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Updated: May 24, 2026

Methods to Evaluate Cytotoxicity and Immunosuppression of Combustible Tobacco Product Preparations
Published on: January 10, 2015
Nicotine modulates the immunological function of dendritic cells through peroxisome proliferator-activated receptor-γ
Manabu Yanagita1, Ryohei Kobayashi, Yuko Kojima
1Department of Periodontology, Division of Oral Biology and Disease Control, Osaka University Graduate School of Dentistry, Yamadaoka 1-8, Suita, Osaka 565-0871, Japan.
Abstract:
We examined the effects of nicotine on differentiation and function of monocyte-derived human dendritic cells (DCs). NiDCs, which were the DCs differentiated in the presence of nicotine, showed lower levels of CD1a. Secretion of IL-12 and TNF-α by lipopolysaccharide (LPS)-stimulated NiDCs was significantly suppressed compared to monocyte-derived DCs grown without nicotine. NiDCs displayed a diminished capacity to induce allogeneic T cell proliferation with a reduced production of IFN-γ, and maintained/enhanced LPS-mediated expression of coinhibitory molecules. Interestingly, NiDCs enhanced the expression of nuclear receptor peroxisome proliferator-activated receptors γ (PPAR γ), which has immunomodulatory properties. Expression of PPAR γ and PPAR γ-target genes was significantly inhibited by pretreatment with d-tubocurarine, antagonist of non-selective nicotinic acetylcholine receptors (nAChR). In addition, reduction of Th1 responses was inhibited after blocking nAChR-mediated signal. These data suggest the effect of nicotine on altering DC immunogenicity by impeding Th1 immunity is partially mediated by upregulation of PPAR γ.
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