Introduction: Dysbiosis of intestinal microbiota likely plays an important role in the development of gut-derived infections, making it a potential therapeutic target against sepsis. However, experience with fecal microbiota transplantation (FMT) in the treatment of sepsis and knowledge of the underlying mechanisms are extremely lacking. In this article, we describe a case of a patient who developed sepsis after a vagotomy and later received an infusion of donor feces microbiota, and we report our findings. Methods: A 44-year-old woman developed septic shock and severe watery diarrhea 4 days after undergoing a vagotomy. Antibiotics, probiotics and supportive treatment strategies were used for about 30 day after surgery, but the patient’s fever, bacteremia and watery diarrhea persisted. Considering the possibility of intestinal dysbiosis, we evaluated the structure and composition of the patient’s fecal microbiota using 16S rDNA-based molecular techniques. As expected, the gut microbiota was extensively disrupted; therefore, a donor fecal suspension was delivered into the patient by nasoduodenal tube. The patient’s clinical outcomes and shifts of the gut microbiota following the treatment were also determined. Results: Dramatically, the patient’s septic symptoms and severe diarrhea were successfully controlled following FMT. Her stool output markedly declined after 7 days and normalized 16 days after FMT. A significant modification in her microbiota composition was consistently seen, characterized by a profound enrichment of the commensals in Firmicutes and depletion of opportunistic organisms in Proteobacteria. Furthermore, we identified a reconstituted bacterial community enriched in Firmicutes and depleted of Proteobacteria members that was associated with fecal output, plasma markers of inflammation and T helper cells. Conclusions: In this report, we describe our initial experience with FMT, in which we successfully used it in the treatment of a patient with sepsis and severe diarrhea after a vagotomy. Our data indicate an association between repaired intestinal microbiota barrier and improvement of clinical outcomes. Our patient’s surprising clinical benefits from FMT demonstrate the role of intestinal microbiota in modulating immune equilibrium. It represents a breakthrough in the clinical management of sepsis and suggests new therapeutic avenues to pursue for microbiota-related indications.

Background: Macrophage polarization represents a promising therapeutic target for inflammatory bowel disease (IBD). This study investigates the role of miRNA-223 (miR-223) in dextran sodium sulfate (DSS)-induced colitis and its regulation of macrophage polarization.Methods: Male C57BL/6 mice were assigned to four groups: Wild-type (WT) control, DSS-treated group (DSS), DSS+miR-223 agomir (DSS+A), and DSS+ miR-223 agomir negative control (DSS+NC). Colitis was induced with 2.5% DSS for 7 days; miR-223 agomir or NC was administered intraperitoneally on days 2–4. We evaluated disease activity index (DAI), colonic inflammation, and the expression of inflammatory mediators, peroxisome proliferator-activated receptor gamma (PPAR-γ) and forkhead box transcription factor O1 (FOXO1). Results: Histopathological analysis showed that miR-223 agomir significantly attenuated DSS-induced colon damage. Proinflammatory cytokines (TNF-α, IL-1β, IL-6) increased in DSS mice, while anti-inflammatory IL-10 decreased—trends reversed by miR-223 supplementation at mRNA/protein levels. Mechanistically, DSS elevated M1 macrophage marker iNOS and FOXO1 but reduced M2 marker Arg-1 and PPAR-γ. miR-223 agomir suppressed M1 polarization while enhancing M2 polarization by downregulating FOXO1 and upregulating PPAR-γ. Conclusion: We identify a novel dual-regulatory mechanism wherein miR-223 ameliorates colitis by shifting macrophage polarization from M1 to M2 via concurrent FOXO1 suppression and PPAR-γ activation. These findings establish a mechanistic basis for miR-223 supplementation as a novel IBD therapeutic strategy.

Background: Anastomotic leakage is a major colorectal surgical complication that may be exacerbated by perioperative inflammatory stress. How transcriptomic profiles and tissue-adherent microbiota change under such stress, and whether postoperative inulin supplementation is associated with microbiota changes and improved healing after inflammatory priming, remain unclear. Methods: Two independent animal experiments were conducted. Experiment 1 compared control (CON) and LPS-primed mice using scheduled, repeated-cross-sectional sampling for microbiota profiling on POD0, 1, 3, 5, 7, and 14 and for RNA-seq on POD0, 1, 3, 5, and 7. Experiment 2 used the same murine colonic anastomosis model to evaluate postoperative exclusive enteral nutrition (EEN) with or without inulin supplementation (dietary fiber, DF) in a 2 × 2 factorial design comprising CON, CON-DF, LPS, and LPS-DF groups. Healing was assessed by survival, recovery scores, anastomotic burst pressure, histology, immunostaining, and short-chain-fatty-acid quantification. Within Experiment 2, a dedicated n = 10/group survival/longitudinal cohort was followed through POD5, and a separate terminal cohort provided six surviving mice/group for POD5 assessments; five microscopy fields were averaged within each mouse. Results: LPS priming impaired healing and induced niche-specific microbiota alterations with altered bacterial microspatial patterns at the suture line. DF supplementation was associated with improved recovery and anastomotic strength, reduced inflammatory infiltration, increased proliferation, decreased apoptosis, and altered inflammatory- and repair-associated immune markers. The planned LPS-DF versus LPS survival comparison in the POD5 four-group cohort was not significant after multiplicity correction. At POD5, DF was associated with lower Shannon diversity and an altered short-chain-fatty-acid profile, including higher acetate; the LPS × inulin interactions for these measures were not significant. Conclusion: Brief postoperative inulin-supplemented EEN improved anastomotic healing following inflammatory priming, concurrent with microbiota remodeling and short-chain-fatty-acid differences, including higher acetate. These concurrent changes do not establish microbiota- or SCFA-mediated causality.