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Bone Marrow-derived Macrophage Production
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Role of plasma, lipopolysaccharide-binding protein, and CD14 in response of mouse peritoneal exudate macrophages to

D Heumann1, Y Adachi, D Le Roy

  • 1Division of Infectious Diseases, CHUV, Lausanne, Switzerland. dheumann@hola.hospvd.ch

Infection and Immunity
|December 19, 2000
PubMed

Insights

Lipopolysaccharide (LPS)-binding protein (LBP) and CD14 are crucial for macrophage responses to low endotoxin levels. This study confirms their essential role in innate immunity against bacterial endotoxins.

Area of Science:

  • Immunology
  • Cell Biology
  • Microbiology

Background:

  • Plasma lipopolysaccharide (LPS)-binding protein (LBP) and membrane CD14 typically enhance monocyte responses to endotoxins.
  • Conflicting reports suggest LBP or CD14 might be dispensable or inhibitory for macrophage responses to LPS.

Purpose of the Study:

  • To investigate the participation of LBP and CD14 in mouse peritoneal exudate macrophage (PEM) responses to LPS stimulation.
  • To clarify the roles of LBP and CD14 in innate immune responses to endotoxins.

Main Methods:

  • Stimulation of mouse peritoneal exudate macrophages (PEM) with varying concentrations of LPS.
  • Assessment of cellular responses in the presence of low (<1%) or high (5-10%) concentrations of plasma/serum or recombinant LBP.
  • Measurement of tumor necrosis factor (TNF) and interleukin-6 (IL-6) production.

Main Results:

  • PEM responded to low LPS concentrations (<5-10 ng/ml) in an LBP- and CD14-dependent manner when low plasma or recombinant LBP was present.
  • Higher plasma/serum concentrations (5-10%) inhibited TNF production, but not IL-6 production, by LPS-stimulated PEM.
  • This inhibitory effect of plasma/serum was independent of LBP.

Conclusions:

  • LBP and CD14 are critical for innate immune responses of both monocytes and tissue macrophages to endotoxins, particularly at low LPS concentrations.
  • While essential for low-dose endotoxin response, high plasma/serum concentrations can modulate macrophage responses, an effect not mediated by LBP.

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