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Archive - Apr 3, 2017

First-Ever Global Symposium on Use of Maple Syrup to Reduce Inflammation Convened at ACS Annual Meeting in San Francisco, shared the results of their research that expands the science of maple's potential impact on several areas affected by chronic inflammation. These include metabolic syndrome, brain health, and liver disease, as well as maple's emerging link to a healthy gut microbiome. The global symposium was organized by Dr. Navindra Seeram, who currently serves as chairman of the Division of Agricultural and Food Chemistry of the ACS, and has extensive experience examining the impact of phytonutrients in foods such as berries and pomegranates. In collaboration with the Federation of Quebec Maple Syrup Producers, Dr. Seeram has been studying the unique properties of maple in his laboratory at the University of Rhode Island since 2009. The results of his research stimulated the interest of the global scientific community, which has uncovered additional health benefits of pure maple products. A new University of Rhode Island study highlighted at the symposium revealed the presence of inulin, a type of carbohydrate recently discovered for the first time in maple syrup. Inulin is a complex carbohydrate (natural dietary fiber) that acts as a prebiotic and works to encourage the growth of "good" or beneficial bacteria in the gut.

Negative Regulator (BATF2) Halts Extreme Immune Response to Trypanosome Parasite, Averting Multi-Organ Damage

Cytokines are proteins secreted by several types of immune cells in response to infection, inflammation, or injury. Interleukin-17 (IL-17) is one such cytokine that causes inflammation, by controlling the production of other cytokines and mobilizing a type of white blood cell (neutrophil) that fights infections. During some parasitic infections, host protection is achieved by an IL-17 response, but too much IL-17 causes chronic tissue damage. This response is therefore tightly regulated by other cytokines, but the precise mechanisms were previously unclear. Now, Japanese research coordinated by Osaka University has unraveled the complex network of cytokine control that prevents multi-organ damage during infection by the protozoan parasite that causes Chagas disease. Trypanosoma cruzi is an intracellular parasite that infects and destroys heart and digestive muscle, causing Chagas disease, which affects 6–7 million people worldwide, mainly in endemic areas of Central and South America. Previous work showed that T. cruzi infection in mice led to production of the cytokine IL-23 by host immune cells. This promoted the generation of CD4+ T cells that produce IL-17. Researchers built on these findings by focusing on the protein BATF2, which they found in an earlier study to be switched on by cytokine signaling in innate immune cells derived from bone marrow during T. cruzi infection. To study the role of BATF2 in this process, the team generated mice lacking the gene encoding this protein. These Batf2 knockout mice produced much more IL-17 in response to the parasite than did control mice. They also produced more IL-23, suggesting that BATF2 normally suppresses expression of the Il23a gene. However, it was not shown to be required for the killing of T. cruzi.

Identification of Protein Crucial to Development of Lymphatic System

Lymphatic vessels form a circulatory system that plays an important role in controlling the amount of fluid in tissues, and in allowing the immune system to identify and target threats. When the lymphatic system malfunctions, fluid accumulates in tissues, producing a condition known as edema. This can be fatal; for example, lung edema can cause respiratory arrest. The molecular mechanisms underlying lymphatic system development are have not been fully understood, with particular uncertainty surrounding the later stages of development, in which the primitive system is remodeled to produce a mature, functional lymphatic vasculature. Osaka University-led Japanese researchers have now identified a protein that is crucial for this lymphatic system remodeling and maturation. “Polydom” is a large protein known to interact with the receptor integrin α9β1, and is found in the extracellular matrix surrounding and supporting cells. The research team found that mice genetically engineered to lack Polydom died immediately after birth because they had lung edema, which prevented them from breathing. Further investigation revealed that a primitive lymphatic system developed in these mice, but branching vessels failed to grow and the mature vasculature did not form, leading to fluid accumulation in tissues. Genetically engineered zebrafish lacking Polydom also exhibited a failure of lymph vessel development. The team then explored the location of Polydom in mice, and found that the protein associates with lymphatic vessels throughout embryonic development. “However, we were interested to find that Polydom was not actually produced by the endothelial cells that line the vessels, but by the surrounding mesenchymal cells,” corresponding author Kiyotoshi Sekiguchi, Ph.D., says.