Bilberry extract modulates cytokine expression in ulcerative colitis

By David Douglas

NEW YORK (Reuters Health) - The anti-inflammatory effects of anthocyanin-rich bilberry extract (ARBE) in patients with ulcerative colitis (UC) may be partly due to inhibition of interferon (IFN) gamma signaling, according to Swiss researchers.

As Dr. Michael Scharl told Reuters Health by email, "We have previously shown that ARBE can be successfully used in the treatment of ulcerative colitis." In the current study, "we present the possible functional mechanisms (by which) ARBE might exert anti-inflammatory effects. So, our findings might be of great importance."

In a paper online May 6 in PLoS ONE, Dr. Scharl of the University of Zurich and colleagues note that anthocyanidins are dietary flavonoids widespread in fruits and flowers where they account for blue, purple, and red colors. Bilberries, which are related to blueberries, are among those with the highest natural anthocyanin content.

The team previously showed that anthocyanin-rich extracts reduce inflammatory gene expression in vitro. Furthermore, in an earlier open-label pilot study in 13 patients, they demonstrated that after six weeks of add-on ARBE treatment, more than half showed significantly reduced endoscopic and histologic disease activity and fecal calprotectin levels.

In the current investigation on the biomolecular mechanisms underlying these anti-inflammatory properties, the researchers established that ARBE suppresses IFN gamma-induced expression of IFN gamma R2 in human monocytic cells (THP-1) and in the intestine of UC patients.

Colon biopsies of UC patients who responded successfully to ARBE treatment further revealed a modified composition of T-cell-derived cytokines.

In fact, there were enhanced levels of Th17-cell specific cytokine interleukin (IL)- 22 and immunoregulatory cytokine IL-10 as well as reduced serum levels of TNF-alpha MCP-1, but enhanced levels of IL-17A.

"We demonstrated," the researchers say, "that daily bilberry ingestion provoked a reduction in (interferon) IFN-gamma and (tumor necrosis factor) TNF-alpha levels in the intestinal tissue in those patients who reached remission while the levels did not decrease in those participants without remission."

However, they go on to point out that as this reduction was seen only in patients reaching remission, "this effect might be the results of reduced disease activity and not a direct effect of the ARBE ingestion."

Also the small number of participants "impedes conclusive statements about the role of ARBE in UC disease control and is a major drawback of this study."

Nevertheless, Dr. Scharl noted that the findings "contribute critically to a better understanding of ARBE-induced anti-inflammatory effects in human subjects and might help to explain the mechanisms of action of a potential novel treatment option for inflammatory bowel disease patients."

He and his colleagues conclude that the results "reinforce the possible therapeutic use of ARBE in UC patients and warrant further prospective, randomized, and controlled clinical studies."

The Swiss National Science Foundation and the Swiss IBD Cohort supported this research. The authors reported no disclosures.

SOURCE: http://bit.ly/1TdGcaG

PLoS ONE 2016.

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