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Biology subjects

Basson, A. R.

Publications and source records attributed to Basson, A. R..

4 recordsLinked to original sources

Mesaconic acid delivery via biomaterials and engineered probiotics to the gut reduces inflammation in Crohn's Diseases mouse models

Mesaconate (MES, an immunosuppressive metabolite) but not itaconate is upregulated in stool of Crohns Disease (CD) patients, albeit below therapeutic levels.. However, colonic MES level is difficult to maintain because of its high absorption rate, limiting its therapeutic potential for CD. Herein, we developed two strategies that elevate MES level and suppress inflammation: EcN-CAD, an engineered probiotic Escherichia coli Nissle 1917 (EcN) that overexpresses cis-aconitate decarboxylase (CAD, produces itaconic acid that is converted to MES); and MES+Zn, a Zinc-MES ionically crosslinked formulation. Mechanistically, MES modulates T cell function by downregulating glycolytic and mitochondrial activity and decrease ROR{gamma}t expression. In preclinical SAMP1/YitFC dexamethasone-withdrawal model and TNFDARE model, MES+Zn decreased gut permeability significantly compared to controls and reduced myeloperoxidase (MPO, an inflammatory marker) 1000-fold compared to controls. EcN-CAD probiotics decreased ROR{gamma}t expression in CD4+ and CD8+ T cells, gut permeability and inflammation in preventive SAMP1/YitFC model, and SAMP1/YitFC dexamethasone-withdrawal model. Overall, MES rewires T cell responses and technologies that enhance MES levels can be effective in gut-related inflammatory diseases.

immunology↗

Clonal Parabacteroides from Gut Microfistulous Tracts as Transmissible Cytotoxic Succinate-Commensal Model of Crohn's Disease Complications

Crohns disease (CD) has been traditionally viewed as a chronic inflammatory disease that cause gut wall thickening and complications, including fistulas, by mechanisms not understood. By focusing on Parabacteroides distasonis (presumed modern succinate-producing commensal probiotic), recovered from intestinal microfistulous tracts (cavernous fistulous micropathologies CavFT proposed as intermediate between mucosal fissures and fistulas) in two patients that required surgery to remove CD-damaged ilea, we demonstrate that such isolates exert pathogenic/pathobiont roles in mouse models of CD. Our isolates are clonally-related; potentially emerging as transmissible in the community and mice; proinflammatory and adapted to the ileum of germ-free mice prone to CD-like ileitis (SAMP1/YitFc) but not healthy mice (C57BL/6J), and cytotoxic/ATP-depleting to HoxB8-immortalized bone marrow derived myeloid cells from SAMP1/YitFc mice when concurrently exposed to succinate and extracts from CavFT-derived E. coli, but not to cells from healthy mice. With unique genomic features supporting recent genetic exchange with Bacteroides fragilis-BGF539, evidence of international presence in primarily human metagenome databases, these CavFT Pdis isolates could represent to a new opportunistic Parabacteroides species, or subspecies ( cavitamuralis) adapted to microfistulous niches in CD.

genomics↗

Patterns of 'Analytical Irreproducibility' in Multimodal Diseases

Multimodal diseases are those in which affected individuals can be divided into subtypes (or data modes); for instance, mild vs. severe, based on (unknown) modifiers of disease severity. Studies have shown that despite the inclusion of a large number of subjects, the causal role of the microbiome in human diseases remains uncertain. The role of the microbiome in multimodal diseases has been studied in animals; however, findings are often deemed irreproducible, or unreasonably biased, with pathogenic roles in 95% of reports. As a solution to repeatability, investigators have been told to seek funds to increase the number of human-microbiome donors (N) to increase the reproducibility of animal studies (doi:10.1016/j.cell.2019.12.025). Herein, through simulations, we illustrate that increasing N will not uniformly/universally enable the identification of consistent statistical differences (patterns of analytical irreproducibility), due to random sampling from a population with ample variability in disease and the presence of disease data subtypes (or modes). We also found that studies do not use cluster statistics when needed (97.4%, 37/38, 95%CI=86.5,99.5), and that scientists who increased N, concurrently reduced the number of mice/donor (y=-0.21x, R2=0.24; and vice versa), indicating that statistically, scientists replace the disease variance in mice by the variance of human disease. Instead of assuming that increasing N will solve reproducibility and identify clinically-predictive findings on causality, we propose the visualization of data distribution using kernel-density-violin plots (rarely used in rodent studies; 0%, 0/38, 95%CI=6.9e-18,9.1) to identify disease data subtypes to self-correct, guide and promote the personalized investigation of disease subtype mechanisms. HighlightsO_LIMultimodal diseases are those in which affected individuals can be divided into subtypes (or data modes); for instance, mild vs. severe, based on (unknown) modifiers of disease severity. C_LIO_LIThe role of the microbiome in multimodal diseases has been studied in animals; however, findings are often deemed irreproducible, or unreasonably biased, with pathogenic roles in 95% of reports. C_LIO_LIAs a solution to repeatably, investigators have been told to seek funds to increase the number of human-microbiome donors (N) to increase the reproducibility of animal studies. C_LIO_LIHerein, we illustrate that although increasing N could help identify statistical effects (patterns of analytical irreproducibility), clinically-relevant information will not always be identified. C_LIO_LIDepending on which diseases need to be compared, random sampling alone leads to reproducible patterns of analytical irreproducibility in multimodal disease simulations. C_LIO_LIInstead of solely increasing N, we illustrate how disease multimodality could be understood, visualized and used to guide the study of diseases by selecting and focusing on disease modes. C_LI

microbiology↗

Understanding artificial mouse-microbiome heterogeneity and six actionable themes to increase study power

The negative effects of data clustering due to (intra-class/spatial) correlations are well-known in statistics to interfere with interpretation and study power. Therefore, it is unclear why housing many laboratory mice ([≥]4), instead of one-or-two per cage, with the improper use/reporting of clustered-data statistics, abound in the literature. Among other sources of artificial confounding, including cyclical oscillations of the cage microbiome, we quantified the heterogeneity of modern husbandry practices/perceptions. The objective was to identify actionable themes to re-launch emerging protocols and intuitive statistical strategies to increase study power. Amenable for interventions, cost-vs-science discordance was a major aspect explaining heterogeneity and the reluctance to change. Combined, four sources of information (scoping-reviews, professional-surveys, expert-opinion, and implementability-score-statistics) indicate that a six-actionable-theme framework could minimize artificial heterogeneity. With a Housing Density Cost Simulator in Excel and fully annotated statistical examples, this framework could reignite the use of study power to monitor the success/reproducibility of mouse-microbiome studies.

scientific communication and education↗