In a Science Immunology Review from earlier this year, researchers discuss how interactions between the nervous and immune systems could impact neurological disorders and allergy-related behaviors like food avoidance.
The nervous and type 2 immune systems regulate each other via cytokines and neurotransmitters, suggesting previously unidentified therapeutic avenues.
Liu et al. report chromosome-level genomes of 11 species across 10 Polygonaceae genera (including four previously published genomes), which encompass diverse habitats. Integrating genomic and transcriptomic analyses, this study provides insights into the evolutionary adaptation strategies of Polygonaceae to thrive in various habitats.
Vascular aging and genetic risk jointly shape coronary artery disease susceptibility across races and sexes.
BackgroundEstimated pulse wave velocity (ePWV), a noninvasive marker of arterial stiffness, reflects vascular aging and has been associated with increased coronary artery disease (CAD) risk. However, the interplay between ePWV and genetic factors, including polygenic risk score (PRS) and apolipoprotein E genotypes, in determining CAD susceptibility remains unclear.
This review examines some of the monogenic disorders that can masquerade as neuroinflammatory phenotypes.
A recent explosion in genomic testing has led to the identification of several genetic disorders that mimic CNS-specific autoimmune disorders. Such monogenic disorders, although rare, represent a diagnostic challenge because of their diverse phenotypes and overlapping features. Early recognition of these disorders is crucial not only to prevent overtreatment with immunotherapy but also to ensure that targeted treatments are available for many of these disorders. This review explores some of the monogenic disorders that can masquerade as neuroinflammatory phenotypes. These clinical vignettes are stratified according to neuroanatomical localization along the neuroaxis: supratentorial white matter, gray matter, brainstem, and spinal cord involvement.
Great paper highlighting key challenges for genetically engineered bacterial therapies in the human gut. It is respectable that this paper was published in Science despite some “negative” results. Although the genetically engineered bacteria were all supposed to die after removal of porphyrin from the diet, they sometimes rebounded. Even with an improved porphyrin pathway which was supposed to resist mutational rebound, the bacteria still persisted in a mouse model, apparently by mysterious non-mutational means. Maybe the microbiomes of the mice somehow supplied porphyrin to the bacteria without the knowledge of the researchers. Furthermore, therapeutic application of the genetically engineered bacteria in humans only resulted in modest (and not statistically significant) decreases in urine oxalate. This was partly due to horizontal gene transfer which replaced the engineered oxalate degradation pathway and partly due to the general fitness burden of the engineered oxalate degradation pathway. As such, this paper revealed a lot of important obstacles which will need to be worked on for bacterial therapies to move forward in the future.
(https://www.science.org/doi/10.1126/science.adu8000)
Precision microbiome programming for therapeutic applications is limited by challenges in achieving reproducible colonic colonization. Previously, we created an exclusive niche that we used to engraft engineered bacteria into diverse microbiota in mice by using a porphyran prebiotic. Building on this approach, we have now engineered conditional attenuation into a porphyran-utilizing strain of Phocaeicola vulgatus by replacing native essential gene regulation with a porphyran-inducible promoter to allow reversible engraftment. Engineering a five-gene oxalate degradation pathway into the reversibly engrafting strain resulted in a therapeutic candidate that reduced hyperoxaluria, a cause of kidney stones, in preclinical models.
Think of cells as the biological answer to battery-powered electronics. Mitochondria are the batteries that supply them with enough energy to keep going. Unfortunately, just like the two standard AAs in your remote control, they eventually run out of power and die—but (much like actual batteries) they can also be recharged and replaced.
Breakdown of mitochondria causes cells to glitch. Wear and tear can happen with age, usually from years of exposure to free radicals that cause oxidative stress and inflammation, but can also be caused by injury from degenerative diseases or mitochondrial toxicity from certain drugs and other harmful substances. When there is damage to the cell, mitochondria begin to lose their capacity to generate energy. Losing mitochondria is detrimental to cell function. This is why biomedical engineer Akhilesh Gaharwar and his research team at Texas A&M University have come up with a way to regenerate them.