Systemic inflammatory protein profiles distinguish IBS and ulcerative colitis,
Potential links between inflammation and IBS-like symptoms in these patient groups are still unclear.
Patients with ulcerative colitis (UC), a chronic inflammatory bowel disease (IBD) involving the colonic mucosa, may suffer from irritable bowel syndrome (IBS)–like symptoms during periods of remission. It has been suggested that UC patients experiencing IBS-like symptoms during remission suffer from inadequately treated inflammation.1 Likewise, there are reports of systemic and intestinal low-grade immune activation in IBS patients.2 Indeed, IBS and UC present some similarities that range from high incidence of clinical depression and/or anxiety to imbalanced microbiome and persistent immune activation.3 However, it is still unclear whether the inflammatory mechanisms of UC and IBS overlap or are part of different spectrums.3
It may sometimes be difficult to differentiate between IBS-like symptoms and an upcoming flare in IBD patients, resulting in mistakes in choice of treatment, increased morbidity, and impaired quality of life. The similarity could also suggest similar underlying immunopathology, ranging from low-grade immune activity to full-scale inflammation. We and others have demonstrated that the serum cytokine profiles of IBS patients, or at least subgroups thereof, are characterized by increased levels of proinflammatory cytokines as compared with healthy subjects.4–7 Moreover, we recently reported that UC patients in deep remission with IBS-like symptoms had higher levels of certain serum cytokines than patients without these symptoms.8
Lately, studies have focused on identifying inflammatory protein profiles, including cytokines and chemokines, in the serum of IBD patients. Interestingly, a study suggests that Crohn’s disease (CD) and UC involve different inflammatory pathways, irrespective of disease activity, based on serum protein levels.9 The same study also identified serum proteins differentiating UC and CD, respectively, from healthy subjects (HS). Increased serum levels of inflammatory proteins such as eotaxin, growth-related oncogene, and tumor necrosis factor α (TNF-α) in UC patients compared with HS has also been reported, although no proteins were found to differ between UC and CD patients.10
We propose that characterization of disease-specific serum protein profiles will improve our understanding of the potential link between inflammation and IBS symptoms in patients with gastrointestinal diseases. Therefore, in this study, we aimed to determine systemic inflammatory protein (SIP) profiles, analyzing a broad panel of inflammation-related proteins, to establish if the profiles differ between UC patients, with presence of inflammation or in remission with or without IBS-like symptoms, and IBS patients.
Characterizing disease-specific immune profiles of UC patients, with and without inflammation and IBS-like symptoms, and IBS patients may help to disentangle the underlying mechanisms possibly linking inflammation and IBS symptoms in these patient groups. In this exploratory study, we demonstrate that SIP profiles discriminate healthy subjects and patients with IBS from patients with UC. Furthermore, we show that SIP profiles vary between UC patients with different inflammatory activities. Additionally, IBS patients deviate from UC patients with IBS-like symptoms and healthy subjects by their SIP profiles. Thus, our data do not support shared inflammatory mechanisms of UC and IBS, or that symptoms of patients with UCR + IBS and IBS, respectively, are driven by similar mechanisms.
Read full study here.