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I am an immunologist by training, have done my graduate work at Sloan Kettering Institute for Cancer Research and worked as post-doctoral fellow with Dr. Max Cooper. In the early days, I worked on T cell subsets, in particular, the T helper-1 and T helper-2 in Leishmania infection. Their balance determines whether the host or this intra-macrophage parasite takes control of the immune defense system. Induction of cell-mediated immunity promotes inflammation and production of nitric oxide for eliminating the parasites. Conversely, the disease will manifest if the parasite potentiates humoral immunity. Leishmaniasis is endemic in India. I found that the anti-inflammatory compound curcumin, active ingredient in the Indian spice turmeric, would increase the infectivity of Leishmania. These findings excited my interest in dietary anti-inflammatory small molecules, their mechanisms of action and their potential as therapeutics. I learned that certain dietary anti-inflammatory agents, parasites and endogenous fatty acids, such as 15d-PGJ2, lipoxins and dietary -3-fatty acid, resolve inflammation by inducing the transcription factor, PPAR, which in turn inhibits activation of NFB and iNOS. More recently, a novel dogma that inflammation does not resolve by dissipation but by active pathways that involve bioactive lipids has emerged. Our laboratory was the first to show that this resolution mechanism is also crucial for controlling chronic inflammation.
Counterbalance in Inflammation, Nitric Oxide Inhibitor and Leishmania Pathogenesis, Nitric Oxide Inhibitor and Leishmania, Pathogenesis, Epigallocatechin-3-gallate for Enhancement of Cisplatin Therapy, Food Processing and Health: Modulation of gene expression of inflammation mediators by processed foods, Modulation of Gene Expression of Inflammation Mediators by Food.
Marion M Chan and Dunne Fong
Editorial: J Autacoids 2013, 3:e122
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