Biology subjects

Jensen, B. A. H.

Publications and source records attributed to Jensen, B. A. H..

5 recordsLinked to original sources

bioRxiv2026

The intestinal immune response is influenced by nutritional-status and increased physical activity level

Beyond its role in digestion and barrier function, the intestine is an energy-responsive organ that actively regulates molecular metabolism. Whether and how lifestyle interventions regulate intestinal metabolism at both tissue and molecular levels remain unclear. Here, we show that both chronic exercise and dietary energy density drive robust, segment-specific intestinal remodeling. Voluntary wheel running in ad-libitum chow fed mice, induced elongation of the small intestine and colon, alongside pronounced, region-specific, transcriptional changes in the proximal, mid, and distal small intestine, particularly within immune and stress-related pathways. Caloric dilution diet also increased intestinal length in mice but elicited transcriptional adaptations, prominently in the proximal small intestine, directly linking energy density and intake to structural and molecular plasticity. In contrast, voluntary wheel running in control-fed and caloric-diluted-fed mice subtly modulated immune-associated gene expression, highlighting that diet and physical activity induce complementary and mechanistically distinct effects on the gut. We further identified an exercise-induced state of intestinal preconditioning. Upon refeeding, sedentary mice mounted robust, segment-specific activation of apoptotic, proliferative, and immune pathways. Similarly, acute treadmill exercise acted as a transient intestinal stressor in sedentary animals by shortening the length of the small intestine and rapidly activating epithelial stress, apoptosis, proliferation, and immune signaling. However, these responses were attenuated in chronically active mice despite higher basal expression of key genes, consistent with adaptive epithelial remodeling. The results suggest that habitual physical activity buffers acute nutritional stress and restrains excessive intestinal immune activation. Finally, translational plasma analyses in humans demonstrate that acute moderate-intensity exercise increases circulating markers of monocyte activation and epithelial stress, including CD14, IL-32, Reg-3-alpha and I-FABP, in both lean and obese individuals. Collectively, these findings suggest that the intestine plays a role as a metabolic organ that integrates energy-sensing signals from diet composition and physical activity.

immunology↗

bioRxiv2026

Saccharomyces boulardii attenuates obesity-associated inflammation and weight gain through coordinated gut ecosystem remodeling

The gut microbiome is a key regulator of metabolic homeostasis and contributes to obesity progression through effects on immune signaling, gut barrier integrity, and systemic inflammation. Microbiome-targeted strategies are therefore being explored as complementary approaches to conventional weight-loss therapies. Here, we investigated the probiotic yeast Saccharomyces boulardii in a murine model of diet-induced obesity (DIO) using an integrated multi-omics framework combining metabolic phenotyping, gut microbiome profiling, cecal metabolomics, colonic transcriptomics, and portal cytokine analysis. S. boulardii reduced food intake, attenuated weight gain, and increased energy expenditure without major changes in circulating metabolic hormone levels. Microbial diversity remained largely preserved, but selective enrichment of Bacteroidales lineages, including Muribaculaceae, was observed alongside functional remodeling of microbial pathways. Cecal metabolomics revealed increased B-vitamins, betaine, and GABA, with reduced stress-associated metabolites. Colonic transcriptomics showed attenuation of TNF/NF-{kappa}B signaling and enrichment of interferon and epithelial programs, while portal cytokine profiling indicated reduced inflammatory chemokines with trends toward increased IL-17A and IL-22. Integrated multi-omics analysis identified coordinated host-microbe interactions across metabolic, transcriptional, and immune layers. Collectively, these findings demonstrate that S. boulardii modulates the gut-immune-metabolic axis in obesity, supporting microbiome-based interventions as potential adjunct strategies targeting metabolic inflammation.

microbiology↗

bioRxiv2025

Dietary fibre promotes chronic whipworm infection through direct and time-dependent modulation of innate immunity

Dietary fibre regulates the microbiome and gut health but increases murine whipworm (Trichuris muris) infection through unclear mechanisms. We show that mice fed inulin-supplemented diets exhibit dysregulated innate antimicrobial defences and altered tryptophan metabolism during T. muris infection. Inhibiting tryptophan catabolism or neutralizing IL-27 and IL-18 in inulin-fed mice restored infection resistance. Notably, inulin led to chronic infection even in microbiota-depleted mice. Removing inulin within a critical immune development window rapidly restored anti-helminth immunity, indicating direct, time-dependent modulation of mucosal immune responses. Our findings reveal a previously unrecognized, direct influence of dietary fibre on mucosal immunity to parasitic infection, independent of the microbiome, highlighting the complex interplay between diet timing and host defence.

microbiology↗

bioRxiv2022

Experimental Diets Dictate the Metabolic Benefits of Lactobacillus Strains in Obesity

BackgroundGrowing evidence supports the use of probiotics to prevent or mitigate obesity-related dysmetabolism and non-alcoholic fatty liver disease (NAFLD). However, frequent reports of responders versus non-responders to probiotic treatment warrant a better understanding of key modifiers of host-microbe interactions. The influence of host diet on probiotic efficacy, in particular against metabolic diseases, remains elusive. MethodWe fed C57BL6/J mice a low fat reference diet or one of two energy-matched high fat and high sucrose diets for 12 weeks; a classical high fat diet (HFD) and a customized fast food-mimicking diet (FFMD). During the studies, mice fed either obesogenic diet were gavaged daily with one of two probiotic lactic acid bacteria (LAB) strains previously classified as Lactobaccillus, namely Limosilactobacillus reuteri (L. reuteri) or Lacticaseibacillus paracasei subsp. paracasei (L. paracasei), or vehicle. ResultsThe tested probiotics exhibited a reproducible efficacy but dichotomous response according to the obesogenic diets used. Indeed, L. paracasei prevented weight gain, improved insulin sensitivity, and protected against NAFLD development in mice fed HFD, but not FFMD. Conversely, L. reuteri improved glucoregulatory capacity, reduced NAFLD development, and increased distal gut bile acid levels associated with changes in predicted functions of the gut microbiota exclusively in the context of FFMD-feeding. ConclusionWe found that the probiotic efficacy of two LAB strains is highly dependent on experimental obesogenic diets. These findings highlight the need to carefully consider the confounding impact of diet in order to improve both the reproducibility of preclinical probiotic studies and their clinical research translatability. Graphical abstract O_FIG_DISPLAY_L [Figure 1] M_FIG_DISPLAY C_FIG_DISPLAY

microbiology↗

bioRxiv2019

Lysates of Methylococcus capsulatus Bath induce a lean-like microbiota, intestinal FoxP3+RORγt+IL-17+ Tregs and improve metabolism

Interactions between host and gut microbial communities may be modulated by diets and play pivotal roles in securing immunological homeostasis and health. Here we show that intake of feed based on whole-cell lysates of the non-commensal bacterium Methylococcus capsulatus Bath (McB) as protein source reversed high fat high sucrose-induced changes in the gut microbiota to a state resembling that of lean, low fat diet-fed mice, both under mild thermal stress (T22{degrees}C) and at thermoneutrality (T30{degrees}C). McB feeding selectively upregulated triple positive (Foxp3+ROR{gamma}t+IL-17+) regulatory T cells in the small intestine and colon, and enhanced mucus production and glycosylation status suggesting improved gut health. Mice receiving McB lysates further exhibited improved glucose regulation, reduced body and liver fat along with diminished hepatic immune infiltration. Collectively, these data points towards profound whole-body effects elicited by the McB lysate suggesting that it may serve as a potent modulator of immunometabolic homeostasis.

immunology↗