In the case of chronic inflammation associated with a Helicobacter infection, however, it could facilitate the development of precancerous lesions," summarizes Prof. In the case of tissue damage, increased cell proliferation can be useful, as it promotes rapid healing. In addition to their well-characterized antimicrobial effects, pro-inflammatory substances such as IFN-γ affect both cell proliferation and tissue stem cell behavior and therefore have a direct impact on tissue homeostasis. "Our findings show that an infection-driven inflammatory response has far more pronounced effects than previously thought. This results in hyperplasia, a precancerous lesion characterized by tissue enlargement. This inflammatory cytokine interferes with the BMP signaling axis, resulting in less BMP signaling activity and stimulating gland stem cell proliferation. Helicobacter infection causes the release of pro-inflammatory substances such as interferon-gamma (IFN-γ). Together, this forms a signaling gradient that guides stem cell turnover and differentiation, and serves as the basis for the gland's structural stability. In contrast, stromal cells at the gland surface were found to activate the signaling pathway, thereby suppressing cell proliferation. The researchers were able to show that stromal cells surrounding the gland base continually inhibit the BMP signaling pathway, thereby stimulating the proliferation of nearby stem cells. These substances include 'bone morphogenetic proteins' (BMPs), which play an important role in tissue development. Instead, they produce various signaling molecules which significantly influence the behavior of the gland cells," explains Prof. "We discovered that 'stromal cells' - a type of cell surrounding the gastric glands - are not only responsible for mechanical stability of the glands, as previously thought. This strategy enabled them to study the effects of various signals on stem cells which are found inside the gastric glands (and which are capable of differentiating into many different cell types). The researchers used these microscopic stomachs to recreate many of the gastric glands' characteristics. In order to minimize the need for animal models, they also developed special organ-like tissue microstructures known as organoids. Using state-of-the art imaging and single-cell sequencing technologies, the researchers were able to visualize and isolate specific gastric gland cells, which they then examined in detail. Sigal and working alongside colleagues from the Max Planck Institute for Infection Biology, the team of researchers used complex mouse models to observe changes occurring inside the gastric glands. Sigal is Professor for Translational Gastrointestinal Oncology and leads an Independent Research Group at Charité's Department of Hepatology and Gastroenterology and the Berlin Institute for Medical Systems Biology (BIMSB), which forms part of the MDC. He continues: "In fact, our team has now discovered that the infection disrupts complex interactions between different cell types and signals which are responsible for tissue stability." Prof. "Until now, researchers had assumed that a Helicobacter infection causes direct damage to the gastric gland cells in the stomach lining and that gastric pathology upon infection is simply the result of this process," explains the study's last author, Prof. As the protective lining inside the stomach is constantly exposed to stomach acid, it has to regenerate completely every few weeks, while maintaining both its structure and composition despite the high cellular turnover. pylori can lead to inflammation of the stomach (gastritis) and increase the risk of developing stomach cancer. Affecting about half the world's population, Helicobacter pylori is one of the most common causes of chronic bacterial infections in humans.
0 Comments
Leave a Reply. |
Details
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |