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Rivista di Medicina Interna
Indexed/Abstracted in: Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,236
Minerva Medica 2016 December;107(6):363-9
Epigallocatechin gallate suppresses Chlamydia pneumoniae mediated IgE responses in peripheral blood mononuclear cells: a pilot study
Tamar A. SMITH-NOROWITZ 1, Kobkul CHOTIKANATIS 1, Elizabeth TAM 1, Yitzchok M. NOROWITZ 1, Rauno JOKS 2, Helen G. DURKIN 3, Margaret R. HAMMERSCHLAG 1, Stephan KOHLHOFF 1 ✉
1 Division of Infectious Diseases, Department of Pediatrics, State University of New York Downstate Medical Center, Brooklyn, New York, NY, USA; 2 Department of Medicine, State University of New York Downstate Medical Center, Brooklyn, New York, NY, USA; 3 Department of Pathology, State University of New York Downstate Medical Center, Brooklyn, New York, NY, USA
BACKGROUND: Chlamydia pneumoniae (C. pneumoniae) causes respiratory infection in children and adults and is associated with asthma and induction of immunoglobulin E (IgE) responses. Previous studies in our laboratory reported that green tea extract (GTE) and its catechin, epigallocatechin gallate (EGCG) have immunoregulatory effects on IgE responses. Whereas tea polyphenols have in vitro inhibitory effects on the proliferation of C. pneumoniae, the in vitro effects of EGCG on C. pneumoniae- mediated IgE responses haven’t been studied. We sought to clarify the in vitro effect of EGCG on C. pneumoniae mediated IgE responses by peripheral blood mononuclear cells (PBMC) in asthma.
METHODS: PBMC from subjects with asthma and non-asthmatic controls were incubated with C. pneumoniae and cultured for 10 days ±EGCG (0.5, 5.0, 50 ng/mL). IgE levels in supernatants were determined (ELISA).
RESULTS: Elevated IgE levels were detected in supernatants of PBMC from an asthma patient (2.6 ng/mL), whereas IgE levels of PBMC from non-asthmatics were low (<2.0 ng/mL) at baseline. When EGCG (0.5-50 ng/mL) was added to PBMC from the asthma patient, IgE production was suppressed in a dose-dependent manner (10-30%), compared with no EGCG. When PBMC from the asthma patient were incubated with C. pneumoniae, IgE production was suppressed (70%); when PBMC from non-asthmatics were incubated with C. pneumoniae, IgE levels remained undetectable (<2.0 ng/mL). When EGCG (0.5-50 ng/mL) was added to PBMC from the asthma patient, C. pneumoniae-induced IgE production was suppressed moderately (35-48%).
CONCLUSIONS: EGCG suppressed C. pneumoniae- mediated IgE responses in PBMC from a patient with asthma.