A study published in Cell Reports demonstrates the potential role of microRNA-223 in reducing, or controlling, inflammation in zebrafish. The microRNA is highly expressed in human blood cells that cause inflammation. Ordinarily, the blood cells protect against infection. On occasion, the cells damage the host tissue, resulting in chronic inflammation and associated diseases.

A team from Purdue University investigated the relationship between MicroRNA-223 and inflammation, by creating a zebrafish totally deficient in the molecule. Inflammation was stimulated by cutting off a small chunk of its fin.

“The inflammation was really robust,” said Qing Deng, a professor of biological sciences at Purdue and corresponding author of the paper. “Neutrophils accumulated at the wound and they just kept coming. This is consistent with the literature, but we wanted to understand why.”

After extensive gene expression analysis, they did find out why. It’s down to pathway NF-kB, which is a protein complex that regulates inflammation and cell proliferation in just about every animal cell type. Increased inflammation is due to the over-activation of the pathway and acts on the basal layer of the epithelium. This means that any therapeutic treatment would need to get deep into the skin to have any effect. In humans, the pathway is linked to the development of asthma. In theory, microRNA-223 could be delivered to epithelial cells to control the inflammation.

“We don’t have human trials yet, but we think it’s promising,” Deng said. “Instead of using steroids to drive away the immune cells, maybe this microRNA could be given.”

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