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Biology subjects

Horvath, T. D.

Publications and source records attributed to Horvath, T. D..

3 recordsLinked to original sources

DEEPNET-LLM: Highly accurate structure prediction of unknown metabolites from mass spectra via their molecular neighborhoods

Most molecular features detected by untargeted mass spectrometry-based metabolomics remain unannotated. This so-called 'dark matter' currently comprises more than 90% and likely holds uncharacterized bioactive chemistry. Structure prediction from fragmentation spectra remains an outstanding challenge, because a spectrum does not uniquely determine a structure and the space of candidate structures is mostly unbounded; correspondingly, existing methods rarely return the correct de novo structure as their top prediction. Here we describe De novo Ego network-Enabled Propagation and Neighborhood Extrapolation of Topology using Large Language Models (DEEPNET-LLM) reasoning approach, which uses Molecular Community Networking (MCN) to restrict the search of a query spectrum to its local neighborhood within the global metabolome, and applies AI reasoning to propagate structural information from neighbors to the query. For a collection of 900 authentic standards (2,249 spectra) that have never been publicly released to exclude possibility of data leakage, DEEPNET-LLM returned the correct structure as its top prediction for 84.7% of spectra. Accuracy was independent of precursor mass across a range over which the number of candidate structures grows by 30 orders of magnitude, and was comparable across ion polarity, adducts and in-source fragmentation. On a random subset of the public MassSpecGym benchmark, DEEPNET-LLM reached 85.9% top-1 accuracy excluding stereochemistry. We showcase the use of DEEPNET-LLM with an example of a discovery of tryptamine amidate of a bile acid in mouse gut, confirmed against a synthetic standard. The DEEPNET-LLM approach is orthogonal to existing in silico methods and can be combined with them.

bioinformatics↗

Infant gut microbiomes contribute to metabolic states that impact brain function

Alterations in the gut microbiome are associated with neurodevelopmental disorders, but causal mechanisms and therapeutic strategies remain undefined. Here, we demonstrate that human infant microbiomes isolated during the first six months of life drive behavioral impairments in mice and that microbiota-based interventions restore mice to normal behavior. Early-life microbiomes from twelve infants who later exhibited cognitive deficits at 2 years old (low-scoring) transferred adverse metabolic, brain, and behavioral phenotypes to mice, in contrast to microbiomes from twenty-three cognitively typical or high-scoring infants. Deficits in mice were rescued by fecal microbiota transplant from high-scoring infants or a rationally designed consortium that promoted amino acid levels. We confirmed lower fecal amino acid concentrations in low-scoring infants and replicated the association between early-life microbiome composition and cognitive outcomes in a second geographically independent infant cohort. Altogether, we discovered an early-life microbiome-mediated metabolic state causally linked to cognitive deficits and amenable to microbial intervention.

microbiology↗

Clostridioides difficile colonization is not mediated by bile salts and requires Stickland fermentation of proline in an in vitro model of infection

Treatment with antibiotics is a major risk factor for Clostridioides difficile infection, likely due to depletion of the gastrointestinal microbiota. Two microbiota-mediated mechanisms thought to limit C. difficile colonization include conversion of conjugated primary bile salts into secondary bile salts toxic to C. difficile growth, and competition between the microbiota and C. difficile for limiting nutrients. Using a continuous flow model that simulates the nutrient conditions of the distal colon, we investigated how treatment with six clinically-used antibiotics influenced susceptibility to C. difficile infection in 12 different microbial communities cultivated from healthy individuals. Antibiotic treatment reduced microbial richness; disruption varied by antibiotic class and microbiota composition, but did not correlate with C. difficile susceptibility. Antibiotic treatment also disrupted microbial bile salt metabolism, increasing levels of the primary bile salt, cholate. However, changes in bile salt did not correlate with increased C. difficile susceptibility. Further, bile salts were not required to inhibit C. difficile colonization. We tested whether amino acid fermentation contributed to persistence of C. difficile in antibiotic- treated communities. C. difficile mutants unable to use proline as an electron acceptor in Stickland fermentation due to disruption of proline reductase (prdB-) had significantly lower levels of colonization than wild-type strains in four of six antibiotic-treated communities tested. Inability to ferment glycine or leucine as electron acceptors, however, was not sufficient to limit colonization in any communities. This data provides further support for the importance of bile salt-independent mechanisms in regulating colonization of C. difficile. IMPORTANCEC. difficile is one of the leading causes of hospital-acquired infections and antibiotic-associated diarrhea. Several potential mechanisms through which the microbiota can limit C. difficile infection have been identified and are potential targets for new therapeutics. However, it is unclear which mechanisms of C. difficile inhibition represent the best targets for development of new therapeutics. These studies demonstrate that in a complex in vitro model of C. difficile infection, colonization resistance is independent of microbial bile salt metabolism. Instead, the ability of C. difficile to colonize is dependent upon its ability to metabolize proline, although proline-dependent colonization is context-dependent and is not observed in all disrupted communities. Altogether, these studies support the need for further work to understand how bile- independent mechanisms regulate C. difficile colonization.

microbiology↗