Open AccessThe α7‐nicotinic receptor is upregulated in immune cells from HIV‐seropositive women: consequences to the cholinergic anti‐inflammatory response
Author(s) -
DelgadoVélez Manuel,
BáezPagán Carlos A,
Gerena Yamil,
Quesada Orestes,
SantiagoPérez Laura I,
CapóVélez Coral M,
Wojna Valerie,
Meléndez Loyda,
LeónRivera Rosiris,
Silva Walter,
LasaldeDominicci José A
Publication year - 2015
Publication title -
clinical and translational immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.321
H-Index - 34
ISSN - 2050-0068
DOI - 10.1038/cti.2015.31
Subject(s) - proinflammatory cytokine , inflammation , immunology , downregulation and upregulation , cholinergic , immune system , medicine , biology , gene , biochemistry
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 gp120 IIIB . Our results demonstrate that HIV gp120 IIIB 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.