Abstract
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 Lps^d^ mice to LPS might be related to an impaired CD14 expression. We compared the in vivo and in vitro 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 macrophages (MΦ), expressed similar amounts of CD14 mRNA and membrane‐bound (m)CD14. LPS enhanced CD14 expression only in Lps^n^ MΦ, while all bacteria, or dsRNA, enhanced CD14 in Lps^n^ and Lps^d^ MΦ. Similarly, in vivo administration of LPS induced or enhanced CD 14 mRNA in different organs of Lps^n^ 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 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 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.