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

• 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
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/cei.13388

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.