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Isolation, Transfection, and Culture of Primary Human Monocytes
Published on: December 16, 2019
Morphine modulates HIV-1 gp160-induced murine macrophage and human monocyte apoptosis by disparate ways
Aditi A Kapasi1, Salvatore A Coscia, Manish P Pandya
1Immunology and Inflammation Center, North Shore-LIJ Research Institute, The Division of Kidney Disease and Hypertension, Long Island Jewish Medical Center, New Hyde Park, NY 11040, USA.
Abstract:
We studied the effect of HIV-1 gp160 protein and morphine on murine macrophage and human monocyte apoptosis. gp160 not only promoted murine macrophage apoptosis but also enhanced macrophage iNOS expression/NO generation. gp160 also altered macrophage bax and bcl-2 expression. Morphine enhanced (P<0.001) the effect of gp160 on macrophage apoptosis as well as iNOS expression/NO generation. Nevertheless, both morphine- and gp160-induced murine macrophage apoptosis was attenuated by nitric oxide synthase (NOS) inhibitors (L-NAME and L-NMMA). On the other hand, free radical scavengers such as superoxide dismutase (SOD), dimethylthiourea (DMTU) and catalase attenuated morphine and gp160-induced human monocyte apoptosis.
Insights
HIV-1 gp160 protein and morphine induce apoptosis in immune cells. Nitric oxide synthase inhibitors reduced this effect in macrophages, while free radical scavengers protected human monocytes.
Area of Science:
- Immunology
- Cell Biology
- Neuropharmacology
Background:
- HIV-1 gp160 protein is a key viral component.
- Morphine is an opioid analgesic with immunomodulatory effects.
- Apoptosis, or programmed cell death, is crucial in immune regulation.
Purpose of the Study:
- To investigate the combined effects of HIV-1 gp160 and morphine on apoptosis in murine macrophages and human monocytes.
- To explore the role of nitric oxide (NO) and reactive oxygen species (ROS) in these cellular responses.
Main Methods:
- Primary cell cultures of murine macrophages and human monocytes were used.
- Cells were treated with HIV-1 gp160 protein and/or morphine.
- Apoptosis was assessed using various assays.
- Expression of inducible nitric oxide synthase (iNOS), bax, and bcl-2 was analyzed.
- Nitric oxide synthase (NOS) inhibitors and free radical scavengers were employed.
Main Results:
- HIV-1 gp160 induced apoptosis and enhanced iNOS expression/NO generation in murine macrophages.
- Morphine potentiated the effects of gp160 on macrophage apoptosis and iNOS expression.
- NOS inhibitors (L-NAME, L-NMMA) attenuated gp160- and morphine-induced macrophage apoptosis.
- Free radical scavengers (SOD, DMTU, catalase) attenuated gp160- and morphine-induced human monocyte apoptosis.
Conclusions:
- HIV-1 gp160 and morphine synergistically induce apoptosis in murine macrophages, mediated partly by NO.
- Apoptosis in human monocytes induced by these agents is attenuated by free radical scavengers, suggesting a role for ROS.
- These findings highlight differential mechanisms of apoptosis induction in macrophages and monocytes by HIV-1 gp160 and morphine.
