Monocyte adherence to fibronectin: role of CD11/CD18 integrins and relationship to other monocyte functions.

摘要: Regulated adherence of monocytes to extracellular matrix macromolecules is a prerequisite for their accumulation at sites pulmonary infection and inflammation. To begin assess the pathobiological importance alterations in monocyte inflammatory lung diseases, properties from patients with an disease (bronchiectasis) healthy subjects representative component (fibronectin) were compared. Spontaneous control was 20 25%, whereas that patients' cells 2 3-fold higher correlated severity airway Endotoxin (LPS) cytokines areas are likely be responsible observed activation since: 1) LPS detected plasma all but none subjects; 2) produced dose-related increases normal vitro. Monocyte fibronectin substantially mediated by CD11/CD18 integrins, via both RGD-dependent RGD-independent mechanisms. These data indicate signals arising foci inflammation determinants lungs chronic diseases. There striking relationship between functions biological Spontaneously adherent had "inflammatory effector" phenotype, non-adherent "immune modulatory" phenotype could stimulated adhere (LPS-adherent cells) intermediate phenotype. In addition, only subpopulations replete HLE these contained substantial (10 11-fold) molar excess compared physiological inhibitor this enzyme (a1-antitrypsin). Maturation vitro increased a1-antitrypsin subpopulations. contrast, proinflammatory mediators up-regulated spontaneously cells, probably translational or post-translational conclusion, heterogeneous ability accumulate capacity related Furthermore, released infection, may induce effector thereby promote resolution tissue infection. Alternatively, recruitment contribute HLE-mediated injury.