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McCormick, B. A.

Publications and source records attributed to McCormick, B. A..

5 recordsLinked to original sources

Analysis of gut bacterial communities leveraging AI methods unveils novel relations between species in Alzheimers disease

The gut microbiome has been increasingly implicated in Alzheimers disease (AD), with studies reporting numerous species- and genus-level differences. These findings established a growing catalog of AD-associated taxa, yet they typically evaluate taxa individually or in small sets rather than across microbial communities. Gut microorganisms act collectively through cross-feeding, competition, and metabolic exchange. Hence, jointly analyzing co-occurring species can reveal community structure and biological insights that a taxon-by-taxon analysis may miss. In 274 stool metagenomes from 119 older adults (18 with AD), we used our Alzheimers disease Analysis Model (ADAM) framework to run Latent Dirichlet Allocation (LDA) 1,000 times with other bioinformatics tools, decomposing species abundances into communities and aligning them into 22 reproducible ones. Of the 50 species that define these communities, 15 showed an AD-associated shift in relative abundance (10 depleted, 5 enriched; Cohens d from -0.91 to +0.67, each 95% CI excluding zero), spanning the depletion of Phocaeicola vulgatus (d - 0.91, 95% CI [-1.23, -0.59]) and the enrichment of Bacteroides fragilis (d +0.67, 95% CI [0.35, 0.99]), the two ends of an AD-associated balance. Separately, P. vulgatus competitively excludes its congener Phocaeicola dorei. In AlzBiom, an independent amyloid-defined cohort, the exclusion reproduced (within the Bacteroidaceae, r = -0.43 vs -0.57 in GAINS) and held in both control and AD participants, a conserved, disease-independent property. The P. vulgatus/B. fragilis balance also reproduced but more modestly (d = -0.24, permutation p = 0.038), whereas the substitution toward P. dorei did not. IMPORTANCEThe gut microbiome, the collection of bacteria living in the human gut, is organized into interacting communities whose members rise and fall together. Reading them jointly is more faithful but yields complex, high-dimensional patterns that standard analysis cannot resolve. Making sense of them means weighing how species move together, what they do, and what the literature reports, a task suited to artificial intelligence. We used our previously developed Alzheimers disease Analysis Model, an artificial intelligence framework customized here for species-community analysis, to integrate this evidence and turn patterns into biological findings. These findings are relationships, not single species, and they separate conserved ecology, shared with and without the disease, such as the competition between Phocaeicola vulgatus and its relatives, from shifts specific to Alzheimers disease. This keeps a general relationship from being mistaken for a disease marker, because the signal lies in the community, not in a single microbe.

microbiology↗

Microbiome functional gene pathways predict cognitive performance in older adults with Alzheimers disease

Disturbances in the gut microbiome is increasing correlated with neurodegenerative disorders, including Alzheimers Disease. The microbiome may in fact influence disease pathology in AD by triggering or potentiating systemic and neuroinflammation, thereby driving disease pathology along the "microbiota-gut-brain-axis". Currently, drivers of cognitive decline and symptomatic progression in AD remain unknown and understudied. Changes in gut microbiome composition may offer clues to potential systemic physiologic and neuropathologic changes that contribute to cognitive decline. Here, we recruited a cohort of 260 older adults (age 60+) living in the community and followed them over time, tracking objective measures of cognition, clinical information, and gut microbiomes. Subjects were classified as healthy controls or as having mild cognitive impairment based on cognitive performance. Those with a diagnosis of Alzheimers Diseases with confirmed using serum biomarkers. Using metagenomic sequencing, we found that relative species abundances correlated well with cognition status (MCI or AD). Furthermore, gene pathways analyses suggest certain microbial metabolic pathways to either be correlated with cognitive decline or maintaining cognitive function. Specifically, genes involved in the urea cycle or production of methionine and cysteine predicted worse cognitive performance. Our study suggests that gut microbiome composition may predict AD cognitive performance.

microbiology↗

Microbiota encoded fatty-acid metabolism expands tuft cells to protect tissues homeostasis during Clostridioides difficile infection in the large intestine

Metabolic byproducts of the intestinal microbiota are crucial in maintaining host immune tone and shaping inter-species ecological dynamics. Among these metabolites, succinate is a driver of tuft cell (TC) differentiation and consequent type 2 immunity-dependent protection against invading parasites in the small intestine. Succinate is also a growth enhancer of the nosocomial pathogen Clostridioides difficile in the large intestine. To date, no research has shown the role of succinate in modulating TC dynamics in the large intestine, or the relevance of this immune pathway to C. difficile pathophysiology. Here we reveal the existence of a three-way circuit between commensal microbes, C. difficile and host epithelial cells which centers around succinate. Through selective microbiota depletion experiments we demonstrate higher levels of type 2 cytokines leading to expansion of TCs in the colon. We then demonstrate the causal role of the microbiome in modulating colonic TC abundance and subsequent type 2 cytokine induction using rational supplementation experiments with fecal transplants and microbial consortia of succinate-producing bacteria. We show that administration of a succinate-deficient Bacteroides thetaiotaomicron knockout ({Delta}frd) significantly reduces the enhanced type 2 immunity in mono-colonized mice. Finally, we demonstrate that mice prophylactically administered with the consortium of succinate-producing bacteria show reduced C. difficile-induced morbidity and mortality compared to mice administered with heat-killed bacteria or the vehicle. This effect is reduced in a partial tuft cell knockout mouse, Pou2f3+/-, and nullified in the tuft cell knockout mouse, Pou2f3-/-, confirming that the observed protection occurs via the TC pathway. Succinate is an intermediary metabolite of the production of short-chain fatty acids, and its concentration often increases during dysbiosis. The first barrier to enteric pathogens alike is the intestinal epithelial barrier, and host maintenance and strengthening of barrier integrity is vital to homeostasis. Considering our data, we propose that activation of TC by the microbiota-produced succinate in the colon is a mechanism evolved by the host to counterbalance microbiome-derived cues that facilitate invasion by intestinal pathogens.

immunology↗

Microcin MccI47 selectively inhibits enteric bacteria and reduces carbapenem-resistant Klebsiella pneumoniae colonization in vivo when administered via an engineered live biotherapeutic

BackgroundThe gastrointestinal (GI) tract is the reservoir for multidrug-resistant (MDR) pathogens, specifically carbapenem-resistant (CR) Klebsiella pneumoniae and other Enterobacteriaceae, which often lead to the spread of antimicrobial resistance genes, severe extraintestinal infections, and lethal outcomes. Selective GI decolonization has been proposed as a new strategy for preventing transmission to other body sites and minimizing spreading to susceptible individuals. ResultsHere, we purify the to-date uncharacterized class IIb microcin I47 (MccI47) and demonstrate potent inhibition of numerous Enterobacteriaceae, including multidrug-resistant clinical isolates, in vitro at concentrations resembling those of commonly prescribed antibiotics. We then genetically modify the probiotic bacterium Escherichia coli Nissle 1917 (EcN) to produce MccI47 from a stable multicopy plasmid by using MccI47 toxin production in a counterselection mechanism to engineer one of the native EcN plasmids, which renders provisions for inducible expression and plasmid selection unnecessary. We then test the clinical relevance of the MccI47-producing engineered EcN in a murine CR K. pneumoniae colonization model and demonstrate significant MccI47-dependent reduction of CR K. pneumoniae abundance after seven days of daily oral live biotherapeutic administration without disruption of the resident microbiota. ConclusionsThis study provides the first demonstration of MccI47 as a potent antimicrobial against certain Enterobacteriaceae, and its ability to significantly reduce the abundance of CR K. pneumoniae in a preclinical animal model, when delivered from an engineered live biotherapeutic product. This study serves as the foundational step towards the use of engineered live biotherapeutic products aimed at the selective removal of MDR pathogens from the GI tract

bioengineering↗

The epithelial-specific ER stress sensor IRE1β enables host-microbiota crosstalk to affect colon goblet cell development

Epithelial cells lining mucosal surfaces of the gastrointestinal and respiratory tracts uniquely express IRE1{beta} (Ern2), a paralogue of the most evolutionarily conserved endoplasmic reticulum stress sensor IRE1. How IRE1{beta} functions at the host-environment interface and why a second IRE1 paralogue evolved remain incompletely understood. Using conventionally raised and germ-free Ern2-/- mice, we found that IRE1{beta} was required for microbiota-induced goblet cell maturation and mucus barrier assembly in the colon. This occurred only after colonization of the alimentary tract with normal gut microflora, which induced IRE1{beta} expression. IRE1{beta} acted by splicing Xbp1 mRNA to expand ER function and prevent ER stress in goblet cells. Although IRE1 can also splice Xbp1 mRNA, it did not act redundantly to IRE1{beta} in this context. By regulating assembly of the colon mucus layer, IRE1{beta} further shaped the composition of the gut microbiota. Mice lacking IRE1{beta} had a dysbiotic microbial community that failed to induce goblet cell development when transferred into germ-free wild type mice. These results show that IRE1{beta} evolved at mucosal surfaces to mediate crosstalk between gut microbes and the colonic epithelium required for normal homeostasis and host defense.

cell biology↗