRP and SAP influence PMN adhesion, migration and expression of CD11b/CD18 and fibronectin receptors, and can modulate the action of IL-8 on PMN attachment to endothelium and fibronectin, and on PMN traffic through the extracellular matrix during transendothelial migration.
Databáze: OpenAIRE