Lipopolysaccharide and tumor necrosis factor-α synergy potentiate serum-dependent responses of rat macrophages

Eben S. Fox, Lei Wang, Thomas Tracy

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) 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-α or IL-1β and activation was determined by detection of TNF-α by specific enzyme-linked immunosorbent assay or TNF-α mRNA by Northern blot analysis. The addition of TNF-α but not IL-1β, 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-α. This study shows that LPS and TNF-α synergize to potentiate serum-mediated macrophage activation. These results demonstrate another element of the control mechanism of cytokine secretion following macrophage activation in sepsis.

Original languageEnglish (US)
Pages (from-to)429-433
Number of pages5
JournalShock
Volume5
Issue number6
DOIs
StatePublished - Jan 1 1996

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Lipopolysaccharides
Tumor Necrosis Factor-alpha
Macrophages
Macrophage Activation
Serum
Interleukin-1
Sepsis
Cytokines
Polymyxin B
Multiple Organ Failure
Protein Binding
Northern Blotting
Blood Proteins
Carrier Proteins
Enzyme-Linked Immunosorbent Assay
Ligands
Messenger RNA
Antibodies

All Science Journal Classification (ASJC) codes

  • Emergency Medicine
  • Critical Care and Intensive Care Medicine

Cite this

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Lipopolysaccharide and tumor necrosis factor-α synergy potentiate serum-dependent responses of rat macrophages. / Fox, Eben S.; Wang, Lei; Tracy, Thomas.

In: Shock, Vol. 5, No. 6, 01.01.1996, p. 429-433.

Research output: Contribution to journalArticle

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