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- W4313383503 abstract "Abstract We have investigated the functionality of the cholinergic anti-inflammatory pathway (CAP) in HIV-1 infected individuals. The pathway plays an important role in regulating inflammatory process in the body. Acetylcholine (ACh), a neurotransmitter, is the main effector molecule of the CAP. It is produced by CD4+ T cells, intestinal epithelial cells as well as by neurons in the body, and exerts its effects via nicotinic (n) and muscarinic (m) Acetylcholine receptors (AChR). Through these receptors, ACh modulates differentiation, proliferation and effector functions of immune cells in the body. Little is known about the regulation of the non-neuronal CAP in HIV infections. To investigate it, we measured concentrations of ACh and the Secreted Ly6/Urokinase type plasminogen activator Receptor-related Peptide-1 (SLURP-1, an allosteric ligand for the α-7nAChR) in the circulation of HIV-infected individuals. The concentrations of both ACh and SLURP-1 were increased in treatment-naïve HIV-infected individuals. In contrast to an increase in the concentrations of ACh and SLURP-1, the expression of the α-7nAChR was significantly decreased on immune cells in the virus-infected individuals. We investigated the effects of gp-120 on the expression of this receptor. We found that the treatment of the human PBMC with recombinant gp120 reduces the expression of α-7nAChR on immune cells. Interestingly, the treatment increases the binding of α-bungarotoxin, a ligand for nAChR. Collectively, these results suggest that the non-neuronal CAP is functionally compromised in HIV-infected individuals and gp120 plays a role in the hypo-functionality by down-regulating the expression of α-7nAChR on the peripheral blood immune cells." @default.
- W4313383503 created "2023-01-06" @default.
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- W4313383503 date "2020-05-01" @default.
- W4313383503 modified "2023-09-27" @default.
- W4313383503 title "Gp120 plays a role in the hypo-functionality of the cholinergic anti-inflammatory pathway in HIV infection" @default.
- W4313383503 doi "https://doi.org/10.4049/jimmunol.204.supp.249.19" @default.
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