Fatemeh Gholizadeh

Conference 2024 Live Talk

Talk Title

Modulatory effect of nicotinic acetylcholine receptors on the human memory T helper 1 and T helper 17 cells

Authors and Affiliations

Fatemeh Gholizadeh1,3, Mehri Hajiaghaei1,3, Jennifer S. Choi2, Aude Pinard3, Peter J. Darlington1,3
1 Department of Biology, Concordia University, Montréal, Québec, Canada
2 Department of Medicine, McGill University, Montréal, Québec, Canada
3 Department of Health, Concordia University, Montréal, Québec, Canada

Abstract

Background

Memory T helper (Th) cells are a crucial component of the adaptive immune system, generated in response to a primary immunogenic challenge. Acetylcholine (ACh), a neurotransmitter produced by the parasympathetic nervous system, influences memory Th cells through muscarinic and nicotinic acetylcholine receptors (nAChRs). This study aims to assess the role of nAChRs in the cytokine production and proliferation of ex vivo isolated memory Th cells.

Methods

Memory Th cells were isolated from the peripheral blood of healthy participants. The average purity of memory Th cells was 98.9% ± 0.64%, as determined by flow cytometry. During activation with anti-CD3/anti-CD28, memory Th cells were exposed to 10μM nicotine for five days. ELISA, flow cytometry, and western blot techniques were employed to analyze the levels of IL-17A, IFN-γ, and NF-κB. Cell proliferation was assessed using CFDASE dye and flow cytometry.

Results

Nicotine significantly decreased IL-17A and IFN-γ levels (p < 0.05). However, nicotine did not change the levels of phosphorylated NF-κB. Moreover, nicotine did not affect the proliferation of memory Th cells. Conclusions Our study reveals that nAChRs play a critical role in regulating memory Th cells towards an anti-inflammatory phenotype. Given the lack of existing cholinergic agonist-based therapies for inflammatory diseases such as multiple sclerosis, our findings suggest the possibility of utilizing nAChR agonists as an approach for ameliorating the clinical symptoms.