Chronic inflammation, or prolonged activation of the immune system, is a major hallmark of many age-related diseases, including heart disease, COVID-19, and neuroinflammation. Typically, the central nervous system (CNS) is protected by a barrier that forms through the coordinated efforts of blood vessel endothelial cells, astrocytes, and pericytes. However, as that barrier breaks down because of chronic inflammation, neuroinflammation can occur. Blood vessel endothelial cells express membrane association proteins, including the cell adhesion molecule Basigin and the transporter protein Monocarboxylate transporter 1 (MCT1). A related MCT protein named MCT4 often increases in expression during chronic inflammation. Basigin associates with both MCT1 and MCT4 in the neural retina. Therefore, the expression of these three proteins (Basigin, MCT1, and MCT4) was investigated in response to chronic inflammation in aged mouse brains. It was hypothesized that the expression of Basigin and MCT1 would decrease and that of MCT4 would increase in response to chronic inflammation. The brains of 6-month-old mice were harvested and exposed to lipopolysaccharide (LPS; 10 g/mL), a known activator of inflammation, or saline control for 3, 6, 12, or 24 hours. The brain proteins were isolated and subjected to ELISA analyses designed to measure each target protein. It was determined that no significant difference in Basigin, MCT1, or MCT4 expression was observed for any treatment time. The hypothesis was not supported, and the data suggest that Basigin, MCT1, and MCT4 may not contribute to the development of neuroinflammatory diseases.
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Falont and Alicia, your project is interesting, well-designed and beautifully executed. The poster is so clearly organized and sharply written that your work is accessible to non-specialists (even historians, like me!). Wishing you all the best in your research efforts going forward.