INDUCTION OF CD14 EXPRESSION IN LPS(N), LPS(D) AND TUMOR-NECROSIS-FACTOR RECEPTOR-DEFICIENT MICE

The involvement of CD14 in lipopolysaccharide (LPS) recognition and si gnaling has been demonstrated in several studies. For this reason, we investigated whether the resistance of Lps(d) mice to LPS might be rel ated to an impaired CD14 expression. We compared the in vivo and in vi tro expression of CD14 in Lps(n) (LPS sensitive) and Lps(d) mice, and its modulation by LPS, killed gramnegative and gram-positive bacteria and double-stranded (ds)RNA. Untreated Lps(n) and Lps(d) cultured macr ophages (M Phi), expressed similar amounts of CP14 mRNA and membrane-b ound (m)CD14. LPS enhanced CD14 expression only in Lps(n) M Phi, while all bacteria, or dsRNA, enhanced CD14 in Lps(n) and Lps(d) M Phi. Sim ilarly, in vivo administration of LPS induced or enhanced CD14 mRNA in different organs of Lps(n) mice only, while bacteria or dsRNA in both types of mouse. Furthermore, exogenous recombinant tumor necrosis fac tor (TNF) induced in vivo and in vitro enhanced CD14 expression in Lps (n), Lps(d) and also in TNF receptor 2-deficient (TNFR2-/-) mice, but failed to do so in TNFR1-/- mice, showing that TNFR1 mediates the effe ct of TNF on CD14. However, LPS, bacteria and dsRNA induced CD14 in bo th TNFR2-/- and TNFR1-/- mice to a similar extent, revealing that this induction does not require TNF signaling.