Immune profile differs during symptom flare for patients with irritable bowel syndrome

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Interferon-&#947; concentrations and T<sub>HELPER</sub> cells are significantly reduced during symptom flares.
Interferon-γ concentrations and THELPER cells are significantly reduced during symptom flares.

(HealthDay News) — For patients with irritable bowel syndrome with diarrhea (IBS-D), interferon-γ concentrations and THELPER cells are inhibited during symptom flare, according to a research letter published in Gut.

Chris Mavrangelos, from the University of Adelaide in Australia, and colleagues conducted a longitudinal study of patients with IBS comparing immune function within patients when they were free of symptoms and when they experienced symptom flare. The authors enrolled 11 patients with long-standing IBS who completed a valid self-report Bowel Disease Questionnaire and donated venous blood samples when free of symptoms and when experiencing a self-reported symptom flare.

The researchers found that symptom scores were significantly higher when subjects had symptom flare compared with being symptom free. When subjects were grouped together or when stratified according to bowel habit, the immune profile did not differ between symptom-flare and symptom-free time points. When subjects were grouped together, cytokine secretion and proliferative capacity did not differ between symptom-free and symptom-flare time points. On stratification by bowel habit, in IBS-D subjects, both interferon-γ concentrations and THELPER proliferation were significantly reduced during symptom-flare versus symptom-free time points.

"In order to accurately characterize immune profiles in IBS, researchers should consistently provide information regarding IBS subtype and symptom profile at the time of tissue sampling," the authors write.

Reference

  1. Mavrangelos C, Campaniello MA, Andrews JM, Bampton PA, Hughes PA. Longitudinal analysis indicates symptom severity influences immune profile in irritable bowel syndrome. Gut. 2017. doi:10.1136/gutjnl-2017-314308
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