Immunomodulation of dendritic cells differentiated in the presence of nicotine with lipopolysaccharide from P orphyromonas gingivalis

Tobacco smoking is a significant risk factor for periodontal diseases. Nicotine, one of the most studied constituents in cigarette smoke, is thought to modify immune responses. Dendritic cells ( DC s), which are key mediators between innate and adaptive immunity, stimulate naive T cells to differentiate to effector T ‐cell subsets that may be actively involved in the immunopathogenesis of periodontal diseases. In this study, we evaluated the effects of nicotine and lipopolysaccharide ( LPS ) from P orphyromonas gingivalis , alone and in combination, on the functions of human monocyte‐derived DC s to elucidate the mechanism of tissue destruction of smoking‐associated periodontal diseases. P . gingivalis LPS ‐stimulated DC s differentiated with nicotine ( N i DC s) induced lower T ‐cell proliferation and human leukocyte antigen ( HLA )‐ DR expression, but elevated expression of programmed cell death ligand 1. Additionally, N i DC s impaired interferon‐ γ production but maintained interleukin ( IL )‐5 and IL ‐10 production in co‐cultured T cells. Furthermore, N i DC s produced lower levels of proinflammatory cytokines compared with DC s differentiated in the absence of nicotine. Interestingly, N i DC s preferentially produced the T helper 2 ( T h2)‐type chemokines macrophage chemotactic protein‐1 and macrophage‐derived chemokine. These results suggest that the presence of nicotine during differentiation of DC s modulates the immunoregulatory functions of P. gingivalis LPS ‐stimulated DC s.