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Archive - Apr 21, 2015

Bitter Taste Sensitivity Regulated by Immune System Protein TNF; Finding May Help Explain Reduced Food Intake During Illness

New research from the Monell Chemical Senses Center in Philadelphia reveals that tumor necrosis factor (TNF), an immune system regulatory protein that promotes inflammation, also helps regulate sensitivity to bitter taste. The finding may provide a mechanism to explain the taste system abnormalities and decreased food intake that can be associated with infections, autoimmune disorders, and chronic inflammatory diseases. In addition to its role in mediating inflammation, TNF has been implicated in the progression of varied diseases ranging from Alzheimer's disease to cancer. "Reduced food intake and associated malnutrition is a significant concern that affects the long-term prognosis of many people who are very ill," said senior author Hong Wang, Ph.D., a molecular biologist at Monell. "Our findings reveal that bitter taste is regulated by the immune system. Specifically, TNF may make sick people more sensitive to bitterness so that foods taste more bitter and less appetizing." Dr. Wang's research focuses on interactions between the taste and immune systems, with the goal of identifying how taste cell function changes in disease states. As part of this effort, previous research from her laboratory had demonstrated that taste buds contain several immune system proteins, including TNF. Because TNF is known to suppress food intake, the current study asked whether TNF affects food intake via the taste system. The findings were published online on April 21, 2015 in the journal Brain, Behavior, and Immunity. To examine whether TNF helps regulate taste responses, the researchers first compared taste responses of normal mice to those of mice engineered to be lacking the gene for TNF (TNF knockout mice).

Genetic Variance in VNN-1 Network Underlies Poor Response to Common Corticosteroid Asthma Medications; Finding May Lay Groundwork for Helping Difficult-to-Treat Children

Researchers have identified a biological basis for asthmatic children who do not respond well to corticosteroid treatment, currently the most effective treatment for chronic asthma and acute asthma attack. Conducted at Cincinnati Children's Hospital Medical Center, the study also identifies a genetic pathway that could open the possibility of new therapies for difficult-to-treat patients. The findings are reported online on April 21, 2015 in The Journal of Allergy and Clinical Immunology, published by the American Academy of Allergy Asthma and Immunology. The article is titled “Vanin-1 Expression and Methylation Discriminate Pediatric Asthma Corticosteroid Treatment Response.” The researchers performed genome-wide analysis of nasal epithelial cells collected from children experiencing acute asthma exacerbation. They compared genetic expression and medical responses in children who responded well to corticosteroids therapy to those who did not. "Genome-wide analysis allowed us to identify a gene, VNN-1, whose expression discriminated between good and poor responders to systemic corticosteroid treatment," said Gurjit Khurana Hershey, M.D., Ph.D., senior author and director of Asthma Research at Cincinnati Children's. "This may serve as a clinically useful biomarker to identify a subset of difficult-to-treat asthmatic children, and targeting the VNN-1 pathway may be useful as a therapeutic strategy." Asthma affects close to 26 million people in the United States, 7 million of them children. Although people suffering from asthma share similar clinical symptoms, it is triggered by multiple genetic and environmental factors.