Health & Medicine
Listening To How The Stomach Responds To Injury Aids Therapy For Gastric Damage
Kathleen Lees
First Posted: Mar 05, 2015 11:41 PM EST
New findings published in Cellular and Molecular Gastroenterology and Hepatology, the basic science journal of the American Gastroenterological Association, show how a better understanding of the stomach's immune response to Helicobater pylori (H. pylori) infection could lead to new therapies that target damage in the stomach.
For the study, researchers used a number of mouse models to determine patterns of immune regulation of gastric pathology.
When H. pylori infection is present, it takes the alarmin Interleukin (IL)-33 to trigger necessary changes that help any injuries related to the infection heal and recovery. More specifically, it results in an inflammatory immune response that begins the process of cell loss that can lead to the onset of metaplasia.
"These (IL-33) immune cell drivers of proliferation and expansion of metaplasia may be a critical target for intervention and further research," said lead study author Jon N. Buzzelli, PhD, Murdoch Children's Research Institute, Department of Pediatrics, Royal Children's Hospital, in a news release.
Findings revealed that IL-3 elevates during acute response to infection, resulting in declines in chronic infection, which may cause alterations observed in patients with chronic infection.
"Since other studies have noted that IL-33 may be elevated in association with metastatic gastric cancer, further investigations will be necessary to determine the changing influences of IL-33 at different stages of cancer development," concluded James R. Goldenring, MD, PhD, AGAF, associate editor of the journal.
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First Posted: Mar 05, 2015 11:41 PM EST
New findings published in Cellular and Molecular Gastroenterology and Hepatology, the basic science journal of the American Gastroenterological Association, show how a better understanding of the stomach's immune response to Helicobater pylori (H. pylori) infection could lead to new therapies that target damage in the stomach.
For the study, researchers used a number of mouse models to determine patterns of immune regulation of gastric pathology.
When H. pylori infection is present, it takes the alarmin Interleukin (IL)-33 to trigger necessary changes that help any injuries related to the infection heal and recovery. More specifically, it results in an inflammatory immune response that begins the process of cell loss that can lead to the onset of metaplasia.
"These (IL-33) immune cell drivers of proliferation and expansion of metaplasia may be a critical target for intervention and further research," said lead study author Jon N. Buzzelli, PhD, Murdoch Children's Research Institute, Department of Pediatrics, Royal Children's Hospital, in a news release.
Findings revealed that IL-3 elevates during acute response to infection, resulting in declines in chronic infection, which may cause alterations observed in patients with chronic infection.
"Since other studies have noted that IL-33 may be elevated in association with metastatic gastric cancer, further investigations will be necessary to determine the changing influences of IL-33 at different stages of cancer development," concluded James R. Goldenring, MD, PhD, AGAF, associate editor of the journal.
For more great science stories and general news, please visit our sister site, Headlines and Global News (HNGN).
See Now: NASA's Juno Spacecraft's Rendezvous With Jupiter's Mammoth Cyclone