Flucytosine-induced colitis is exceedingly rare with very few cases reported in the literature. We present a case of a 56-year-old male with history of ulcerative colitis and seronegative spondyloarthropathy who developed abdominal pain, diarrhoea and rectal bleeding following commencement of flucytosine and amphotericin B for cryptococcal empyema. The clinical features and biochemistry initially raised concern for an ulcerative colitis flare. Histopathology demonstrated features of an acute colitis. Subsequent cessation of flucytosine without alteration to management of his underlying ulcerative colitis led to a rapid and complete resolution of symptoms, supporting a diagnosis of flucytosine-induced colitis. This case highlights the importance of considering a drug-induced colitis in patients with inflammatory bowel disease presenting with new or worsening gastrointestinal symptoms. Accurate differentiation from disease flare is essential to avoid unnecessary changes or escalation in immunosuppressive therapy.

Ulcerative colitis (UC) is a prevalent chronic inflammatory bowel disease globally, driven mainly by immune dysregulation and gut microbiota dysbiosis. This study focused on Lactiplantibacillus plantarum BF_15, an infant-derived strain with potential to alleviate UC. Four experimental groups were established, including the control group, DSS group, BF_15 group, and LGG group. Probiotics were administrated at a dosage of 1 × 10[9] CFU/mL and 0.1 mL/10 g body weight (BW) for 21 days. The therapeutic effects and mechanisms of BF_15 against UC were explored based on physiological indicators, gut microbiota, and tandem mass tag (TMT)-based quantitative proteomics. The results showed that BF_15 intervention significantly reduced the disease activity index (DAI) from 3.00 ± 0.50 to 1.16 ± 0.36 (p < 0.05) and mitigated UC-related symptoms including body weight loss and colon shortening, with colon length restored from 4.43 ± 0.32 cm to 5.41 ± 0.26 cm (p < 0.05). Meanwhile, BF_15 downregulated the levels of pro-inflammatory factors such as interleukin IL-6 and IL-17A, and upregulated the levels of IL-10 (from 565.92 ± 79.40 pg/mL to 656.84 ± 66.01 pg/mL) and secretory immunoglobulin A (SIgA, from 9.75 ± 1.29 μg/mL to 12.79 ± 1.77 μg/mL) (p < 0.05), with a therapeutic effect comparable to that of LGG. Further, gut microbiota analysis demonstrated that BF_15 restored the relative abundance of Bacteroidetes (from 28.02% to 30.85%) and regulated gut microbiota homeostasis. Finally, TMT-based proteomic analysis indicated that BF_15 regulated 528 differentially expressed proteins (DEPs) and exhibited a superior regulatory effect on the antigen presentation and processing (APC) pathway compared with LGG. The above findings provide potential novel therapeutic targets and probiotic strain resources for the treatment of UC.

Inflammatory bowel disease (IBD) severely impairs patients' quality of life and elevates colorectal cancer risk, where early diagnosis and timely intervention are vital to control disease remission. Peroxynitrite (ONOO[-]), a critical reactive nitrogen species closely involved in IBD pathogenesis, is an attractive biomarker for biological detection. Herein, we rationally constructed a turn-on near-infrared fluorescent probe HCY-PO targeting ONOO[-]. Upon ONOO[-]-triggered cleavage of the diphenylphosphinamide recognition group, HCY-PO exhibited a distinct fluorescence enhancement at 750 nm within 60 s, with a detection limit of 90 nM and strong anti-interference capability in complex biological systems. Using HCY-PO, we achieved real-time tracking of endogenous ONOO[-] fluctuations in inflamed NCM460 cells, zebrafish enteritis models, and early diagnosis of ulcerative colitis in mouse models. Importantly, the probe's fluorescent signal intensity was positively correlated with IBD severity. Moreover, HCY-PO achieved the sensitive detection of ONOO[-] in mouse feces, enabling non-invasive monitoring of IBD progression. Based on this superior analytical performance, an integrated fluorescence sensing platform was first established to semi-quantitatively evaluate the therapeutic efficacy of the traditional Chinese medicine formula Bu-Zhong-Yi-Qi-Tang. Consistent results among fluorescence, pathology and inflammatory factor tests verified the method reliability, and five anti-enteritis bioactive constituents from the formula were efficiently screened via this platform. Collectively, this work provides a powerful analytical tool for non-invasive early IBD diagnosis, drug efficacy evaluation, and rapid screening of anti-enteritis bioactive components.

Hematochezia has a broad differential, including nonsteroidal anti-inflammatory drug (NSAID)-induced, infectious, and inflammatory colitis. Colonoscopy with biopsy is primarily used to evaluate suspected colitis or inflammatory bowel disease (IBD) in patients with hematochezia, rather than to diagnose all causes of hematochezia. While the inflammatory bowel disease serology, genetics, and inflammation (IBD-SGI) blood panel test has been studied and marketed by laboratories, it is not widely implemented in routine clinical practice due to the restriction of current clinical guidelines, lack of FDA clearance/approval, and limited medical insurance coverage. Thus, we report a case of the utility of the IBD-SGI panel in the evaluation of atypical ulcerative colitis (UC) with active NSAID use. A 39-year-old man with hematochezia, diarrhea, and chronic high-dose NSAID use developed anemia, elevated fecal calprotectin, and endoscopic evidence of inflammation. Biopsies by colonoscopy showed focal colitis with features suggestive of both NSAID injury and IBD. To provide additional diagnostic support in this challenging case, an IBD-SGI blood panel was used. When interpreted with the patient's clinical presentation, elevated fecal calprotectin level, colonoscopic findings, and histopathologic features, the panel results supported a diagnosis of UC. Based on the overall clinic-pathological assessment, including continuous circumferential inflammation on colonoscopy and histopathologic evidence of chronic IBD, the patient was diagnosed with UC and treatment with vedolizumab was initiated. Anemia attributed to hematochezia was also managed. At the three-month follow-up, the patient had resumed his daily activities and returned to work. In the setting of overlapping features of UC and possible NSAID-associated colitis, the IBD-SGI panel provided adjunctive diagnostic information. This case highlights the panel's potential value as a supportive tool when endoscopic biopsy findings are inconclusive and multiple possible etiologies coexist.

Changes in cell-cell communication during disease can result from shifts in tissue composition, variations in the proportion of cells engaged in signaling, and differences in ligand-receptor expression. To address this, we developed community, an R package designed for differential communication analysis in multi-sample case-control scRNAseq datasets. Community reconstructs interactions by evaluating cell type abundance, the active fraction of cells, and their expression levels. This method identifies communication patterns that are upregulated, downregulated, unchanged, or compensated. Applied to ulcerative colitis, melanoma under immune checkpoint inhibitor treatment, and acute myeloid leukemia, community captured disease- and response-associated communication changes, including increased communication in ulcerative colitis, reduced immunosuppressive signaling in melanoma responders, and decreased immune communication in AML. Comparisons with existing tools showed improved robustness to outlier-driven signals and better scalability. These component-level analyses help connect altered communication patterns to biological mechanisms in healthy and disease states.

Granulomonocytapheresis (GMA) is an extracorporeal leukocyte adsorption therapy that selectively removes activated granulocytes and monocytes through interactions involving Fcγ receptors (FcγR) and complement receptor 3 (CR3). Initially developed for chronic inflammatory diseases such as ulcerative colitis, GMA has recently attracted attention as a potential adjunctive therapy for sepsis. Contemporary understanding of sepsis emphasizes thromboinflammation, immunothrombosis, endothelial injury, and inflammatory cell death as central mechanisms underlying organ dysfunction. Activated FcγR-positive and CR3-positive myeloid cells contribute to cytokine storm, neutrophil extracellular trap (NET) formation, oxidative injury, coagulation activation, and release of damage-associated molecular patterns (DAMPs). These processes amplify endothelial dysfunction, microvascular thrombosis, and disseminated intravascular coagulation. GMA may interrupt these self-amplifying inflammatory and thromboinflammatory loops by selectively depleting activated inflammatory leukocytes while relatively preserving adaptive immunity. Mechanistically, removal of FcγR-positive cells may suppress inflammasome activation, pyroptosis, and DAMP-mediated cytokine amplification, whereas removal of CR3-positive cells may attenuate NETosis, oxidative burst, endothelial adhesion, and microvascular injury. Although preliminary clinical and experimental studies suggest potential benefits in sepsis, important concerns remain regarding patient selection, optimal timing, infection risk, thrombocytopenia, and cost-effectiveness. Further phenotype-oriented clinical trials are required to define the therapeutic role of GMA in sepsis and thromboinflammatory critical illness.