Green tea catechins and peroxisome proliferator-activated receptor (PPAR) agonists have been shown to reduce inflammation associated with collagen-induced arthritis in mice ( ; ) and to inhibit other markers of inflammation ( ; ; ; ). We are investigating the mechanisms by which catechins and PPAR agonists interfere with the signalling pathways of the pro-inflammatory cytokines, IL-1 and TNF. Epigallocatechin gallate (EGCG), epicatechin gallate (ECG), epigallocatechin (EGC), epicatechin (EC) and fenofibrate were from Sigma Aldrich, Poole, UK. Rosiglitazone was from Cayman Chemical, Ann Arbor, MI, USA. Cytokines and IL-8 ELISA were from NIBSC. IL-6 ELISA from eBiosciences (San Diego, CA, USA). Cells used were primary fibroblasts from inflamed periodontal tissue or osteoarthritic chondrocytes from discarded tissue following surgery. We show the significant suppression of cytokine-induced IL-6 and IL-8 release by EGCG, which is dose- and cell-type dependent. The other three catechins have a much lesser effect. Preliminary results show that PPAR agonists also interfere with TNF-induced IL-8 production. Green tea has a long history of human consumption, and epidemiological studies have shown that it can reduce inflammatory diseases ( ). Our results confirm that EGCG has the strongest anti-inflammatory effect, compared with the other three catechins. They also indicate that the mechanism of action of EGCG is cell-type dependent. This could be because the compound targets components of pro-inflammatory signalling pathways whose expression is restricted to certain differentiated cell types. Alternatively, the different sensitivities of cells to EGCG could reflect differences in their ability to metabolize the compound. Further experiments are needed to discriminate between these hypotheses. [ABSTRACT FROM AUTHOR]