Lack of SHIP1 Protein May Contribute to Inflammatory Process in Crohn’s Disease

Lack of SHIP1 Protein May Contribute to Inflammatory Process in Crohn’s Disease

A protein called SHIP1 may be involved in the progression of Crohn’s disease, according to a study conducted by researchers at SUNY Upstate Medical University and the Erasmus Medical Center, in the Netherlands.

The results of the study titled “Analysis of SHIP1 expression and activity in Crohn’s disease” that appeared in the journal PLOS One, showed that some patients with Crohn’s disease either lack the SHIP1 protein or the protein has lower activity than normal. This aberrant SHIP1 activity can contribute to the deregulation of the immune system and the inflammatory mechanisms that characterize this disease.

SHIP1 is mainly expressed by immune cells, and is necessary to regulate immune cell function and intestinal fibrosis. Previous studies have showed that mice lacking this protein develop intestinal inflammation, with symptoms similar to those observed in Crohn’s disease.

In the present study led by William G. Kerr, PhD, professor at SUNY Upstate Medical University, the research team analyzed the activity and levels of SHIP1 protein in 34 patients with diagnosed Crohn’s disease and 25 healthy people in a control group.

First, they analyzed the total activity of SHIP1 protein, but found no differences between patients and controls. Next, they examined the levels of the protein and found that some patients had very low levels of the protein, while other patients had similar or higher levels of the protein than the control group.

Since the total activity of a protein depends on the amount of the protein itself, the research team correlated the SHIP1 activity measured in each sample with its respective amount.

This new analysis revealed that the intrinsic activity of the protein in the Crohn’s disease patients was reduced as compared to those in the healthy control group. This means that although some patients had higher levels of the protein, it was actually less active.

“We followed a larger cohort of individuals with Crohn’s disease in our second study and again found that SHIP1 expression is absent or drastically reduced in a subset of Crohn’s disease and ulcerative colitis patients,” Kerr said in news release. “We are continuing our efforts to determine the molecular and genetic basis for this defect,”

Additional studies are still necessary on the role SHIP1 plays in inflammatory bowel disease. If its involvement is confirmed, SHIP1 may be a suitable therapeutic target and may also be useful as a potential biomarker for early detection of bowel inflammation.

This study was supported by Crohn’s & Colitis Foundation of America, Paige’s Butterfly Run and the National Institutes of Health.

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