Understanding the stomach’s immune response to Helicobacter pylori infection may help develop new treatments against gastric damage, according to a recent report published in Cellular and Molecular Gastroenterology and Hepatology.
Researchers evaluated interleukin (IL)-33 levels in mouse and human biopsy specimens infected with H. pylori and in mice after dosing with aspirin. IL-33 is an important signal expressed in gastric mucosa that triggers necessary changes for handling the injuries caused by infection. Mice were given one or seven daily doses of recombinant IL-33 (1mcg/dose) and the stomach and spleen responses were quantified morphologically.
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They found that during an acute response to an infection in mice, interleukin (IL)-33 levels were elevated four-fold but reduced two-fold in chronic infection. Human biopsy specimens with H. pylori presence also showed a reduced IL-33 expression.
Authors concluded that the decreased IL-33 expression after prolonged H. pylori infection may enable the T helper 1-biased immune response seen during H. pylori infection and the precancerous progression. Further studies are needed to determine the impact of IL-33 in different stages of gastric cancer.
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