Search bioRxiv⌕ Search

Biology subjects

Kleigrewe, K.

Publications and source records attributed to Kleigrewe, K..

At least 19 recordsLinked to original sources

Post-Weaning Gut Microbiota Colonization Reveals Divergent Recovery of Skeletal Muscle and Peripheral Nerves

We previously demonstrated that the absence of a complex gut microbiota (CGM) impairs the postnatal development of peripheral nerves and motor targets in germ-free (GF) mice. In this study, we investigated whether establishing a complex gut microbiota after weaning could reverse these developmental alterations. To address this question, GF mice were colonized with a complex gut microbiota by co-housing with conventionally raised mice. Microbiota composition, peripheral nerve morphology and transcriptional profiles, skeletal muscle proteome, neuromuscular junction architecture and circulating metabolites were comprehensively analyzed and compared with those of GF, gnotobiotic OMM12 and CGM mice. Post-weaning colonization partially restored microbial diversity and resulted in a compositionally distinct microbial community with reduced alpha diversity and enrichment of Duncaniella muris strain B8. Despite successful microbial colonization, peripheral nerve abnormalities persisted, including axon hypermyelination, transcriptional alterations in sciatic nerves, elongated nodes of Ranvier, and dysregulated axon-glia interactions. In contrast, skeletal muscle defects were largely rescued, with restoration of muscle mass, normalization of proteomic profiles, recovery of metabolic and structural pathways, and reduced fragmentation of the postsynaptic neuromuscular junction, although presynaptic abnormalities persisted. These findings demonstrate that microbiota-dependent developmental alterations differ markedly in their reversibility across the neuromuscular system. Specifically, post-weaning colonization with a complex gut microbiota resulted in broad recovery of skeletal muscle but failed to rescue peripheral nerve abnormalities. Our findings provide a framework for future studies investigating how the timing of microbial colonization, microbiota composition, and microbiota-derived signals influence the reversibility of microbiota-dependent neuromuscular alterations.

neuroscience↗

Distinct colorectal cancer genotypes shape microbial ecosystems and reveal stage-specific microbiota dependencies

The gut microbiota has emerged as an important modifier of colorectal cancer (CRC), yet how tumor genotype influences host-microbiota interactions and whether microbial signals are required throughout tumor progression remain unclear. Here, we combined genetically engineered mouse models, microbial multi-omics and a germ-free-compatible orthotopic transplantation system to define the functional contribution of the microbiota across distinct stages of CRC evolution. Across multiple CRC genotypes, we identified tumor-associated microbial ecosystem states characterized by distinct taxonomic, functional and metabolic configurations. To directly test their contribution to tumor progression, we established the first orthotopic CRC transplantation platform compatible with long-term experimentation in germ-free mice, enabling side-by-side comparison of genetically identical tumors in the presence or absence of microbiota. Using organoids spanning low-grade adenoma, high-grade adenoma and adenocarcinoma states, we found that the dependence on the presence of microbiota progressively decreases during malignant evolution. Whereas adenoma-derived organoids exhibited profound dependence on microbial exposure and failed or were markedly impaired in establishing tumors under germ-free conditions, adenocarcinoma organoids engrafted and metastasized in both germ-free and specific pathogen-free (SPF) hosts. Unexpectedly, comprehensive histological, immunological and transcriptomic analyses revealed highly similar tumor ecosystem states in advanced tumors arising under both microbial conditions, arguing against broad immune or epithelial defects as a primary explanation for the observed phenotype. Together, our findings demonstrate that distinct oncogenic drivers establish specific microbial ecosystem states and reveal a stage-dependent role of the microbiota during colorectal tumorigenesis. Whereas microbial signals are critical during early stages of tumor progression and may promote malignant transformation, advanced tumors progressively acquire microbiota-independent growth programs and increasingly impose genotype-specific ecological signatures on the surrounding microbial ecosystem. More broadly, we establish a versatile framework for the causal dissection of tumor-microbiota interactions in cancer.

cancer biology↗

A microbial metabolite protects against graft-versus-host disease via mTORC1 and STING-dependent intestinal regeneration

Changes in the intestinal microbiome and microbiota-derived metabolites predict clinical outcomes after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Here, we report that desaminotyrosine (DAT), a product of bacterial flavonoid metabolism, correlates with improved overall survival and reduced relapse rates in allo-HSCT patients. In preclinical mouse models, treatment with synthetic DAT prevents graft-versus-host disease by protecting the intestinal barrier and promoting intestinal regeneration and contributes to graft-vs.-leukemia responses. DATs beneficial effects on intestinal regeneration remain effective despite broad-spectrum antibiotics-induced dysbiosis, also when administered by fecal microbiota transfer with flavonoid-degrading F. plautii. Mechanistically, DAT promotes mTORC1-dependent activation and proliferation of intestinal stem cells, with concomitant engagement of the innate immune receptor STING required to mitigate metabolic stress and maintain an undifferentiated stem cell state independently of type-I interferon responses. Additionally, DAT can skew T cells towards an effector phenotype to modulate graft-versus-leukemia responses. Our data uncover DATs dual, tissue- and immune-modulating properties and underscore its potential in precision microbiome-based therapies to improve tissue regeneration and minimize immune-mediated side effects.

immunology↗

Microbial metabolite-guided CAR T cell engineering enhances anti-tumor immunity via epigenetic-metabolic crosstalk

The microbiome is a complex host factor and key determinant of the outcome of antibody-based and cellular immunotherapy. Its postbiotics are a blend of soluble commensal byproducts that are released into the host environment and have been associated with the regulation of immune homeostasis, particularly through impacts on epigenetics and cell signaling. In this study, we show that the postbiotic pentanoate is metabolized to citrate within the TCA cycle via both the acetyl- and succinyl-CoA entry points, a feature uniquely enabled by the chemical structure of the C5 aliphatic chain. We identified ATP-citrate lyase as the crucial factor that redirects pentanoate-derived citrate from the succinyl-CoA route to the nucleus, thereby linking metabolic output and histone acetylation. This epigenetic-metabolic crosstalk mitigated T cell exhaustion and promoted naive-like differentiation in pentanoate-programmed chimeric antigen receptor (CAR) T cells. The predictive and therapeutic potential of pentanoate was corroborated in two independent patient cohorts and three syngeneic models of CAR T adoptive therapy. Our data demonstrate that postbiotics are integrated into mitochondrial metabolism and subsequently incorporated as epigenetic imprints. This bridge between microbial and mammalian interspecies communication can ultimately impact T cell differentiation and efficacy.

immunology↗

Dietary fiber intervention modulates the formation of the cardiovascular risk factor trimethylamine-N-oxide after beef consumption

The gut-microbiota-dependent metabolite trimethylamine-N-oxide (TMAO) has emerged as a potential risk factor for cardiovascular disease (CVD). Conversely, dietary fiber has been associated with a reduced risk of CVD and been proposed to exhibit beneficial effects on gut health. Considering these associations, we conducted an intervention study to investigate the influence of fiber supplementation on intestinal TMAO formation and its response after beef consumption. Our randomized, double blind, pilot study MEATMARK included thirteen volunteers who underwent a dietary fiber and placebo intervention over two weeks. We assessed the effect of fiber supplementation on the gut microbiota and expression of the enzyme cutC, a key enzyme for microbial TMA formation, a precursor for TMAO. We measured the TMAO response following beef consumption after the two-week intervention. We further investigated the impact of three human single nucleotide polymorphisms (SNPs) in the expression of the hepatic enzyme FMO3 on TMAO plasma levels, as this factor is responsible for the final oxidation step from TMA to TMAO. Our findings indicate that dietary fiber supplementation attenuated TMAO formation after beef intake, particularly in participants with habitual lower daily meat consumption. Furthermore, we observed a significant downregulation of cutC expression in response to the fiber intervention, suggesting a potential mechanism to reduce plasma TMAO. Considering these findings, a high fiber, low meat diet presents a promising dietary strategy for reducing this CVD risk factor. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/602621v1_ufig1.gif" ALT="Figure 1"> View larger version (77K): org.highwire.dtl.DTLVardef@1f8fd4eorg.highwire.dtl.DTLVardef@1be2baborg.highwire.dtl.DTLVardef@24fae8org.highwire.dtl.DTLVardef@1d4cac2_HPS_FORMAT_FIGEXP M_FIG C_FIG

physiology↗

Microbiota metabolized Bile Acids accelerate Gastroesophageal Adenocarcinoma via FXR inhibition

BackgroundThe incidence of Barrett esophagus (BE) and Gastroesophageal Adenocarcinoma (GEAC) correlates with obesity and a diet rich in fat. Bile acids (BA) support fat digestion and undergo microbial metabolization in the gut. The farnesoid X receptor (FXR) is an important modulator of the BA homeostasis. The capacity of inhibiting cancer-related processes when activated, make FXR an appealing therapeutic target. In this work, we assess the role of diet on the microbiota-BA axis and evaluate the role of FXR in disease progression. ResultsHere we show that high fat diet (HFD) accelerated tumorigenesis in L2-IL1B mice (BE- and GEAC- mouse model) while increasing BA levels and enriching gut microbiota that convert primary to secondary BA. While upregulated in BE, expression of FXR was downregulated in GEAC in mice and humans. In L2-IL1B mice, FXR knockout enhanced the dysplastic phenotype and increased Lgr5 progenitor cell numbers. Treatment of murine organoids and L2-IL1B mice with the FXR agonist obeticholic acid (OCA) deacelerated GEAC progression. ConclusionWe provide a novel concept of GEAC carcinogenesis being accelerated via the diet-microbiome-metabolome axis and FXR inhibition on progenitor cells. Further, FXR activation protected with OCA ameliorated the phenotype in vitro and in vivo, suggesting that FXR agonists have potential as differentiation therapy in GEAC prevention. Statement of significanceIf its inhibition is linked to disease progression and its activation to cancer prevention, exploring the potential of FXR as a therapeutic target has great clinical relevance in GEAC context.

cancer biology↗

Sex-specific fear acquisition following early life stress is linked to amygdala glutamate metabolism

Early life stress (ELS) adversely affects physiological and behavioral outcomes, increasing the vulnerability to stress-related disorders, such as post-traumatic stress disorder (PTSD). PTSD prevalence is significantly higher in women and is partially mediated by genetic risk variants. Understanding how sex influences the interaction of PTSD risk genes, such as FKBP5, with trauma-related behaviors is crucial for uncovering PTSDs neurobiological pathways. The development of in-depth behavioral analysis tools using unsupervised behavioral classification is thereby a crucial tool to increase the understanding of the behavioral outcomes related to stress-induced fear memory formation. The current study investigates the sex-specific effects of ELS exposure by using the limited bedding and nesting (LBN) paradigm. The LBN exposure disrupted different facets of the hypothalamic-pituitary-adrenal (HPA) axis in a sex-specific manner directly after stress and at adult age. Moreover, freezing was altered by LBN exposure in both the acquisition and the retrieval of fear in a sex-dependent manner. Unsupervised behavioral analysis revealed a higher active fear response after LBN exposure during fear acquisition in females, but not in males. The regulation of the HPA axis is closely intertwined with cellular metabolism and core regulatory cascades. To investigate the impact of LBN exposure on tissue-specific metabolism, a metabolomic pathway analysis in the basolateral amygdala revealed a specific sex- and stress-dependent effect on purine, pyrimidine, and glutamate metabolism. The present study highlights the intricate interplay between metabolic pathways and the neurobiological substrates implicated in fear memory formation and stress regulation. Overall, these findings highlight the importance of considering sex-specific metabolic alterations in understanding the neurobiological mechanisms underlying stress-related disorders and offer potential avenues for targeted interventions.

animal behavior and cognition↗

Diurnal rhythmicity of fecal microbiota and metabolite profiles in the first year of life: a randomized controlled interventional trial with infant formula

Microbiota assembly in the infant gut is influenced by time and duration of dietary exposure to breast-milk, infant formula and solid foods. In this randomized controlled intervention study, longitudinal sampling of infant stool (n=998) showed similar development of fecal bacterial communities (16S rRNA/shallow metagenomics sequencing) between formula- and breast-fed infants during the first year of life (N=210). Infant formula supplemented with galacto-oligosaccharides (GOS) was most efficient to sustain high levels of bifidobacteria compared to formula containing B. longum and B. breve or placebo. In addition to primary endpoints, metabolite and bacterial profiling revealed 24-hour oscillations and data integration identified circadian networks. Rhythmicity in bacterial diversity, specific taxa and functional pathways increased with age and was strongest following breast-feeding and GOS-supplementation. Circadian rhythms in dominant taxa were discovered ex-vivo in a chemostat model. Hence, microbiota rhythmicity develops early in life, likely via bacterial intrinsic clock mechanism and is affected by diet.

microbiology↗

Untargeted metabolomics reveals PTI-associated metabolites in cultivated tomato

Plants employ a multi-layered innate immune system to detect and fend off invading fungal pathogens. In one such layer, recognition of Pathogen- or Microbe-Associated Molecular Patterns or elicitors, triggers a signaling cascade that leads to defence against the pathogen and ultimately Pattern-Triggered Immunity (PTI). Secondary Metabolites (SMs) are expected to play an important role in this kind of resistance, because they are potentially mycotoxic compounds. Tomato plants inoculated with Alternaria solani show clear symptoms of infection 5 days after inoculation. Whereas plants inoculated with Alternaria alternata remain symptomless. We hypothesized that pattern-triggered induction of resistance-related metabolites in Solanum lycopersicum contribute to the resistance against A. alternata, yet such SMs are suppressed in a compatible interaction. We compared the metabolomic profile (metabolome) of S. lycopersicum at two time points (3 and 24 hours) after treatments with A. alternata, A. solani and the fungal elicitor chitin and identified SMs that are involved in the early defence response of tomato plants. Our study revealed differential metabolome fingerprints and shows that the molecular composition of A. alternata and chitin-induced indeed show larger overlap with each other than with the A. solani-induced metabolome. We identify 65 candidate metabolites possibly associated with pattern-triggered resistance in tomato plants, including the alkaloid, trigonelline, for which we can confirm that it inhibits fungal growth in vitro when supplied at physiological concentrations. Our findings show that a true, pattern-triggered, chemical defence is mounted against A. alternata and that it contains mycotoxin compounds previously unidentified in tomato, that could be interesting for future crop protection strategies.

plant biology↗

The Intestinal Clock Regulates Host Metabolism through the Fiber-Dependent Microbiome and Macronutrient Transcriptome.

Circadian disruption, e.g. through shift work, causes microbial dysbiosis and increases the risk of metabolic diseases. Microbial rhythmicity in mice depends on a functional intestinal clock and frequent jetlag as well as high-caloric energy intake induces loss of these oscillations. Similarly, arrhythmic microbiota was found in obese and T2D populations. However, the interplay between the intestinal circadian clock, the microbiome, diet and host metabolism is poorly understood. In intestinal-specific Bmal1 knockout mice (Bmal1IEC-/-) we demonstrate the relevance of the intestinal clock in microbiome oscillations and host and microbial nutrient metabolism. Microbiota transfer from Bmal1IEC-/- mice into germ-free recipients led to obesity, reflected by increased bodyweight and fat mass. Western diet-fed Bmal1IEC-/- mice increased bodyweight likely through mechanisms involving the intestinal clock-control of lipid and hexose transporters. Additionally, we identified dietary fiber as novel link between circadian microbial rhythmicity, intestinal clock functioning and host physiology. Thus, revealing the potential of fiber-rich diet intervention as a non-invasive strategy targeting microbial oscillations in metabolic disease prevention.

molecular biology↗

Secondary bile acid production by gut bacteria promotes Western diet-associated colorectal cancer

Western diet is an important risk factor for the development of sporadic colorectal cancer (CRC). Dietary fat stimulates bile acid (BA) production by the host and their conversion to secondary BAs by 7-dehydroxylating (7DH+) bacteria, but causal proof of their tumor-promoting effects in vivo is lacking. To address this, we performed feeding studies in a genetically engineered pig model of CRC combined with multi-omics analyses and gnotobiotic mouse studies. Western diet worsened the disease phenotype in APC1311/+ pigs. This was accompanied by microbiota changes, increased levels of the secondary bile acid deoxycholic acid (DCA), and higher colonic epithelial cell proliferation. The latter was counteracted by using the BA-scavenging drug colestyramine. Metagenomic analysis across multiple cohorts revealed higher occurrence of bai (BA inducible) operons from Clostridium scindens and close relatives in stool of CRC subjects (n = 1,034). Using two gnotobiotic mouse models of CRC, we demonstrate that colonization with 7DH+ bacteria (C. scindens or Extibacter muris) increased colonic tumor loads. This work provides clear evidence for the causal role of microbiome-derived DCA production in CRC under detrimental dietary conditions, opening avenues for future preventive strategies.

microbiology↗

Targeting the intestinal circadian clock by meal timing ameliorates gastrointestinal inflammation

ObjectiveImpaired clock genes expression has been observed in biopsy samples from patients with inflammatory bowel disease (IBD). Disruption of circadian rhythms, which occurs in shift workers, has been linked to an increased risk of gastrointestinal diseases, including IBD. The intestinal clock balances gastrointestinal homeostasis by regulating the microbiome. Here we characterize intestinal immune functions in mice lacking the intestinal clock and IBD-relevant mouse model under different feeding conditions to describe the functional impact of the intestinal clock in the development of gastrointestinal inflammation. DesignTissues and fecal samples from intestinal clock-deficient mice (Bmal1IEC-/-) and mouse models for colitis (IL-10-/-, Bmal1IEC-/-xIL-10-/-, dextran sulfate sodium (DSS) administration) under ad libitum and restricted feeding (RF) conditions were used to determine the causal role of the intestinal clock for colitis. ResultsIn IL-10-/- mice, inflammation correlated with disrupted colon clock genes expression. Genetic loss of intestinal clock functions promoted DSS and IBD inflammatory phenotypes and dramatically reduces survival, and colonization with disease-associated microbiota in germ- free Bmal1IEC-/- hosts increased their inflammatory responses, demonstrating the causal role of colonic clock disruption and the severity of IBD. RF in IL-10-/- mice restored the colon clock and related immune functions, improved the inflammatory responses and rescued the histopathological phenotype. In contrast, RF failed to improve IBD symptoms in Bmal1IEC-/- xIL-10-/- demonstrating the significance of the colonic clock to gate the effect of RF. ConclusionWe provide evidence that inflammation-associated intestinal clock dysfunction triggers host immune imbalance and promotes the development and progression of IBD-like colitis. Enhancing intestinal clock function by RF modulates the pathogenesis of IBD and thus could become a novel strategy to ameliorate the symptoms in IBD patients.

physiology↗

Skeletal muscle hypertrophy rewires glucose metabolism in mice: an experimental investigation and systematic review

BackgroundProliferating cancer cells shift their metabolism toward glycolysis even in the presence of oxygen to especially generate glycolytic intermediates as substrates for anabolic reactions. We hypothesize that a similar metabolic remodeling occurs during skeletal muscle hypertrophy. MethodsWe used mass spectrometry in hypertrophying C2C12 myotubes in vitro and plantaris mice muscle in vivo and assessed metabolomic changes and the incorporation of [U-13C6]glucose tracer. We performed enzyme inhibition of the key serine synthesis pathway enzyme phosphoglycerate dehydrogenase (Phgdh) for further mechanistic analysis and conducted a systematic review to align any changes in metabolomics during muscle growth with published findings. Finally, UK Biobank was used to link the findings to population level. ResultsThe metabolomics analysis in myotubes revealed IGF-1 induced altered metabolite concentrations in anabolic pathways such as in the pentose phosphate (ribose-5-phosphate/ribulose-5-phosphate: +40%; p=0.01) and serine synthesis pathway (serine: - 36.8%; p=0.009). Like the hypertrophy-stimulation with IGF-1 in myotubes in vitro, the concentration of the dipeptide L-carnosine was decreased by 26.6% (p=0.001) during skeletal muscle growth in vivo. However, phosphorylated sugar (glucose-6-phosphate, fructose-6-phosphate or glucose-1-phosphate) decreased by 32.2% (p=0.004) in the overloaded muscle in vivo, while increased in the IGF-1 stimulated myotubes in vitro. The systematic review revealed that 10 metabolites linked to muscle hypertrophy were directly associated with glycolysis and its interconnected anabolic pathways. We demonstrated that labelled carbon from [U-13C6]glucose is increasingly incorporated by [~]13% (p=0.001) into the non-essential amino acids in hypertrophying myotubes, which is accompanied by an increased depletion of media serine (p=0.006). The inhibition of Phgdh suppressed muscle protein synthesis in growing myotubes by 58.1% (p<0.001) highlighting the importance of the serine synthesis pathway for maintaining muscle size. Utilizing data from the UK Biobank (n=450,243), we then discerned genetic variations linked to the serine synthesis pathway (PHGDH and PSPH) and to its downstream enzyme (SHMT1), revealing their association with appendicular lean mass in humans (p<5.0e-8). ConclusionUnderstanding the mechanisms that regulates skeletal muscle mass will help in developing effective treatments against muscle weakness. Our results provide evidence for metabolic rewiring of glycolytic intermediates into anabolic pathways during muscle growth, such as in the serine synthesis.

molecular biology↗

Nutritional and host environments determine community ecology and keystone species in a synthetic gut bacterial community

Microbe-microbe interactions are critical for gut microbiome function. A challenging task to understand health and disease-related microbiome signatures is to move beyond descriptive community-level profiling towards disentangling microbial interaction networks. Here, we aimed to determine members taking on a keystone role in shaping community ecology of a widely used synthetic bacterial community (OMM12). Using single-species dropout communities and metabolomic profiling, we identified Bacteroides caecimuris I48, Blautia coccoides YL58 and Enterococcus faecalis KB1 as major drivers of in vitro community assembly and elucidated underlying mechanisms of these keystone functions. Importantly, keystone species and bacterial strain relationships were found to strongly vary across different nutritional conditions, depending on the strains potential to modify the corresponding environment. Further, gnotobiotic mice transplanted with communities lacking B. caecimuris I48 and B. coccoides YL58 exhibited morphological anomalies and altered intestinal metabolomic profiles, exposing physiologically relevant functions of these keystone community members. In summary, the presented study experimentally confirms the strong interdependency between bacterial community ecology and the biotic and abiotic environment, underlining the context-dependency and conditionality of bacterial interaction networks.

ecology↗

Bacteriophages targeting protective commensals impair resistance against Salmonella Typhimurium infection in gnotobiotic mice

Gut microbial communities protect the host against a variety of major human gastrointestinal pathogens. Bacteriophages (phages) are ubiquitous in nature and frequently ingested via food and drinking water. Moreover, they are an attractive tool for microbiome engineering due to the lack of known serious adverse effects on the host. However, the functional role of phages within the gastrointestinal microbiome remain poorly understood. Here, we investigated the effects of microbiota-directed phages on infection with the human enteric pathogen Salmonella enterica serovar Typhimurium (S. Tm), using a gnotobiotic mouse model (OMM12) for colonization resistance (CR). We show that phage cocktails targeting Escherichia coli and Enterococcus faecalis acted in a strain-specific manner. They transiently reduced the population density of their respective target before establishing coexistence for up to 9 days. Infection susceptibility to S. Tm was markedly increased at an early time point after phage challenge. Surprisingly, OMM12 mice were more susceptible 7 days after a single phage inoculation, when the targeted bacterial populations were back to pre-phage administration density. The presence of phages that dynamically modulates the density of protective members of the gut microbiota provides opportunities for invasion of bacterial pathogens.

microbiology↗

Genetic and environmental circadian disruption induce metabolic impairment through changes in the gut microbiome

ObjectiveInternal clocks time behavior and physiology, including the gut microbiome in a circadian ([~]24 h) manner. Mismatch between internal and external time, e.g. during shift work, disrupts circadian system coordination promoting the development of obesity and type 2 diabetes (T2D). Conversely, body weight changes induce microbiota dysbiosis. The relationship between circadian disruption and microbiota dysbiosis in metabolic diseases, however, remains largely unknown. MethodsCore and accessory clock gene expression in different gastrointestinal (GI) tissues were determined by qPCR in two different models of circadian disruption - mice with Bmal1 deficiency in the circadian pacemaker, the suprachiasmatic nucleus (Bmal1SCNfl/-), and wild-type mice exposed to simulated shift work (SSW). Body composition and energy balance were evaluated by nuclear magnetic resonance (NMR), bomb calorimetry, food intake and running-wheel activity. Intestinal permeability was measured in an Ussing chamber. Microbiota composition and functionality were evaluated by 16S rRNA gene amplicon sequencing, PICRUST2.0 analysis and targeted metabolomics. Finally, microbiota transfer was conducted to evaluate the functional impact of SSW-associated microbiota on the hosts physiology. ResultsBoth chronodisruption models show desynchronization within and between peripheral clocks in GI tissues and reduced microbial rhythmicity, in particular in taxa involved in short-chain fatty acid (SCFA) fermentation and lipid metabolism. In Bmal1SCNfl/- mice, loss of rhythmicity in microbial functioning associates with previously shown increased body weight, dysfunctional glucose homeostasis and adiposity. Similarly, we observe an increase in body weight in SSW mice. Germ-free colonization experiments with SSW- associated microbiota mechanistically link body weight gain to microbial changes. Moreover, alterations in expression of peripheral clock genes as well as clock-controlled genes (CCGs) relevant for metabolic functioning of the host were observed in recipients, indicating a bidirectional relationship between microbiota rhythmicity and peripheral clock regulation. ConclusionsCollectively, our data suggest that loss of rhythmicity in bacteria taxa and their products, which likely originates in desynchronization of intestinal clocks, promotes metabolic abnormalities during shift work.

physiology↗

The intestinal circadian clock drives microbial rhythmicity to maintain gastrointestinal homeostasis

Diurnal (i.e., 24-hour) oscillations of the gut microbiome have been described in various species including mice and humans. However, the driving force behind these rhythms remains less clear. In this study, we differentiate between endogenous and exogenous time cues driving microbial rhythms. Our results demonstrate that fecal microbial oscillations are maintained in mice kept in the absence of light, supporting a role of the hosts circadian system rather than representing a diurnal response to environmental changes. Intestinal epithelial cell-specific ablation of the core clock gene Bmal1 disrupts rhythmicity of microbiota. Targeted metabolomics functionally link intestinal clock-controlled bacteria to microbial-derived products, in particular branched-chain fatty acids and secondary bile acids. Microbiota transfer from intestinal clock-deficient mice into germ-free mice altered intestinal gene expression, enhanced lymphoid organ weights and suppressed immune cell recruitment. These results highlight the importance of functional intestinal clocks for circadian microbiota composition and function, which is required to balance the hosts gastrointestinal homeostasis.

physiology↗

Exploring the interaction network of a synthetic gut bacterial community

A key challenge in microbiome research is to predict functionality from microbial community composition. As central microbiota functions are determined by bacterial community networks it is important to gain insight into the principles that govern bacteria-bacteria interactions. Here, we focused on growth and metabolic interactions of the Oligo-Mouse-Microbiota (OMM12) synthetic bacterial community, which is increasingly used as model system in gut microbiome research. Using a bottom-up approach, we uncovered the directionality of strain-strain interactions in mono- and pairwise co-culture experiments, as well as in community batch culture. Metabolomics analysis of spent culture supernatant of individual strains in combination with genome-informed pathway reconstruction provided insights into the metabolic potential of the individual community members. Thereby, we could show that the OMM12 interaction network is shaped by both, exploitative and interference competition in vitro. In particular, Enterococcus faecalis KB1 was identified as important driver of community composition by affecting the abundance of several other consortium members. Together, this study gives fundamental insight into key drivers and mechanistic basis of the OMM12 interaction network, which serves as knowledge base for future mechanistic studies.

microbiology↗