In Vitro Therapeutic Effect of Epigallocatechin Gallate on Nicotine-Induced Impairment of Resistance to Legionella pneumophila Infection of Established MH-S Alveolar Macrophages

Epigallocatechin gallate (EGCg), a major form of tea catechins, has a variety of biological activities. Tobacco smoking, nicotine in particular, is one of the risk factors for respiratory infections. In the present study, a possible immunotherapeutic effect of EGCg on the nicotine-induced impairment...

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Bibliographic Details
Published in:The Journal of infectious diseases 2002-01, Vol.185 (2), p.229-236
Main Authors: Matsunaga, Kazuto, Klein, Thomas W., Friedman, Herman, Yamamoto, Yoshimasa
Format: Article
Language:English
Subjects:
Alveolar macrophages
Animals
Antibacterial agents
Antibiotics. Antiinfectious agents. Antiparasitic agents
Antibodies
Antimicrobials
Antiseptics
Bacteria
Biological and medical sciences
Catechin - analogs & derivatives
Catechin - pharmacology
Cell Line
Cytokines
Cytokines - biosynthesis
Epigallocatechin gallate
Gallates
Infections
Interferon-gamma - pharmacology
Legionella pneumophila
Legionella pneumophila - growth & development
Legionella pneumophila - immunology
Macrophages
Macrophages, Alveolar - drug effects
Macrophages, Alveolar - immunology
Macrophages, Alveolar - microbiology
Major Articles
Medical sciences
Mice
Nicotine - toxicity
Pharmacology. Drug treatments
Tea
Tobacco smoking
Tumor Necrosis Factor-alpha - pharmacology
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Summary:Epigallocatechin gallate (EGCg), a major form of tea catechins, has a variety of biological activities. Tobacco smoking, nicotine in particular, is one of the risk factors for respiratory infections. In the present study, a possible immunotherapeutic effect of EGCg on the nicotine-induced impairment of alveolar macrophages regarding antimicrobial activity, as well as immune function, was examined. The treatment of MH-S macrophages with nicotine significantly enhanced Legionella pneumophila replication in the cells and selectively down-regulated the production of interleukin (IL)–6, IL-12, and tumor necrosis factor (TNF)–α induced by infection but did not alter IL-10 production. The EGCg treatment of nicotine-suppressed macrophages reconstituted the resistance to the infection. Furthermore, EGCg diminished the nicotine-induced inhibition of cytokine production. Experiments with TNF-α treatment, neutralization of cytokines with antibodies, and analysis of interferon (IFN)–γ messenger RNA showed that the mechanism of the EGCg-induced recovery of anti–L. pneumophila activity impaired by nicotine may be due to the recovery of TNF-α and IFN-γ production by the macrophages
ISSN:0022-1899
1537-6613
DOI:10.1086/338449