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Involvement of microglial CD40 in murine retrovirus-induced peripheral neuropathy
1Department of Biomedical Sciences, College of Osteopathic Medicine, University of New England, 11 Hills Beach Road, Biddeford, ME 04005, USA. lcao@UNE.edu
Abstract:
B6 mice infected with LP-BM5 develop severe immunodeficiency (termed murine acquired immunodeficiency syndrome (MAIDS)) and peripheral neuropathy. To determine whether microglial CD40 is involved in LP-BM5-induced peripheral neuropathy, B6-CD40 knockout (KO) mice and B6-CD40 KO mice adoptively transferred either total leukocytes or B cells were examined for behavioral sensitivity, tissue viral loads, cytokine responses, and the development of MAIDS. All three CD40 KO groups developed MAIDS, the severity of which was correlated with peripheral cytokine responses. CD40 KO mice displayed significantly reduced mechanical hypersensitivity post-infection compared to wild-type mice regardless of cell transfer. These findings support microglial CD40 involvement in LP-BM5-induced peripheral neuropathy.
Insights
Microglial CD40 plays a role in LP-BM5-induced peripheral neuropathy in mice. CD40 knockout mice showed reduced pain sensitivity, suggesting CD40
Area of Science:
- Immunology
- Neuroscience
- Virology
Background:
- LP-BM5 retrovirus infection in B6 mice causes murine acquired immunodeficiency syndrome (MAIDS) and peripheral neuropathy.
- Microglia, the immune cells of the central nervous system, are implicated in neuroinflammation and neuropathic pain.
- The specific role of microglial CD40 in the pathogenesis of LP-BM5-induced peripheral neuropathy remains unclear.
Purpose of the Study:
- To investigate the involvement of microglial CD40 in the development of LP-BM5-induced peripheral neuropathy.
- To assess the impact of CD40 deficiency on MAIDS development, viral load, and cytokine responses.
Main Methods:
- Utilized B6-CD40 knockout (KO) mice and B6-CD40 KO mice with adoptive transfer of leukocytes or B cells.
- Infected mice with LP-BM5 retrovirus.
- Evaluated behavioral sensitivity (mechanical hypersensitivity), tissue viral loads, and peripheral cytokine responses.
Main Results:
- All CD40 KO groups developed MAIDS, with severity correlating to peripheral cytokine levels.
- CD40 KO mice exhibited significantly reduced mechanical hypersensitivity compared to wild-type mice post-infection.
- This reduction in hypersensitivity was observed irrespective of adoptive cell transfer.
Conclusions:
- Microglial CD40 is involved in the development of LP-BM5-induced peripheral neuropathy.
- CD40 deficiency attenuates neuropathic pain without preventing MAIDS development.
- These findings highlight CD40 as a potential therapeutic target for neuropathic pain associated with viral infections.
