Thanks to epidemiological studies, researchers now know that obesity and inflammatory bowel disease (IBD) are linked. Animal models also show that a maternal high-fat diet and maternal obesity make offspring more likely to be obese. A team at the Institut Pasteur and Inserm is now reporting that excess calorie intake by neonatal mice born to mothers on a high fat diet or made to force feed have more permeable intestines during weaning. These mice also express pro-inflammatory cytokines and microbiota that produce hydrogen sulphide.
These intestinal changes lead to an increased susceptibility to colitis in adults and long-term susceptibility to IBD.
The research is reported in Nature Metabolism.
Meanwhile, in a new paper in Nature Microbiology, researchers at Michigan Medicine tgether with colleagues at Insem describe how bad bacteria gain a foothold over good bacteria in irritable bowel syndrome (IBD) and how something as simple as a diet change might reverse it. “The same bacteria are present in healthy and inflamed digestive tracts,” says Nobuhiko Kamada, of the division of gastroenterology in the Department of Internal Medicine at Michigan. “They just change their competition.”
Finally, researchers in Catherine Robin’s group at the Hubrecht Institute and Thierry Jaffredo’s group at UPMC, LBD IBPS in Paris are reporting on a hitherto unappreciated hematopoietic wave that occurs in the bone marrow of late foetuses and young adults that produces hematopoietic stem cells (HSCs) from resident haemogenic endothelial cells of somite origin. This transient haematopoietic wave lies in between the end of embryonic blood production and the beginning of adult bone marrow hematopoietic production in both chicken and mice. The research is published in Nature Cell Biology.
Hematopoietic stem cells (HSCs) are responsible for constantly replenishing blood cells throughout life. One of the major challenges in regenerative medicine is to produce tailor-made HSCs to replace defective ones in patients suffering from blood related diseases. This would overcome the shortage of donor HSCs available for the clinic. To produce bona fide HSCs in vitro, researchers need to better understand where, when and how HSCs are physiologically produced in vivo.