A team of scientists at Mount Sinai says it has officially published one of the first studies to examine the significance of reactive oxygen species (ROS) in preserving stem cell functionality.
The researchers believe their findings, which also emphasize the importance of ROS in preventing inflammation during wound repair, could help with averting and treating inflammatory bowel disease (IBD).
The umbrella term “reactive oxygen species” describes an array of extremely reactive chemicals formed from oxygen. They are among the telltale signs of cellular dysfunction that leads to various diseases and illnesses. The secretion of ROS in the intestines is required to maintain the healthy functioning of stem cells and to facilitate wound healing. But the downside is that there’s a potential to cause inflammatory effects.
Senior author Judy Cho, MD, noted: “While it’s clear that regulation of oxygen and reactive oxygen species plays a critical role in chronic diseases generally, and IBD in particular, this study provides a major advance in defining the key role of oxygen species in maintaining a healthy epithelial barrier for IBD. Loss-of-function mutations in genes generating reactive oxygen species (ROS), such as NOX1, are associated with IBD. Mechanisms whereby loss of ROS drive IBD are incompletely defined.”
The researchers looked into the role of ROS and NOX1 – the protein that creates these chemicals – by examining single-cell gene expression in both living organisms and those in test tubes. They also studied human intestinal biopsies, which were gathered through basic colonoscopies.
The researchers used both mice as well as human patients with ulcerative colitis – a category of IBD, and assessed the amount of ROS and the intestine barrier’s gene profile expression. In addition to aiding in food digestion and nutrient absorption, these cells also serve as barriers against internal bacterial invasion.
The team found that three factors work in tandem to cause an abnormal increase in microfold cells, namely NOX1, a loss of function (that causes the amount of ROS to go down), and the existence of tumor necrosis factor (TNF), which leads to high inflation levels.
Microfold cells – also called M cells, are of critical importance when it comes to the regulation of gut immune response. One of the major findings of the research team was that the anomalous increase in M cells, in both mice and human models – was because of the loss of reactive oxygen species. The upturn in the M cell volume, in turn, leads to a more efficient accumulation of immune cells in mice. The scientists succeeded in reversing the initial problem caused by the loss of ROS as a result of inflammation.
Lead author Nai-Yun Hsu, Ph.D, said that the importance of reactive oxygen species lies in the fact that they are crucial in maintaining a healthy gut through the maintenance of intestine barrier cell types.
It’s still too early to say for sure whether or not ROS treatment could be effective as a therapy for IBD patients. However, the team is optimistic that future findings, coupled with the current ones, can potentially lead to a breakthrough in finding new and improved treatments.
