The α7-nicotinic Receptor is Upregulated Inimmune Cells from HIV-seropositive Women: Consequences to the Cholinergic Anti-inflammatory Response.
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Authors
Delgado-Vélez, Manuel
Báez-Pagán, Carlos A.
Gerena, Yamil
Quesada, Orestes
Santiago-Pérez, Laura I.
Capó-Vélez, Coral M.
Wojna, Valerie
Meléndez, Loyda
León-Rivera, Rosiris
Silva, Walter
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Nature Publishing Group
DOI
10.1038/cti.2015.31
Abstract
Antiretroviral therapy partially restores the immune system and markedly increases life expectancy of HIV-infected patients. However, antiretroviral therapy does not restore full health. These patients suffer from poorly understood chronic inflammation that causes a number of AIDS and non-AIDS complications. Here we show that chronic inflammation in HIV+ patients may be due to the disruption of the cholinergic anti-inflammatory pathway by HIV envelope protein gp120IIIB. Our results demonstrate that HIV gp120IIIB induces α7 nicotinic acetylcholine receptor (α7) upregulation and a paradoxical proinflammatory phenotype
in macrophages, as activation of the upregulated α7 is no longer capable of inhibiting the release of proinflammatory cytokines. Our results demonstrate that disruption of the cholinergic-mediated anti-inflammatory response can result from an HIV protein. Collectively, these findings suggest that HIV tampering with a natural strategy to control inflammation could contribute to a crucial, unresolved problem of HIV infection: chronic inflammation.
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Delgado-Vélez, M., Báez-Pagán, C. A., Gerena, Y., Quesada, O., Santiago-Pérez, L. I., Capó-Vélez, C. M., … Lasalde-Dominicci, J. A. (2015). The α7-nicotinic receptor is upregulated in immune cells from HIV-seropositive women: consequences to the cholinergic anti-inflammatory response. Clinical & Translational Immunology, 4(12), e53–. http://doi.org/10.1038/cti.2015.31
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© 2015 Australasian Society for Immunology Inc.
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