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Green Tea Protects Rats Against Autoimmune Arthritis by Modulating Disease-Related Immune Events - Source: The Journal of Nutrition, Nov 2008

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By Hong Ro Kim, Kamal D Moudgil, et al. • www.ProHealth.com • November 25, 2008


Green tea, a product of the dried leaves of Camellia sinensis, is the most widely consumed beverage in the world. The polyphenolic compounds from green tea (PGT) possess antiinflammatory properties.

We investigated whether PGT can afford protection against autoimmune arthritis and also examined the immunological basis of this effect using the rat adjuvant arthritis (AA) model of human rheumatoid arthritis (RA). AA can be induced in Lewis rats (RT.1) by immunization with heat-killed Mycobacterium tuberculosis H37Ra (Mtb), and arthritic rats raise a T cell response to the mycobacterial heat-shock protein 65 (Bhsp65).

Rats consumed green tea (2–12 g/L) in drinking water for 1–3 weeks and then were injected with Mtb to induce disease. Thereafter, they were observed regularly and graded for signs of arthritis. Subgroups of these rats were killed at defined time points and their draining lymph node cells were harvested and tested for T cell proliferative and cytokine responses. Furthermore, the sera collected from these rats were tested for anti-Bhsp65 antibodies.

Feeding 8 g/L PGT to Lewis rats for 9 d significantly reduced the severity of arthritis compared with the water-fed controls. Interestingly, PGT-fed rats had a lower concentration of the proinflammatory cytokine interleukin (IL)-17 but a greater concentration of the immunoregulatory cytokine IL-10 than controls. PGT feeding also suppressed the anti-Bhsp65 antibody response.

Thus, green tea induced changes in arthritis-related immune responses. We suggest further systematic exploration of dietary supplementation with PGT as an adjunct nutritional strategy for the management of RA.

Source: The Journal of Nutrition, Nov 2008. 138:2111-2116. PMID:18936206, by Kim HR, Rajaiah R, Wu Q, Satpute SR, Tan MT, Simon JE, Berman BM, Moudgil KD. Department of Microbiology and Immunology, Division of Rheumatology, Department of Medicine, Department of Epidemiology and Preventive Medicine, University of Maryland Greenebaum Cancer Center; Center for Integrative Medicine, University of Maryland School of Medicine, Baltimore, Maryland; Department of Plant Biology and Pathology, School of Environmental and Biological Sciences, Rutgers University, New Brunswick, New Jersey, USA. [E-mail: kmoud001@umaryland.edu]





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