Semaphorins guide the entry of dendritic cells into the lymphatics by activating myosin II.
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Human T lymphocyte isolation, culture and analysis of migration in vitro.
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Selective activation of the prostaglandin E2 circuit in chronic injury-induced pathologic angiogenesis.
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Mechanisms of force generation and force transmission during interstitial leukocyte migration.
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Effect of exogenous galectin-1 on leukocyte migration: modulation of cytokine levels and adhesion molecules.
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The effect of exogenous Gal-1 on cellular response and adhesion molecule expression was investigated in a classical model of acute inflammation induced by zymosan. C57BL6 mice, treated or not with human recombinant (hr) Gal-1, received i.p. injection of zymosan and peritoneal exudate, blood and mesentery were processed for cellular, biochemical, light and electron microscopic analysis after 4 and 24 h. Zymosan peritonitis provoked the expected signs of inflammation at 4 h, including a significant increase in extravasated PMNs in the mesentery and peritoneal exudate, mirrored by blood neutrophilia. These changes subsided after 24 h. Ultrastructural immunocytochemical analysis of PMNs showed significant Gal-1 expression and co-localization with L-selectin and beta2-integrin in the plasma membrane and cytoplasm. Pharmacological treatment with hrGal-1 at 4 h produced an inhibition of PMN migration, associated with diminished expression of adhesion molecules, particularly beta2-integrin, and TNF-alpha and IL-1beta release by peritoneal cells. At 24 h, Gal-1 induced an increase in mononuclear phagocytic cell recruitment. In conclusion, our data propose an important mechanism of anti-inflammatory action of Gal-1, initially by modulation of pro-inflammatory cytokine release and PMN migration through an imbalance between adhesion molecule expression and, later, by promoting monocyte-macrophage recruitment. (+info)
Attenuation of human neutrophil migration and function by uropathogenic bacteria.
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Activation of adenosine A2A receptors inhibits neutrophil transuroepithelial migration.
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Kaposi's sarcoma-associated herpesvirus-encoded latency-associated nuclear antigen reduces interleukin-8 expression in endothelial cells and impairs neutrophil chemotaxis by degrading nuclear p65.
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