Signal transduction mechanisms for leukotriene B4 induced hyperadhesiveness of endothelial cells for neutrophils.

摘要: We have previously demonstrated that leukotriene B4 (LTB4) induces in vitro a transient state of hyperadhesiveness cultured human umbilical vein endothelial cells (HUVEC) for neutrophils (PMN). The magnitude this response is intermediate conferred by thrombin and platelet-activating factor (PAF). This report shows the LTB4 was neither related to HUVEC expression PAF (because it could not be blocked receptor antagonist WEB-2086), nor access receptors on (as shown desensitization experiments). However, partly treating with an (SC-41930). evoked rise intracellular calcium concentrations, [Ca2+]i, HUVEC, hyperadhesive abrogated buffering [Ca2+]i Quin-2. inhibited pertussis toxin before LTB4. Neutrophils showed no signs activation when adhering LTB4-treated because they did i) release lactoferrin, or ii) react increase iii) bound equally well stimulated after having been treated so up-regulation PMN adhesion abolished. shed factors modulated neutrophil adherence chemotaxis. Thus, promotes PMN, transduction mechanism involves ions, may depend surface LTB4, but does involve toxin-sensitive G proteins activation.