• CD14;
  • Lpsd mice;
  • Bacteria;
  • Double-stranded;
  • Tumor necrosis factor receptor −/− mice


The involvement of CD14 in lipopolysaccharide (LPS) recognition and signaling has been demonstrated in several studies. For this reason, we investigated whether the resistance of Lpsd mice to LPS might be related to an impaired CD14 expression. We compared the in vivo and in vitro expression of CD14 in Lpsn (LPS sensitive) and Lpsd mice, and its modulation by LPS, killed gramnegative and gram-positive bacteria and double-stranded (ds)RNA. Untreated Lpsn and Lpsd cultured macrophages (MΦ), expressed similar amounts of CD14 mRNA and membrane-bound (m)CD14. LPS enhanced CD14 expression only in Lpsn MΦ, while all bacteria, or dsRNA, enhanced CD14 in Lpsn and Lpsd MΦ. Similarly, in vivo administration of LPS induced or enhanced CD 14 mRNA in different organs of Lpsn mice only, while bacteria or dsRNA in both types of mouse. Furthermore, exogenous recombinant tumor necrosis factor (TNF) induced in vivo and in vitro enhanced CD 14 expression in Lpsn, Lpsd and also in TNF receptor 2-deficient (TNFR2−/−) mice, but failed to do so in TNFR1−/− mice, showing that TNFR1 mediates the effect of TNF on CD14. However, LPS, bacteria and dsRNA induced CD14 in both TNFR2−/− and TNFR1−/− mice to a similar extent, revealing that this induction does not require TNF signaling.