Microbiota and Gut Inflammatory Markers (Zonulin and Fecal Calprotectin) Exhibit Age-Dependent Variation in Patients with Ulcerative Colitis

Abstract

Patients with bowel diseases (inflammatory bowel disease (IBD) in general) tend to seek medical, nursing, and/or physiotherapeutic consultations. Physiotherapists specialized in gastrointestinal (visceral) therapy can help reduce inflammation in patients with ulcerative colitis (UC). In this study, we divided UC patients into three groups according to their age: the youngest (18-35 years old), middle-aged (36-49 years old), and oldest (50-70 years old). Our hypothesis was that gut inflammatory markers (zonulin and fecal calprotectin levels) and microbiota strains would exhibit age-dependent variations in UC patients. We compared differences in zonulin, calprotectin, and vitamin D levels, together with a plethora of microbiota strains, based on age. Calprotectin is a marker of intestinal inflammation and zonulin identifies gut permeability; as IBD is characterized by gastrointestinal inflammation, these are useful markers for diagnosing and monitoring treatment/s in IBD patients, including ulcerative colitis (UC). Dysbiosis can alter the normal balance of intestinal function, and thus, several microbiota strains were compared between different age ranges in UC patients. The results indicated that the middle-aged UC (36-49) patients had the highest endogenous vitamin D levels, as well as lower zonulin and calprotectin levels than the youngest (18-35) and oldest (50-70) UC participants, respectively. The middle-aged group also had lower Enterococcus, E. Coli biovare, and Pseudomonas spp. levels than the youngest UC participants. Meanwhile, the most LPS microbiota producers were found in middle-aged patients. Finally, a higher number of Candida albicans and elevated LPS were found in the oldest UC participants than in the middle-aged (36-49) group. This study was, however, limited by uneven age-group sizes, which may have may limited the power in the youngest cohort. Although altered gut microbiota levels can increase gut inflammation in rodent models of UC, a definitive cause-effect relationship between UC and intestinal microbiota alteration is difficult to demonstrate in human