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Nitric oxide production and apoptosis by GP120

A Mansur1, C M Chu, A Karnik

  • 1Department of Pathology, Nassau County Medical Center, East Meadow, New York 11554, USA.

Allergy and Asthma Proceedings
|July 13, 2000
PubMed

Insights

The gp120 fragment F1 significantly increases nitric oxide (NO) and apoptosis in immune cells. This finding helps understand HIV-induced apoptosis mechanisms.

Area of Science:

  • Immunology
  • Neuroscience
  • Virology

Background:

  • Nitric oxide (NO) production is elevated in astrocytes and macrophages by gp120.
  • gp120 also induces apoptosis in CD4+ T cells.
  • Specific gp120 fragments (F1, F2, F3) are investigated for their roles.

Purpose of the Study:

  • To determine the relative contribution of gp120 and its fragments (F1, F2, F3) to nitric oxide production.
  • To assess the impact of gp120 fragments on apoptosis in peripheral blood mononuclear cells (PBMCs).
  • To elucidate the mechanisms underlying HIV-induced apoptosis.

Main Methods:

  • Incubation of PBMCs with gp120 and its fragments (F1, F2, F3) at varying concentrations and time points (24 and 72 hours).
  • Measurement of nitric oxide (NO) production in cell supernatants.
  • Detection of apoptosis using in situ hybridization, with and without lipopolysaccharide (LPS) stimulation.

Main Results:

  • Fragment F1 significantly increased NO production at 24 hours (1.9-fold increase).
  • Both F1 and F2 showed significant contributions to NO production at 72 hours (1.5-fold increase).
  • F1 demonstrated the most substantial contribution to apoptosis, both with and without LPS.

Conclusions:

  • gp120 fragment F1 is a major contributor to NO production and apoptosis in PBMCs.
  • Fragment F2 also plays a role in NO production at later time points.
  • These findings offer insights into the molecular mechanisms of HIV-associated immune dysregulation and apoptosis.

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