Welcome to this week’s Research Roundup. These Friday posts aim to inform our readers about the many stories that relate to animal research each week. Do you have an animal research story we should include in next week’s Research Roundup? You can send it to us via our Facebook page or through the contact form on the website.
- Pathogenic gut bacteria can translocate to organs and trigger autoimmune diseases. Researchers at Yale have identified that the gut bacteria, Enterococcus gallinarum can break through cell junctions of the intestinal wall and infect lymph nodes and the liver, in both mice and humans. Once the bacteria enters these organs, the infection then triggers autoimmune disease (e.g. systemic lupus erythematosus) in hosts that are genetically predisposed to certain forms of autoimmune disease. Thankfully, the triggering of autoimmune disease via this pathway can be prevented by a vaccine targeting E. gallinarum. This study was conducted in mice genetically predisposed to autoimmune disease and using tissue from liver biopsies of human patients with autoimmune disease. Future research will investigate other autoimmune disease and other organs that may be infected. Published in Science.
- Social Deficits in Mice Reversed by Anti-cancer Drug. A study by researchers at the University of Buffalo were able to reverse social deficits in mice that were not able to express a gene called, Shank 3 — a key risk factor for autism spectrum disorders (ASD). The team found that a very low dose of romidepsin was able to restore gene expression and function using an epigenetic mechanism. There are currently no treatments for social difficulties in patients diagnosed with ASD. Dr. Zhen Yan, a researcher leading the study, says, “Autism involves the loss of so many genes. To rescue the social deficits, a compound has to affect a number of genes that are involved in neuronal communication.” Zan and her colleagues will continue to pursue research to find and develop new therapies for autism. Published in Nature Neuroscience.
- Mice lacking a key brain protein are resistant to Multiple Sclerosis. By examining donated brain tissue from human patients with Multiple Sclerosis (MS), scientists identified that the tissue had extremely high levels of a protein named calnexin. They then used a mouse model of human MS (experimental autoimmune encephalomyelitis) to compare mice with and without calnexin, and found that the mice without calnexin were completely resistant to MS. The calnexin deficient mice also had reduced trafficking of T-cell lymphocytes across the blood-brain barrier, however it remains unclear whether this reduction of trafficking prevents MS. Future research will study what specific roles calnexin plays in relation to MS, and if it is a potential target for MS treatment. Published in JCI Insight.
- Link between body temperature and obesity found. A new study has found that mice housed from a young age in a cold environment consumed more food in the day (when they are usually asleep) and that this led to obesity and high blood sugar in adulthood. To understand this association, these researchers compared TRPM8 deficient mice lacking cold sensing ion channels to control mice with TRPM8 and found that compared to control mice, TRPM8 mice lost body heat more quickly. These researchers stated, “This research reveals a previously unrecognized link between thermal sensing systems, thermoregulation and food intake, which may open up new avenues for preventing and treating obesity.” Published in the Journal of Neuroscience.
- Clearing of protein waste in neural stem cells improves their activity. A new study using mice has found that neural stem cells, which make new neurons, become less efficient in the disposal of “protein waste” with age. Such “protein waste” are byproducts of metabolic and other cellular processes and are stored in lysosomes. This discovery is important because a similar process is associated with the onset of neurodegenerative diseases, such as Alzheimer’s. Anne Brunet, the lead researched on this work stated, “….if we remove these aggregates [waste], we can improve the cells’ ability to activate and make new neurons. So if one were able to restore this protein-processing function, it could be very important to bringing older, more dormant neural stem cells ‘back to life.” Published in Science.
Speaking of Research 