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Porras, A. M.

Publications and source records attributed to Porras, A. M..

4 recordsLinked to original sources

Comparative Genomic and Functional Profiling of ECM-Targeting Enzymes in Bacteroides, a Key Genus of the Human Gut Microbiome

Purpose The human extracellular matrix (ECM) provides essential cues for intestinal homeostasis. While most studies focus on ECM degradation by host cells, our prior work suggests that commensal gut microbes may also contribute to these remodeling processes. Here, we continue exploring this novel dimension of host-microbe interactions by profiling the proteolytic diversity and substrate-specific activity of ECM-targeting enzymes across species of Bacteroides, a dominant and metabolically versatile gut genus. MethodsWe curated a custom ECM-specific enzyme database from the BRENDA repository and used it to perform comparative genomic analyses across 11 Bacteroides species, mapping the diversity and abundance of candidate ECM-degrading proteases and carbohydrate active enzymes (CAZymes). Functional activity was evaluated via in vitro degradation assays using purified substrates. Family-specific protease inhibitors were used to confirm the major catalytic classes involved. ResultsECM-targeting CAZymes and proteases were broadly encoded across all 11 genomes, with gene counts positively correlated with genome size and GAG-associated genes comprising the largest substrate category. Experimental degradation assays revealed species- and substrate-specific activity patterns, including elastin degradation restricted to a subset of species, a capacity previously undocumented in intestinal Bacteroides. Genomic predictions showed limited concordance with measured enzymatic activity, suggesting context-dependent regulation of ECM-degrading enzymes. Inhibitor experiments confirmed that collagen degradation is driven primarily by metalloproteases and secondarily by serine proteases across representative species. ConclusionsOur findings position commensal Bacteroides as a rich, yet underappreciated, source of ECM-degrading enzymes. This work underscores the need to consider microbiota as key modulators of host tissue homeostasis and potential targets for therapeutic modulation. BIOGRAPHYDr. Ana Maria Porras is an Assistant Professor of Biomedical Engineering at the University of Florida, where she leads the Tissue-Microbe Interactions lab. Her group leverages cell and tissue engineering, bioinformatics, and statistical modeling to understand how microorganisms regulate human extracellular matrix remodeling. Her work centers primarily on the gut microbiome, cardiovascular health, and tropical infectious diseases. Dr. Porras is also a science artist, and a science communicator, particularly in interested in evidence-based, culturally informed, and multilingual practices to improve public engagement with science. She is the co-founder and Senior Advisor of the Latinx in Biomedical Engineering community, and the recipient of multiple awards, including the UF Excellence Award for Assistant Professors, the NSF Faculty Early Career Development (CAREER) Award, the NIH Maximizing Investigators Research Award (MIRA), the AAAS Early Career Award for Public Engagement with Science, and and the Rising Star Award from the Academy of Science, Engineering, and Medicine of Florida. Prior to arriving in Florida, Dr. Porras was a Presidential Postdoctoral Fellow at Cornell University. She holds a B.S. in biomedical engineering from the University of Texas at Austin, and a Ph.D. from the University of Wisconsin-Madison, where she was an American Heart Association Predoctoral Fellow.

microbiology↗

Supplementation with a Limosilactobacillus fermentum K73 synbiotic modulates gut microbiota function and behavior in gnotobiotic mice transplanted with microbiota from children diagnosed with autism spectrum disorder

BackgroundGut dysbiosis has been implicated in numerous pathological conditions, including neurodevelopmental and neurodegenerative disorders. Recently, dietary interventions targeted at restoring microbial balance have therefore gained attention as potential therapeutic strategies. We recently demonstrated that an encapsulated synbiotic containing high-oleic palm oil and Limosilactobacillus fermentum K73 can modulate the metabolic activity and composition of human-derived gut microbiota in an in vitro batch bioreactor. Here, we extended this work through an in vivo supplementation pilot study using gnotobiotic mice colonized with gut microbiota from Colombian pediatric patients diagnosed with autism spectrum disorder (ASD) or age-matched neurotypical (NT) donors. Behavioral assessments and analyses of gut microbiota composition and function were performed before and after synbiotic supplementation. ResultsFirst, we found that the gut microbiota from Colombian ASD patients exhibited significantly reduced richness relative to NT donors, consistent with reports from other geographical regions, and displayed distinct compositional features unique to this population. Humanization of the gnotobiotic mice with this donor microbiota was successful, with murine gut communities reflecting features of their corresponding donor microbiota. Notably, synbiotic supplementation induced significant increases in the abundance of beneficial taxa and the production of short chain fatty acids that were more pronounced in mice colonized with ASD-derived microbiota, with concurrent behavioral changes associated with beneficial modulation of gut microbiota. ConclusionsOverall, we provide evidence that supports synbiotic supplementation as a viable strategy to positively modulate gut microbiome in conditions of dysbiosis. Our study also expands the body of knowledge of gut microbiome to understudied populations such as Latin America.

microbiology↗

Trymethylamine-N-oxide, a gut-derived metabolite, induces myofibroblastic activation of valvular interstitial cells through endoplasmic reticulum stress

Calcific aortic valve disease currently lacks effective treatments beyond surgical valve replacement, due to an incomplete understanding of its pathogenesis. Emerging evidence suggests that the gut microbiome influences cardiovascular health through the production of metabolites derived from dietary components. Among them, trimethylamine-N-oxide (TMAO) has been identified as a potential causal factor for several cardiovascular conditions. However, its role in the development of aortic valve disease remains poorly understood. This study sought to investigate the impact of TMAO on valvular interstitial cells (VICs), the most abundant cell type in the aortic valve. Here, we demonstrate that TMAO activates VICs towards a myofibroblastic profibrotic phenotype. Using an in vitro protocol to generate quiescent VICs, we found that TMAO induces the upregulation of myofibroblastic markers in a sex-independent manner. These quiescent VICs were more sensitive to TMAO than conventionally cultured VICs. Treatment with TMAO also elevated extracellular matrix production and oxidative stress, phenotypic hallmarks of an activated profibrotic state. Finally, inhibition of the endoplasmic reticulum stress kinase prior to TMAO treatment blocked all effects of this metabolite. These findings suggest that TMAO contributes to the early stages of valve disease by promoting VIC activation through endoplasmic reticulum stress mechanisms. Understanding the role of TMAO and other gut-derived metabolites in the pathogenesis of valve disease could inform the development of novel preventive or therapeutic strategies to modify or delay disease progression. Furthermore, these insights underscore the importance of host-microbiome interactions and highlight the potential for targeted dietary interventions to mitigate cardiovascular disease risk.

cell biology↗

Inflammatory bowel disease-associated gut commensals degrade components of the extracellular matrix

Extracellular matrix (ECM) remodeling has emerged as a key feature of inflammatory bowel disease (IBD), and ECM fragments have been proposed as markers of clinical disease severity. Recent studies report increased protease activity in the gut microbiota of IBD patients. Nonetheless, the relationship between gut microbiota and ECM remodeling has remained unexplored. We hypothesized that members of the human gut microbiome can degrade host ECM, and that bacteria-driven remodeling, in turn, can enhance colonic inflammation. Through a variety of in vitro assays, we first confirmed that multiple bacterial species found in the human gut are capable of degrading specific ECM components. Clinical stool samples obtained from ulcerative colitis patients also exhibited higher levels of proteolytic activity in vitro compared to those of their healthy counterparts. Furthermore, culture supernatants from bacteria species capable of degrading human ECM accelerated inflammation in a dextran sodium sulfate (DSS)-induced colitis. Finally, we identified several of the bacterial proteases and carbohydrate degrading enzymes (CAZymes) potentially responsible for ECM degradation in vitro. Some of these protease families and CAZymes were also found in increased abundance in a metagenomic cohort of IBD. These results demonstrate that some commensal bacteria in the gut are indeed capable of degrading components of human ECM in vitro and suggest this proteolytic activity may be involved in the progression of IBD. A better understanding of the relationship between nonpathogenic gut microbes, host ECM, and inflammation could be crucial to unravel some of the mechanisms underlying host-bacteria interactions in IBD and beyond.

microbiology↗