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Clinical and Diagnostic Laboratory Immunology, July 2002, p. 864-871, Vol. 9, No. 4
1071-412X/02/$04.00+0     DOI: 10.1128/CDLI.9.4.864-871.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Epigallocatechin Gallate, a Potential Immunomodulatory Agent of Tea Components, Diminishes Cigarette Smoke Condensate-Induced Suppression of Anti-Legionella pneumophila Activity and Cytokine Responses of Alveolar Macrophages

Kazuto Matsunaga, Thomas W. Klein, Herman Friedman, and Yoshimasa Yamamoto*

Department of Medical Microbiology and Immunology, University of South Florida College of Medicine, Tampa, Florida

Received 17 January 2002/ Returned for modification 11 March 2002/ Accepted 3 April 2002

Even though cigarette smoking has been shown to suppress immune responses in the lungs, little is known about the effect of cigarette smoke components on respiratory infections. In the present study, the effects of cigarette smoke condensate (CSC) on bacterial replication in alveolar macrophages and the immune responses of macrophages to infection were examined. Furthermore, a possible immunotherapeutic effect of epigallocatechin gallate (EGCg), a major form of tea catechins, on the CSC-induced suppression of antimicrobial activity and immune responses of alveolar macrophages was also determined. The treatment of murine alveolar macrophage cell line (MH-S) cells with CSC significantly enhanced the replication of Legionella pneumophila in macrophages and selectively down-regulated the production of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-{alpha}) induced by bacterial infection. The treatment of macrophages with EGCg not only overcame the CSC-induced suppression of antimicrobial activity but also strengthened the resistance of macrophages to infection. EGCg also markedly up-regulated the CSC-suppressed IL-6 and TNF-{alpha} production by macrophages in response to infection. The results of exogenous TNF-{alpha} treatment and neutralization treatment with anti-TNF-{alpha} and anti-gamma-interferon (IFN-{gamma}) antibodies and the determination of IFN-{gamma} mRNA levels indicate that CSC-suppressed macrophages can be activated by EGCg to inhibit L. pneumophila growth by up-regulation of TNF-{alpha} and IFN-{gamma} production. Thus, this study revealed that CSC selectively alters the immune responses of macrophages to L. pneumophila infection and leads to an enhancement of bacterial replication in macrophages. In addition, the tea catechin EGCg can diminish such suppressive effects of CSC on alveolar macrophages.

* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, University of South Florida College of Medicine, 12901 Bruce B. Downs Blvd., Tampa, FL 33612-4799. Phone: (813) 974-2332. Fax: (813) 974-4151. E-mail: yyamamot{at}hsc.usf.edu.

Clinical and Diagnostic Laboratory Immunology, July 2002, p. 864-871, Vol. 9, No. 4
1071-412X/02/$04.00+0     DOI: 10.1128/CDLI.9.4.864-871.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Rogers, J., Perkins, I., van Olphen, A., Burdash, N., Klein, T. W., Friedman, H. (2005). Epigallocatechin Gallate Modulates Cytokine Production by Bone Marrow-Derived Dendritic Cells Stimulated with Lipopolysaccharide or Muramyldipeptide, or Infected with Legionella pneumophila. Exp. Biol. Med. 230: 645-651 [Abstract] [Full Text]  


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