Research reveals protective role of CD14 in IBD
Researchers at Hannover Medical School, along with those from the University of Erlangen-Nürnberg, have found that the CD14 protein appears to play a protective role in the development of inflammatory bowel disease (IBD) by enhancing intestinal barrier function. Their findings are detailed April 12, 2017 in The American Journal of Pathology.
IBD, which involves inflammation of part or all of the digestive tract, is a result of genetic, microbial, and environmental factors. Many genetic loci have been implicated in IBD development in both humans and mouse models. In particular, a gene called Cd14, which encodes the CD14 protein, has been suggested to be a candidate gene for IBD susceptibility. The CD14 protein is preferentially expressed by monocytes and macrophages. As part of the innate immune system, it functions to enhance activation of cells by bacterial LPS.
In this work, the team used a mouse-model system for IBD to better elucidate the disease's pathogenesis. Genetic and candidate gene analyses confirmed that Cd14 is a potentially protective candidate gene. Mice lacking CD14 exhibited more severe inflammation in their gut in comparison to the controls. In contrast, increasing CD14 expression strengthened the integrity of the intestinal barrier.
There is a hypothesis that intestinal homeostasis disturbance through intestinal barrier disruption contributes to IBD development. Epithelial barrier function is regulated and maintained by various molecules. Loss of barrier integrity, which can be caused by bacteria, drugs, and toxic chemicals, leads to bacterial invasion and inflammation.
For this work, the researchers found that CD14 appears to regulate intestinal barrier function and prevent against intestinal inflammation. Therefore, CD14 might be a promising target for IBD treatment.
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CD14 recombinant protein
, CD14 antibody