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Assessment of Morphine-induced Hyperalgesia and Analgesic Tolerance in Mice Using Thermal and Mechanical Nociceptive Modalities
Published on: July 29, 2014
Effect of morphine on the neuropathogenesis of SIVmac infection in Indian Rhesus Macaques
Joanne K Marcario1, Mariam Riazi, Istvan Adany
1Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Mail Stop 3043, 3901 Rainbow Blvd., Kansas City, KS 66160, USA.
Abstract:
Morphine is known to prevent the development of cell-mediated immune (CMI) responses and enhance expression of the CCR5 receptor in monocyte macrophages. We undertook a study to determine the effect of morphine on the neuropathogenesis and immunopathogenesis of simian immunodeficiency virus (SIV) infection in Indian Rhesus Macaques. Hypothetically, the effect of morphine would be to prevent the development of CMI responses to SIV and to enhance the infection in macrophages. Sixteen Rhesus Macaques were divided into three experimental groups: M (morphine only, n = 5), VM (morphine + SIV, n = 6), and V (SIV only, n = 5). Animals in groups M and VM were given 2.5 mg/kg of morphine sulfate, four times daily, for up to 59 weeks. Groups VM and V were inoculated with SIVmacR71/17E 26 weeks after the beginning of morphine administration. Morphine prevented the development of enzyme-linked immunosorbent spot-forming cell CMI responses in contrast to virus control animals, all of which developed CMI. Whereas morphine treatment had no effect on viremia, cerebrospinal fluid viral titers or survival over the time course of the study, the drug was associated with a tendency for greater build-up of virus in the brains of infected animals. Histopathological changes in the brains of animals that developed disease were of a demyelinating type in the VM animals compared to an encephalitic type in the V animals. This difference may have been associated with the immunosuppressive effect of the drug in inhibiting CMI responses.
Insights
Morphine suppressed cell-mediated immune responses to simian immunodeficiency virus (SIV) in macaques. While not affecting viral load or survival, morphine was linked to increased SIV in the brain and altered neuropathology.
Area of Science:
- Neuroscience
- Immunology
- Virology
Background:
- Morphine is known to suppress cell-mediated immune (CMI) responses and upregulate CCR5 receptors on macrophages.
- Simian immunodeficiency virus (SIV) infection in macaques serves as a model for HIV pathogenesis.
Purpose of the Study:
- To investigate the impact of morphine on the neuropathogenesis and immunopathogenesis of SIV infection in Indian Rhesus Macaques.
- To determine if morphine exacerbates SIV infection by inhibiting CMI responses.
Main Methods:
- Sixteen Rhesus Macaques were divided into three groups: morphine only (M), morphine + SIV (VM), and SIV only (V).
- Animals received morphine sulfate (2.5 mg/kg) for up to 59 weeks.
- Groups VM and V were inoculated with SIVmacR71/17E.
Main Results:
- Morphine treatment inhibited the development of SIV-specific CMI responses.
- Morphine did not significantly alter viremia, cerebrospinal fluid viral titers, or survival rates.
- A trend towards increased SIV accumulation in the brain was observed in morphine-treated, SIV-infected macaques.
- Histopathological analysis revealed demyelinating changes in the brains of VM animals versus encephalitic changes in V animals.
Conclusions:
- Morphine's immunosuppressive effect, specifically the inhibition of CMI responses, may influence SIV neuropathogenesis.
- The observed differences in brain pathology suggest morphine could alter the disease course in SIV-infected macaques, potentially by modulating immune responses.
