Taurine is a semi-essential micronutrient that acts as an anti-inflammatory molecule. The oral administration of taurine to colitic mice attenuates ongoing mucosal inflammation. This study aimed to determine whether inflammatory bowel diseases (IBDs) are marked by changes in the circulating levels of taurine. We measured the serum concentrations of taurine in 92 IBD patients [46 with ulcerative colitis (UC) and 46 with Crohn’s disease (CD)] and 33 healthy controls with a commercial ELISA kit. The taurine levels were significantly decreased in both patients with UC and patients with CD compared to the controls, while there was no difference between CD and UC. Taurine levels declined with age in healthy controls but not in IBDs. IBD patients younger than 50 years had levels of taurine reduced compared to their age-matched controls. In the IBD group, taurine levels were not influenced by the body mass index of the patients and the consumption of taurine-rich nutrients, while they were significantly reduced in UC patients with clinically active disease compared to those in clinical remission. These findings indicate that IBDs are marked by serum taurine deficiency, which would seem to reflect the activity of the disease, at least in UC.

Inflammatory Bowel Diseases (IBD), most notably ulcerative colitis (UC) and Crohn’s disease (CD), are long-standing disorders driven by dysregulated immune responses within the gastrointestinal tract and characterized by several metabolic disturbances, which are believed to influence disease progression. We have recently shown that a systemic deficiency of taurine, a semi-essential amino acid with anti-inflammatory properties, marks IBD. To characterize the temporal dynamics and determinants of taurine deficiency in IBD, we conducted a prospective longitudinal study assessing serum taurine levels in a cohort of 47 patients with IBD compared with 33 healthy controls. Serum taurine concentrations were measured at baseline and after a median follow-up period of 45 months using ELISA. Patients were stratified by disease subtype (UC and CD), age group, and clinical activity status at baseline and follow-up. Serum taurine levels were significantly lower in IBD patients at both baseline and the end of follow-up (p < 0.05), and remained stable over time within the CD and UC cohorts. In healthy individuals, but not in IBD patients, taurine concentrations declined with age, suggesting that age-related metabolic regulation of taurine is altered in the context of chronic intestinal inflammation. Stratification by disease activity revealed that taurine deficiency was present in both active and inactive IBD, particularly among younger patients, and differences between active and inactive disease were minimal. These findings indicate that the persistent reduction in serum taurine in IBD is independent of age, disease subtype, or clinical activity, and remains relatively constant over time across most patient subgroups, suggesting an underlying alteration in taurine metabolism or homeostasis associated with IBD pathophysiology. Further investigation is needed to elucidate the mechanisms linking taurine dysregulation to IBD progression.

Colorectal cancer (CRC) progression is shaped by dynamic interactions between tumor-intrinsic metabolic adaptations and immune remodeling within the tumor microenvironment. In CRC, the expression of SMAD7, a classical inhibitor of TGF-β1 signaling, is increased and has been associated with tumor-associated inflammatory responses and malignant progression. In this study, we investigated the potential role of SMAD7 in regulating glycolytic metabolism and macrophage phenotype in CRC. Knockdown of SMAD7 in CRC cell lines resulted in reduced glycolytic activity, as demonstrated by decreased extracellular acidification rate, basal glycolysis, and glycolytic capacity. These metabolic changes were associated with reduced expression of the basal and IL-6- and IL-22-induced glycolytic enzyme hexokinase 2 (HK2), while glucose uptake was increased. Similar reductions in HK2 expression were observed in patient-derived CRC organoids following SMAD7 inhibition, supporting the relevance of this pathway in human tumor-derived models. Functionally, SMAD7 knockdown reduced lactate production by CRC cells and diminished the ability of tumor cell-derived conditioned medium to induce the expression of macrophage-associated immunoregulatory markers, including CD163, CD206, and ARG1. The addition of exogenous lactate restored these effects, indicating that tumor-derived lactate contributes to SMAD7-dependent control of the expression of macrophage-associated immunoregulatory markers. Analysis of human CRC transcriptomic datasets revealed positive associations between SMAD7 expression and macrophage-related signatures, including profiles associated with immunoregulatory tumor-associated macrophages. Together, these findings support a potential role for SMAD7 in controlling tumor metabolism and macrophage-associated immunoregulatory markers in CRC.