LIPOPOLYSACCHARIDE AND TUMOR NECROSIS FACTOR-± SYNERGY POTENTIATE SERUM-DEPENDENT RESPONSES OF RAT MACROPHAGES

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Abstract
Tumor necrosis factor-± (TNF-±) and interleukin-1± (IL-1 ±) are major mediators of sepsis and multiple organ failure. Serum-mediated macrophage activation requires lipopolysaccharide (LPS) and its serum binding protein, lipopolysaccharide binding protein as a ligand for the receptor CD14. This study was designed to determine whether cytokines participate in regulation of serum-mediated LPS activation. Rat macrophages were stimulated with LPS with and without TNF-± or IL-1± and activation was determined by detection of TNF-± by specific enzyme-linked immunosorbent assay or TNF-± mRNA by Northern blot analysis. The addition of TNF-± but not IL-1±, in the presence of serum, leads to potentiation of macrophage activation after LPS stimulation. This effect could be specifically inhibited by neutralization of LPS with polymyxin B or an antibody against TNF-±. This study shows that LPS and TNF-± synergize to potentiate serum-mediated macrophage activation. These results demonstrate another element of the control mechanism of cytokine secretion following macrophage activation in sepsis.

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