Lipopolysaccharide LPS-mediated soluble TNF receptor release and TNF receptor expression by monocytes. Role of CD14, LPS binding protein, and bactericidal/permeability-increasing protein.

摘要: Previously we demonstrated that two soluble(s) tumor necrosis factor receptors, TNF-R55 as well sTNF-R75, are constitutively released in vitro by monocytes, and this release was markedly enhanced after activation. Because LPS is an important activator of investigated the effect on sTNF-R monocytes. It found but not (or minimally) sTNF-R55, activation with LPS, reaching plateau levels approximately 2 days. CD14, one membrane receptors for intermediate process, shown experiments using mAb directed against CD14. Under serum-free conditions, LPS-induced sTNF-R75 less compared presence serum, suggesting involvement serum proteins. Addition binding protein (LBP) under had no serum. On other hand, bactericidal/permeability-increasing (BPI), known to possess neutralizing activity, inhibited release. Furthermore, cell surface expression both types TNF-R be controlled LBP, BPI. caused, within 1 h, a complete reduction TNF-R75 expression, followed re-expression 24 h. The down-modulation increased whereas BPI counteracted down-regulation. LPS-enhanced capable inactivation TNF, initial leading postulated temporary unresponsiveness TNF may share physiological mechanism carefully control effects TNF.