ArticleMolecular and cellular biochemistry2010
Inflammatory cytokines decrease the expression of nicotinic acetylcholine receptor during the cell maturation.
Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Bone health in asthma: a twofold effect of disease and pharmacotherapy.Frontiers in endocrinology · 2026Review
- The post-septic peripheral myeloid compartment reveals unexpected diversity in myeloid-derived suppressor cells.Frontiers in immunology · 2024Article
- Cigarette Smoking Contributes to Th1/Th2 Cell Dysfunction via the Cytokine Milieu in Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023Article
- Inflammation has synergistic effect with nicotine in periodontitis by up-regulating the expression of α7 nAChR via phosphorylated GSK-3β.Journal of cellular and molecular medicine · 2020Article
- The Cholinergic and Adrenergic Autocrine Signaling Pathway Mediates Immunomodulation in OysterFrontiers in immunology · 2018Article
- Article
- The α4 nicotinic receptor promotes CD4+ T-cell proliferation and a helper T-cell immune response.Molecular pharmacology · 2014Article
- Effect of the smell of Seirogan, a wood creosote, on dermal and intestinal mucosal immunity and allergic inflammation.Journal of clinical biochemistry and nutrition · 2012Article
- Cytokine-induced alterations of α7 nicotinic receptor in colonic CD4 T cells mediate dichotomous response to nicotine in murine models of Th1/Th17- versus Th2-mediated colitis.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is known that the nervous system significantly attenuates systemic inflammatory responses through the parasympathetic nervous system. Furthermore, it has been reported that the alpha 7 subunit of a nicotinic acetylcholine receptor is required for a cholinergic inhibition against cytokine synthesis in a macrophage. As antigen-presenting cells (APCs) play a central role in the generation of primary T cell responses and the maintenance of immunity, in this study, we investigated the expression level of nicotinic receptors of a p53-deficient APC cell line (JawsII) derived from a mouse bone marrow. We showed that stimulation of the JawsII cells with lipopolysaccharide (LPS) and tumor necrosis factor alpha (TNF-alpha) led increase of CD80 and CD86 expression while diminishment of the surface nicotinic receptor. On the other hand, stimulation of nicotinic receptor had no effect on these phenomena. Furthermore, we examined the ability of the cells to release cytokine when stimulated with both nicotine and LPS and showed that the stimulation with LPS augmented the secretion of IL-1a, IL-1b, IL-6, and TNF-alpha. These results suggested that nicotinic stimulation had no effect on the diminishment of alpha 7 nicotinic acetylcholine receptor on JawsII cells by LPS stimulation.
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