Syndicate content

Archive - Nov 27, 2018

Date

Sugars & Microbiome in Mother's Milk Influence Neonatal Rotavirus Infection

Using a multidisciplinary approach, an international team of researchers from several institutions, including Baylor College of Medicine, reveals that complex interactions between sugars and the microbiome in human milk influence neonatal rotavirus infection. Reported online on November 27, 2018 in the journal Nature Communications, this study provides new understanding of rotavirus infections in newborns and identifies maternal components that could improve the performance of live, attenuated rotavirus vaccines. The open-access article is titled “Human Milk Oligosaccharides, Milk Microbiome and Infant Gut Microbiome Modulate Neonatal Rotavirus Infection.” "Rotavirus infection causes diarrhea and vomiting primarily in children younger than 5, with the exception of babies younger than 28 days of age, who usually have no symptoms. However, in some places, infections in newborns are associated with severe gastrointestinal problems. What factors mediate differences between newborns with and without symptoms are not clearly understood," said first and corresponding author Dr. Sasirekha Ramani (photo), Assistant Professor of Molecular Virology and Microbiology at Baylor College of Medicine. "We began our investigation years ago by determining that a particular strain of rotavirus was associated with both asymptomatic infections and clinical symptoms in newborns." Dr. Ramani and her colleagues first looked for answers from the perspective of the virus. They investigated whether factors such as the amount of virus in newborns or the genome of the virus could be linked to the presence of symptoms in newborns, but did not find any connection between those factors. The researchers then posed the question from the perspective of the newborn.

International Society for Extracellular Vesicles (ISEV) Releases 2018 Update of 2014 Guidelines for Studies of Extracellular Vesicles

On November 23, 2018, The International Society for Extracellular Vesicles (ISEV) published online an open-access position paper titled “Minimal Information for Studies of Extracellular Vesicles 2018 (MISEV2018); A Position Statement of the International Society for Extracellular Vesicles and Update of the MISEV2014 Guidelines.” The article is scheduled for hard-copy publication in Volume 8, Issue 1, of the 2019 Journal of Extracellular Vesicles. In the article abstract, the authors note the following: “The last decade has seen a sharp increase in the number of scientific publications describing physiological and pathological functions of extracellular vesicles (EVs), a collective term covering various subtypes of cell-released, membranous structures, called exosomes, microvesicles, microparticles, ectosomes, oncosomes, apoptotic bodies, and many other names. However, specific issues arise when working with these entities, whose size and amount often make them difficult to obtain as relatively pure preparations, and to characterize properly. The ISEV proposed Minimal Information for Studies of Extracellular Vesicles (“MISEV”) guidelines for the field in 2014. We now update these “MISEV2014” guidelines based on evolution of the collective knowledge in the last four years. An important point to consider is that ascribing a specific function to EVs in general, or to subtypes of EVs, requires reporting of specific information beyond mere description of function in a crude, potentially contaminated, and heterogeneous preparation.

Researching Rare Genetic Disease, Scientists Uncover Key Immune Regulator

Scientists at Scripps Research in California have found an important immune system-regulating protein that in principle could be targeted to treat cancers and chronic viral infections. In a study published online on November 12, 2018 in Nature Chemical Biology, the scientists set out to determine the function of a protein, ABHD12 (abhydrolase domain containing protein 12), whose absence causes a rare genetic disease featuring a host of brain and nerve problems. The article is titled “Selective Blockade of the Lyso-PS Lipase ABHD12 Stimulates Immune Responses in Vivo.” The researchers found that ABHD12 normally acts as a powerful "brake" on the immune system to keep it from becoming harmfully overactive. Mice engineered without the protein have signs of elevated inflammation, and their immune systems are more likely to overreact to a viral infection. The discovery suggests that the absence of ABHD12 in people with mutant versions of its gene may cause neurological disease at least in part via excessive immune activity. It also indicates that ABHD12 may be a useful target for drugs that boost the immune system--for example against cancers and viruses that normally persist by shutting down people's immune defenses. "This is a good example of how the study of a rare genetic disease can reveal a pathway that plays a key role in human biology," says study co-senior author Benjamin Cravatt, PhD, Professor and Chair of the Department of Chemical Physiology at Scripps Research. The rare disease in this case is a mix of progressive brain, peripheral nerve, and eye problems that scientists have given the acronym PHARC (polyneuropathy, hearing loss, ataxia, retinitis pigmentosa, and cataract). Since 2010, researchers have known that PHARC is caused by gene mutations that prevent ABHD12 from being made.