Systemic inflammatory protein (SIP) profiles indicate that ulcerative colitis (UC) and inflammatory bowel syndrome (IBS) may have different underlying inflammatory mechanisms, according to study results published in Inflammatory Bowel Diseases.

Persistent immune activation is common in both UC and IBS; however, it is unclear whether the inflammatory mechanisms of these conditions overlap or are part of different spectrums. The objective of this study was to establish whether SIP profiles differ between patients with IBS and patients with UC with the presence of inflammation or in remission, with or without symptoms of IBS.

In this study, researchers obtained serum samples from patients with UC and IBS, and from healthy controls without gastrointestinal symptoms at 4 outpatient clinics in Sweden. Patients were stratified into groups based on whether they had IBS, active ulcerative colitis (UCA), UC in remission with or without symptoms of IBS (UCR + IBS and UCR – IBS, respectively), or were healthy controls. Serum levels of 92 inflammation-related proteins were analyzed using the ProSeek Multiplex Inflammation Kit.


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The study cohort consisted of 166 patients: 105 with UC, 40 with IBS, and 21 healthy controls. There were 40 patients with UCA, 45 with UCR – IBS, and 20 with UCR + IBS. In multivariate analysis, SIP profiles were used to separate patients with and without UC.

The variables found most important for the clustering were caspase 8, axin 1, sulfotransferase 1A1, and tumor necrosis factor superfamily member 14. Loading scatter plots defined interleukin (IL) 17C, IL17A, chemokine ligand 9, and transforming growth factor–α as the best proteins to characterize active inflammation in UCA, though there were no specific proteins that characterized UCR + IBS or UCR – IBS. SIP profiles generated a weak model with moderate differences between the IBS and healthy control groups, though serum levels of fibroblast growth factor 21 and IL6 were higher in the IBS group. Results were tested and confirmed using a validation cohort consisting of 14 patients with IBS, 15 patients with UCA, and 9 patients with UCR + IBS.

There were several limitations to this study. First, the method used to measure serum proteins was based on relative quantification, and researchers could not compare absolute levels between different proteins or with other studies that used traditional enzyme-linked immunosorbent assays. Second, a significant number of patients with UC were receiving treatment that may have regulated immune activity and affected serum levels of inflammatory proteins. Third, researchers were unable to measure fecal calprotectin in patients with UCR + IBS, which may have affected patient selection. Fourth, only SIP profiles were determined, and not intestinal immune protein profiles. Lastly, there were sex and age differences between the groups that may have influenced the data.

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The study researchers concluded that SIP profiles may differentiate between patients with IBS and patients with UC regardless of the presence of inflammation or IBS symptoms, and that SIP profiles may reflect different underlying inflammatory mechanisms of IBS and UC.

References

Moraes L, Magnusson MK, Mavroudis G, et al. Systemic inflammatory protein profiles distinguish irritable bowel syndrome (IBS) and ulcerative colitis, irrespective of inflammation or IBS-like symptoms [published online January 4, 2020]. Inflamm Bowel Dis. doi: 10.1093/ibd/izz322