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Researchers have established a new defense mechanism to explain how Escherichia coli can thrive during flare ups in patients with inflammatory bowel disease (IBD). Findings from the study are published in Nature Communications.
The typically innocuous E. coli can proliferate during a flare up and contribute to disease in patients with IBD. A team from Penn State University examined the interactions between enterobactin, myeloperoxidase, and lipocalin 2, and how they regulate E. coli in the intestine.
Enterobactin, a chemical secreted by E. coli, takes iron from host proteins in the body and helps the proliferation of E. coli. Myeloperoxidase is an antibacterial protein that is produced by white blood cells. Lipocalin 2 is also a protein produced by white blood cells that groups enterobactin so that the bacteria cannot gather enough iron for their survival.
Enterobactin was found to inhibit myeloperoxidase from carrying out its function. Researchers also found that lipocalin 2 can counter the effects of enterobactin on myeloperoxidase. The way enterobactin inhibits myeloperoxidase could explain the defense mechanism of E. coli living in a human or animal host, researchers concluded. In addition, future enterobactin-based drugs may help alleviate other inflammatory diseases.
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This article originally appeared on MPR
