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Induction of apoptosis in a macrophage cell line RAW 264.7 by acemannan, a beta-(1,4)-acetylated mannan

L Ramamoorthy1, I R Tizard

  • 1Department of Veterinary Pathobiology, Texas A & M University, College Station, Texas 77843, USA. l0r7859@nigel.tamu.edu

Molecular Pharmacology
|April 4, 1998
PubMed

Insights

Acemannan, an antiviral immunomodulator, triggers apoptosis in macrophages when combined with interferon-gamma (IFNγ). This process involves inhibiting bcl-2 expression, independent of nitric oxide.

Area of Science:

  • Immunology
  • Cell Biology
  • Virology

Background:

  • Acemannan is a beta-(1,4)-linked acetylated mannan with known antiviral properties.
  • It functions as an immunomodulator, activating macrophages in preliminary studies.
  • The interaction between acemannan, interferon-gamma (IFNγ), and macrophage apoptosis requires further elucidation.

Purpose of the Study:

  • To investigate the mechanism by which acemannan induces apoptosis in RAW 264.7 macrophage cells, particularly in the presence of IFNγ.
  • To determine the role of nitric oxide (NO) in acemannan-induced apoptosis.
  • To examine the effect of acemannan and IFNγ on the expression of the anti-apoptotic protein bcl-2.

Main Methods:

  • RAW 264.7 cells were treated with acemannan and IFNγ.
  • Apoptosis was assessed by observing chromatin condensation, DNA fragmentation, and DNA laddering.
  • The effect of nitric oxide inhibition (using N-nitro-L-arginine methyl ester) on apoptosis was evaluated.
  • The expression of bcl-2 protein was analyzed.

Main Results:

  • Acemannan, in combination with IFNγ, induced apoptosis in RAW 264.7 cells, evidenced by characteristic apoptotic morphological and molecular changes.
  • The induction of apoptosis was not mediated by nitric oxide, as NO inhibition did not alter the effect.
  • Acemannan and IFNγ co-treatment led to the inhibition of bcl-2 expression.

Conclusions:

  • Acemannan, alongside IFNγ, effectively induces apoptosis in RAW 264.7 macrophages.
  • The apoptotic pathway activated by acemannan and IFNγ does not rely on nitric oxide signaling.
  • Inhibition of bcl-2 expression is a key component of the mechanism through which acemannan and IFNγ induce apoptosis.

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