Volvulus of Midgut

CHICAGO--( BUSINESS WIRE )--ClostraBio, a biotech company focused on developing novel therapeutic solutions for diseases of the gut, is excited to announce a major breakthrough in targeted metabolite delivery to transform intestinal health. This first-in-class, oral, targeted metabolite delivery platform enables butyrate to achieve its maximum therapeutic potential with an initial focus on helping patients who struggle with gastrointestinal issues like mild to moderate ulcerative colitis and food allergies. This groundbreaking development of an oral nanoparticle platform has the potential to revolutionize the treatment of gut-related diseases and marks a significant step forward in the field of gastrointestinal health ( source: University of Chicago release ). Until now, oral delivery of sodium butyrate had been a challenge due to not only its foul odor and taste, but because it metabolized too rapidly to maintain a pharmacologic effect in the small intestine and colon, the areas of the gut where it has a therapeutic effect. “We have created an innovative way to use polymeric nanoparticles to address delivery of butyrate to the lower gut to help patients with mild to moderate ulcerative colitis and food allergy,” said ClostraBio founder, Dr. Cathryn Nagler. “This new therapeutic has the potential to help patients by restoring normal barrier protective function over time.” In a recent study published in the journal Nature Biomedical Engineering , ClostraBio’s founders, Dr. Cathryn Nagler, Dr. Jeffrey Hubbell, and co-authors demonstrated that the use of polymeric nanoscale micelles can effectively restore intestinal homeostasis in mouse models of colitis and peanut allergy. Butyrate was selected for its ability to alleviate inflammatory diseases of the gut through multiple mechanisms. ClostraBio co-founder, Dr. Jeffrey Hubbell said, “In today’s options for gastrointestinal issues, targeted drug delivery has become key in pharmaceutical product development. Innovative, sustained-release technologies allow for increased performance of new and existing compounds.” In addition to this exciting news, ClostraBio is pleased to announce a key addition to its management team with the appointment of CEO, Ritu Shah, Managing Director at Portal Innovations and taking on leadership roles at Portal’s portfolio companies. “I’m honored to serve as the CEO at ClostraBio. The science and technology behind their metabolite delivery platform, along with Dr. Nagler and Dr. Hubbell’s long-term vision is what attracted me to the company,” said Shah. “After the successful delivery of the drug in mice as featured in Nature Biomedical Engineering, I’m excited to execute a go-to-market plan to help bring visibility of ClostraBio to the marketplace where more than 33 million Americans suffer from inflammatory bowel disease (IBD) and food allergies.” Shah joins ClostraBio with over two decades of experience in multiple leadership roles in drug development for pharma and biotech. She was recently Chief Operating Officer at Pyxis Oncology. To date, Shah helped take Pyxis public, while also completing mergers and acquisitions with four biotech and pharmaceutical companies. “At ClostraBio, our novel delivery platform is designed to transform the treatment of lower gut disease —starting with ulcerative colitis,” finished Shah. About ClostraBio ClostraBio is a late-preclinical stage biopharma company focused on targeted metabolite delivery to transform intestinal health in patients with inflammatory bowel disease (IBD) and food allergy. Founded on seminal science originating from Dr. Cathryn Nagler’s and Dr. Jeffrey Hubbell’s labs at the University of Chicago, the company is developing a novel nanoparticle platform that enables oral delivery of short-chain fatty acids (SCFAs) to targeted locations in the gastrointestinal tract. For more information about the company, please visit: http://clostrabio.com

New research has found a better education has a strong genetic correlation and a protective causal association with several gut disorders. We've long known education is important for many aspects of life, but now a new benefit has been discovered: it can look after your gut health. Landmark Edith Cowan University (ECU) research has found a better education has a strong genetic correlation and a protective causal association with several gut disorders. A previous study from ECU's Centre for Precision Health (CPH) discovered a genetic link between gut health and Alzheimer's Disease (AD) but couldn't conclude whether one caused the other. This study breaks new ground by finding that a higher level of education protects against gut disorders. CPH Director and study supervisor Professor Simon Laws said these findings build upon the centre's previous work to provide further evidence of the strong links between the brain and gut, known as the gut-brain axis. "Gut disorders and Alzheimer's may not only share a common genetic predisposition but may be similarly influenced by genetic variations underpinning educational attainment," Professor Laws said. This large-scale study examined the genetic information of more than 766,000 individuals, with an emphasis on AD, cognitive traits and gut disorders, including peptic ulcer disease (PUD), gastritis-duodenitis, gastroesophageal reflux disease (GERD), irritable bowel syndrome, diverticulosis and inflammatory bowel disease (IBD). It found higher levels of education and cognitive functioning reduced the risk of gut disorders. Lead researcher Dr Emmanuel Adewuyi said the findings have significant implications. "The results support education as a possible avenue for reducing the risk of gut disorders by, for example, encouraging higher educational attainment or a possible increase in the length of schooling," he said. "Hence, policy efforts aimed at increasing educational attainment or cognitive training may contribute to a higher level of intelligence, which could lead to better health outcomes including a reduced risk of gut disorders." It goes both ways ECU's study further revealed the gut may also influence the brain. GERD showed evidence of causing a decline in cognitive function across a number of cognitive traits assessed in the study, such as intelligence, cognitive performance, educational attainment and educational qualification. Although this is the first study to report this finding, the results support recent research reporting an increased incidence of dementia and GERD, which Dr Adewuyi said could help with earlier diagnoses and potential treatments. "GERD may be a risk factor for cognitive impairment, so it's important for health workers to look for signs or symptoms of cognitive dysfunction in patients presenting with the gut disorder," he said. "This could lead to earlier detection of cognitive decline and therefore earlier interventions aimed at reducing the rate of cognitive decline. "More studies are needed to investigate whether treatment for, cure or remission of GERD can contribute to a reduced risk of cognitive decline." The curious case of IBD Interestingly, higher levels of education and cognitive function protecting against gut disorders was true of all the disorders examined in the study -- but largely with the exception of inflammatory bowel disease. Further analysis reveals different effects of IBD on cognitive traits and AD at different genomic locations, indicating its relationship depend on effects at specific locations across the genome. This new understanding may explain the lack of significant genetic correlation of IBD with cognitive traits and AD, and the inconsistency reported in previous observational studies. Dr Adewuyi said this finding was also important, as it brings a new insight into the relationship of IBD with cognitive traits (and AD), which may shape the direction of future studies. "For example, some risk genes for AD may be protective against IBD, and vice versa," he said. 'Relationship of cognition and Alzheimer's disease with gastrointestinal tract disorders: a large-scale genetic overlap and Mendelian randomisation analysis' was published in the International Journal of Molecular Sciences.

Innate lymphoid cells are a recently discovered family of white blood cells that reside in the skin, gastrointestinal tract, airways and other barrier tissues of the body. Group 2 innate lymphoid cells (ILC2s) have an essential role in protecting these tissues from parasitic infections as well as damage associated with allergic inflammation and asthma, according to a new study. Innate lymphoid cells are a recently discovered family of white blood cells that reside in the skin, gastrointestinal tract, airways and other barrier tissues of the body. Group 2 innate lymphoid cells (ILC2s) have an essential role in protecting these tissues from parasitic infections as well as damage associated with allergic inflammation and asthma, according to a new study led by Weill Cornell Medicine researchers. The finding resolves a controversy about the possible redundancy of ILC2s with other cells in the body. The study also suggests that a unique set of regulatory networks controlled by neurons in the gut may be viable targets for future drug therapies to combat chronic inflammatory diseases including asthma, allergy and inflammatory bowel disease (IBD). The study, published Nov. 2 in Nature, shows that although ILC2s have many functional similarities to immune cells called T helper type 2 cells (Th2 cells), the latter cell type cannot adequately compensate for loss of the protective response of ILC2s against parasitic worm infection in the gut as well as gut inflammation. Underscoring the clinical relevance of the study, the researchers found evidence that ILC2s in humans respond in a manner similar to mouse ILC2s. "This advances our understanding of the complexity of the immune system, and gives us a potential new set of targets for future therapies," said study senior author Dr. David Artis, director of the Jill Roberts Institute for Research in Inflammatory Bowel Disease, director of the Friedman Center for Nutrition and Inflammation and the Michael Kors Professor of Immunology at Weill Cornell Medicine. ILC2s are part of a family of cells, innate lymphoid cells, that were discovered by multiple groups only about 12 years ago. With their strong presence in barrier tissues, innate lymphoid cells are generally considered to serve as sentinels and first responders against various types of infection. But scientists also recognize that ILCs may hold the keys to understanding common inflammatory and autoimmune conditions such as asthma and IBD. It is thought that both ILC2s and Th2 cells evolved at least in part to defend the body from parasitic worm infections, biting insects and other environmental triggers. When triggered by such challenges, both help marshal what is called a type 2 immune response. These similarities have led researchers to suggest that they are functionally almost the same but ILC2s specialize in earlier, more localized responses, whereas T cells are more blood-borne and mobile, concentrating in multiple tissues where needed. However, in the new study, the researchers found that ILC2s have an essential immune role rather than being redundant as type 2 immune responders. When ILC2s and Th2 cells are activated by a worm infection, they both produce an anti-worm, tissue-protecting protein called amphiregulin (AREG). To determine if Th2 cells can compensate for loss of this protein from ILC2s, the researchers engineered mice in which AREG production is selectively deleted in ILC2s, but not in Th2 cells. They found that these mice were more susceptible to parasitic worm infection in the gut due to reduced capacity to mount an anti-parasitic immune response, compared with mice with normal ILC2s. The mice lacking ILC2 AREG were also much more susceptible to gut damage from inflammation. "This finding clarifies that ILC2s are playing the major role in this tissue protective response -- without them the response is inadequate," said study co-first author Dr. Hiroshi Yano, a postdoctoral research associate in the Artis laboratory. Clarifying the functional importance of a major immune cell type is a significant achievement in basic immunology and the results of the study also suggest clinical applications. The researchers showed that the ILC2 immune response, either to worm infection or inflammatory gut damage, is selectively controlled by a signaling molecule produced by neurons in the gut. Giving the molecule to mice with experimental gut inflammation boosted AREG production in ILC2s and protected the animals from gut damage. Preliminary experiments with gut ILC2s taken from patients with inflammatory bowel disease showed that the molecule could boost the protective response in the human cells as well. These findings suggest that neurons in the gut communicate with ILC2s to generate a protective response that cannot be replaced by other immune cells, thus offering new therapeutic opportunities, Dr. Artis said. This work was supported in part by the National Institutes of Health (DK126871, AI151599, AI095466, AI095608, AI142213, AR070116, AI172027, DK132244), a WCM Department of Pediatrics Junior Faculty Pilot Award, the Jill Roberts Center Pilot Award for Research in IBD, a Thomas C. King Pulmonary Fellowship, the LEO foundation, Cure for IBD, Jill Roberts Institute, the Sanders Family, and the Rosanne H. Silbermann Foundation.