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Based on findings published Oct.
3 in the journal Gut, researchers at Mount Sinai have published one of the earliest studies demonstrating the importance of reactive oxygen species in maintaining stem cell function and preventing inflammation during wound repair, which could provide greater insights
into the prevention and treatment of inflammatory bowel disease (IBD).
Reactive oxygen species are highly reactive chemicals
formed from oxygen.
They are the main signals
of cellular dysfunction that lead to disease.
The secretion of reactive oxygen species in the intestine is necessary to maintain stem cell function and is also important for wound repair; However, it can also cause inflammation
.
The team at Mount Sinai College of Medicine has identified key transcription factors that drive abnormal changes in stem cells, suggesting that reactive oxygen species play an important role
in maintaining gut health.
"While it is clear that the regulation of oxygen and reactive oxygen species plays a key role in chronic diseases, especially IBD, this study has made significant progress
in identifying the critical role of oxygen in maintaining the healthy epithelial barrier of IBD.
" Senior author Judy H.
Cho said
.
The team studied the role of reactive oxygen species and NOX1 (the protein used to produce these chemicals) by detecting single-cell gene expression in vitro and in vivo in mouse models, as well as human intestinal biopsies
obtained after routine colonoscopy.
They measured the number of reactive oxygen species and analyzed the gene expression profiles
of intestinal barrier cells in mice and humans with subtypes of IBD with ulcerative colitis.
Intestinal barrier cells cover the surface of the intestines to help digest food, absorb nutrients, and prevent intestinal bacteria from invading
.
Researchers at Mount Sinai School of Medicine compared gene expression data
from inflammatory and non-inflammatory colon tissue.
The researchers found that the combination of NOX1, loss of function led to a decrease in the species of reactive oxygen species, which, combined with the presence of a substance called TNF, led to an abnormal increase
in microfolded cells.
Microfolded cells, also known as M cells, are essential
for regulating the gut immune response.
The team found that in stem cells from human and mouse models, M cells increased
abnormally due to loss of reactive oxygen species.
The increase in epithelial M cells drove the increase in
mouse immune cells.
By treating intestinal cells with reactive oxygen species, they were able to reverse the initial defects
caused by the loss of reactive oxygen species during inflammation.
"Reactive oxygen species released by stem cells are essential for maintaining proper balance in intestinal barrier cell types," said
Dr.
Nai-Yun Hsu, an associate scientist in Judy Cho's lab.
The researchers encourage further research, which they say may include direct reactive oxygen species-stem cell-modulated therapies for IBD patients in future
treatments.
Nai-Yun Hsu, Shikha Nayar, Kyle Gettler, Sayali Talware, Mamta Giri, Isaac Alter, Carmen Argmann, Ksenija Sabic, Tin Htwe Thin, Huai-Bin Mabel Ko, Robert Werner, Christopher Tastad, Thaddeus Stappenbeck, Aline Azabdaftari, Holm H Uhlig, Ling-Shiang Chuang, Judy H Cho.
NOX1 is essential for TNFα -induced intestinal epithelial ROS secretion and inhibits M cell signatures.
Gut, 2022; gutjnl-2021-326305