Nicotine modulates molecules of the innate immune response in epithelial cells and macrophages during infection with M. tuberculosis

Summary Smoking increases susceptibility to becoming infected with and developing tuberculosis. Among the components of cigarette smoke, nicotine has been identified as the main immunomodulatory molecule; however, its effect on the innate immune system is unknown. In the present study, the effect of...

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Published in:	Clinical and experimental immunology Vol. 199; no. 2; pp. 230 - 243
Main Authors:	Valdez‐Miramontes, C. E., Trejo Martínez, L. A., Torres‐Juárez, F., Rodríguez Carlos, A., Marin‐Luévano, S. P., Haro‐Acosta, J. P., Enciso‐Moreno, J. A., Rivas‐Santiago, B.
Format:	Journal Article
Language:	English
Published:	England Oxford University Press 01-02-2020 John Wiley and Sons Inc
Subjects:	A549 Cells Alveolar Epithelial Cells - immunology Alveolar Epithelial Cells - microbiology Alveolar Epithelial Cells - pathology Chemokines Cigarette smoke CXCL10 protein Cytokines Cytokines - immunology Epithelial cells Gene Expression Regulation - drug effects Gene Expression Regulation - immunology Humans Immune response Immune system Immunity, Innate - drug effects Immunomodulation Infections Innate immunity Ligands Macrophages Macrophages - immunology Macrophages - microbiology Macrophages - pathology Monocyte chemoattractant protein 1 Monocytes Mycobacterium tuberculosis Mycobacterium tuberculosis - immunology Nicotine Nicotine - pharmacology Nod2 Signaling Adaptor Protein - immunology Original Pneumocytes Toll-Like Receptor 2 - immunology Toll-Like Receptor 4 - immunology Tuberculosis Tuberculosis, Pulmonary - immunology Tuberculosis, Pulmonary - pathology Tumor necrosis factor Tumor necrosis factor-TNF epithelial cells macrophages nicotine Mycobacterium tuberculosis cigarette smoke
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Summary:	Summary Smoking increases susceptibility to becoming infected with and developing tuberculosis. Among the components of cigarette smoke, nicotine has been identified as the main immunomodulatory molecule; however, its effect on the innate immune system is unknown. In the present study, the effect of nicotine on molecules of the innate immune system was evaluated. Lung epithelial cells and macrophages were infected with Mycobacterium tuberculosis (Mtb) and/or treated with nicotine. The results show that nicotine alone decreases the expression of the Toll‐like receptors (TLR)‐2, TLR‐4 and NOD‐2 in all three cell types, as well as the production of the SP‐D surfactant protein in type II pneumocytes. Moreover, it was observed that nicotine decreases the production of interleukin (IL)‐6 and C‐C chemokine ligand (CCL)5 during Mtb infection in epithelial cells (EpCs), whereas in macrophages derived from human monocytes (MDMs) there is a decrease in IL‐8, IL‐6, tumor necrosis factor (TNF)‐α, IL‐10, CCL2, C‐X‐C chemokine ligand (CXCL)9 and CXCL10 only during infection with Mtb. Although modulation of the expression of cytokines and chemokines appears to be partially mediated by the nicotinic acetylcholine receptor α7, blocking this receptor found no effect on the expression of receptors and SP‐D. In summary, it was found that nicotine modulates the expression of innate immunity molecules necessary for the defense against tuberculosis. Nicotine modulates the expression of innate immunity molecules necessary for the defense against tuberculosis.
ISSN:	0009-9104 1365-2249
DOI:	10.1111/cei.13388