Related Experiment Video
Updated: Aug 10, 2026

Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
Published on: June 23, 2013
Protein phosphorylation pathways involved during lipopolysaccharide-induced expression of CD14 in mouse bone marrow
1Molecular Immunophysiology Unit, URA-1961, National Center for Scientific Research, Pasteur Institute, Paris, France.
Abstract:
Lipopolysaccharide (LPS) of Gram-negative bacteria interacts with a CD14-independent receptor of mouse bone marrow granulocytes (BMC), and triggers in these cells the expression of CD14, an inducible type of LPS receptor (iLpsR). This particular response of BMC to LPS required the activation of protein tyrosine kinase and p38 MAP kinase. The inhibition of the LPS effect by the MEK inhibitor PD-98059 suggested that the ERK pathway was also involved. Unexpectedly, protein kinase C, myosin light chain kinase, cAMP-, cGMP-, and Ca(2+)/calmodulin-dependent kinases, as well as ecto-protein kinases, were not required for iLpsR expression. However, other yet unidentified serine/threonine protein kinase(s) were implied since the BMC response to LPS was markedly reduced after exposure to three inhibitors of such kinases (K-252a, H-7, and KT-5823). The atypical kinase requirements observed in this study may be due either to a novel signaling LPS receptor complex present in BMC, or to the particular events involved in CD14 biosynthesis.
Insights
Lipopolysaccharide (LPS) triggers CD14 expression in mouse bone marrow granulocytes via a novel kinase pathway. This response involves protein tyrosine kinase and p38 MAP kinase, but not conventional kinases, suggesting unique signaling mechanisms.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Gram-negative bacteria possess lipopolysaccharide (LPS), a potent immune stimulant.
- CD14 is a key receptor for LPS, mediating inflammatory responses.
- Mouse bone marrow granulocytes (BMC) express CD14 upon LPS stimulation, termed inducible LPS receptor (iLpsR).
Purpose of the Study:
- To elucidate the intracellular signaling pathways involved in LPS-induced CD14 expression in BMC.
- To identify the specific kinases required for iLpsR expression.
Main Methods:
- Treatment of BMC with LPS.
- Inhibition of specific kinase pathways using chemical inhibitors (e.g., PD-98059, K-252a, H-7, KT-5823).
- Assessment of CD14 expression levels.
Main Results:
- LPS-induced iLpsR expression in BMC requires protein tyrosine kinase and p38 MAP kinase activation.
- The ERK pathway is also implicated in this response.
- Conventional kinases like protein kinase C, myosin light chain kinase, and Ca(2+)/calmodulin-dependent kinases are not essential for iLpsR expression.
- Inhibition of certain serine/threonine protein kinases significantly reduced BMC response to LPS.
Conclusions:
- The signaling pathway for LPS-induced CD14 expression in BMC is atypical, involving novel kinase requirements.
- This atypical signaling may stem from a unique LPS receptor complex or specific CD14 biosynthesis events in BMC.
Related Concept Videos
Amplifying Signals via Enzymatic Cascade
The JAK-STAT Signaling Pathway
cAMP-dependent Protein Kinase Pathways
IP3/DAG Signaling Pathway

