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Clin Transl Immunology. 2015 Dec 11;4(12):e53. doi: 10.1038/cti.2015.31. eCollection 2015 Dec.

The α7-nicotinic receptor is upregulated in immune cells from HIV-seropositive women: consequences to the cholinergic anti-inflammatory response.

Author information

1
Department of Biology, University of Puerto Rico, Río Piedras Campus , San Juan, Puerto Rico.
2
School of Medicine, Department of Pharmacology, University of Puerto Rico , San Juan, Puerto Rico.
3
Department of Physical Sciences, University of Puerto Rico , San Juan, Puerto Rico.
4
Specialized Neuroscience Research Program in Neuro AIDS, University of Puerto Rico , San Juan, Puerto Rico ; Internal Medicine, Neurology Division, University of Puerto Rico , San Juan, Puerto Rico.
5
Specialized Neuroscience Research Program in Neuro AIDS, University of Puerto Rico , San Juan, Puerto Rico ; Department of Microbiology and Medical Zoology, University of Puerto Rico , San Juan, Puerto Rico.
6
Department of Physiology, University of Puerto Rico , San Juan, Puerto Rico.
7
Department of Biology, University of Puerto Rico, Río Piedras Campus , San Juan, Puerto Rico ; Specialized Neuroscience Research Program in Neuro AIDS, University of Puerto Rico , San Juan, Puerto Rico ; Department of Chemistry, University of Puerto Rico , San Juan, Puerto Rico.

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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