Browsing by Person "Schmidt, Nina S."

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Contamination-controlled upper gastrointestinal microbiota profiling reveals salivary-duodenal community types linked to opportunistic pathogen carriage and inflammation
(2025) Schmidt, Nina S.; Dörner, Elisabeth; Podlesny, Daniel; Bohlhammer, Elisabeth; Bubeck, Alena M.; Ruple, Hannah K.; Tetzlaff-Lelleck, Vivian; Sina, Christian; Schmidt, Herbert; Fricke, Florian W.
The upper gastrointestinal (uGI) microbiota has been implicated in infectious, metabolic, and immunological conditions, yet remains poorly characterized due to invasive sampling and low microbial biomass. We developed and validated a contamination-controlled 16S rRNA gene and transcript-based protocol to profile the murine and human uGI microbiota from low-biomass samples. We applied this protocol to murine esophageal, gastric, and duodenal tissues, and to human saliva, gastric, and duodenal aspirates from patients undergoing endoscopy for suspected food-related, mild GI symptoms. Our objective was to identify conserved compositional and structural uGI microbiota patterns and assess their clinical relevance in relation to pathogen burden and inflammation. In mice, we found evidence for transcriptionally inactive and active intestinal taxa along the uGI tract, supporting horizontal microbiota transfer. In humans, we identified two distinct, inversely correlated salivary microbiota types – one dominated by the Prevotella 7 genus – which were conserved in the duodenum. The Prevotella 7-dominated uGI microbiota type was associated with lower relative abundances of gastrointestinal and extraintestinal opportunistic pathogens. These patterns were reproducible in an independent cohort and associated with lower systemic TNF-α levels. Our findings suggest that noninvasive salivary microbiota profiling can stratify individuals based on uGI microbiota composition and inflammation-associated risk traits, offering new opportunities for clinical applications and translational studie
The gut microbiota predicts and time-restricted feeding delays experimental colitis
(2025) Ruple, Hannah K.; Haasis, Eva; Bettenburg, Anna; Maier, Carina; Fritz, Carolin; Schüle, Laura; Löcker, Sarah; Soltow, Yvonne; Schintgen, Lynn; Schmidt, Nina S.; Schneider, Celine; Lorentz, Alex; Fricke, W. Florian
The etiology of inflammatory bowel disease (IBD) remains unclear, treatment options unsatisfactory and disease development difficult to predict for individual patients. Dysbiosis of the gastrointestinal microbiota and disruption of the biological clock have been implicated and studied as diagnostic and therapeutic targets. Here, we examine the relationship of IBD to biological clock and gut microbiota by using the IL-10 deficient (IL-10-/-) mouse model for microbiota-dependent spontaneous colitis in combination with altered (4 h/4 h) light/dark cycles to disrupt and time-restricted feeding (TRF) to restore circadian rhythmicity. We show that while altered light/dark cycles disrupted the intestinal clock in wild type (WT) mice, IL-10-/- mice were characterized by altered microbiota composition, impaired intestinal clock, and microbiota rhythmicity irrespective of external clock disruption, which had no consistent colitis-promoting effect on IL-10-/- mice. TRF delayed colitis onset reduced the expression of inflammatory markers and increased the expression of clock genes in the intestine, and increased gut microbiota rhythmicity in IL-10-/- mice. Compositional changes and reduced rhythmicity of the fecal microbiota preceded colitis and could predict colitis symptoms for individual IL-10-/- mice across different experiments. Our findings provide perspectives for new diagnostic and TRF-based, therapeutic applications in IBD that should be further explored.