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In Vitro Therapeutic Effect of Epigallocatechin Gallate on Nicotine-Induced Impairment of Resistance to Legionella pneumophila Infection of Established MH-S Alveolar Macrophages
Kazuto Matsunaga, Thomas W. Klein, Herman Friedman and Yoshimasa Yamamoto
The Journal of Infectious Diseases
Vol. 185, No. 2 (Jan. 15, 2002), pp. 229-236
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/30137263
Page Count: 8
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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 nicotineinduced 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.
The Journal of Infectious Diseases © 2002 Oxford University Press