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Fernando, S. C.

Publications and source records attributed to Fernando, S. C..

2 recordsLinked to original sources

Insights into rumen microbial biosynthetic gene cluster diversity through genome-resolved metagenomics

Ruminants are critical to global food security as they transform lignocellulosic biomass into high-quality protein products. The rumen microbes ferment feed to provide necessary energy and nutrients for the ruminant host. However, we still lack insight into the metabolic processes encoded by most rumen microbial populations. In this study, we implemented metagenomic binning approaches to recover 2,809 microbial genomes from cattle, sheep, moose, deer, and bison. By clustering genomes based on average nucleotide identity, we demonstrate approximately one-third of the metagenome-assembled genomes (MAGs) to represent species not present in current reference databases and rumen microbial genome collections. Combining these MAGs with other rumen genomic datasets permitted a phylogenomic characterization of the biosynthetic gene clusters (BGCs) from 8,160 rumen microbial genomes, including the identification of 5,346 diverse gene clusters for nonribosomal peptide biosynthesis. A subset of Prevotella and Selenomonas BGCs had higher expression in steers with lower feed efficiency. Moreover, the microdiversity of BGCs was fairly constant across types of BGCs and cattle breeds. The reconstructed genomes expand the genomic representation of rumen microbial lineages, improve the annotation of multi-omics data, and link microbial populations to the production of secondary metabolites that may constitute a source of natural products for manipulating rumen fermentation.

microbiology

Establishing the phenotypic basis of adherent-invasive Escherichia coli (AIEC) pathogenicity in intestinal inflammation

Background & AimsAdherent-invasive Escherichia coli (AIEC) are enriched in ileal Crohns disease patients and implicated in disease etiology. However, AIEC pathogenesis is poorly understood, and it is unclear if the expansion of these organisms contributes to inflammatory bowel disease (IBD). Questions also remain as to what extent the various in vitro phenotypes used to classify AIEC are pathologically relevant.\n\nMethodsWe utilized a combination of in vitro phenotyping and a murine model of intestinal inflammation to systematically relate AIEC phenotypes to pathogenicity for 30 mucosa-associated human-derived E. coli strains. In vitro assays used included survival/replication in and TNF- production by J774 macrophages as well as invasion/replication in Caco2 intestinal epithelial cells.\n\nResultsAIEC do not form a phenotypic group that is clearly separated from non-AIEC. However, E. coli strains displaying in vitro AIEC phenotypes caused, on average, more severe intestinal inflammation. Survival/replication of strains in J774 and Caco2 cells were positively correlated with disease in vivo, while adherence to Caco2 cells and TNF- production by J774 cells were not. Importantly, co-colonization with adherent non-AIEC strains ameliorated AIEC-mediated disease.\n\nConclusionOur findings do not support the existence of an AIEC pathovar that can be clearly separated from commensal E. coli. However, intracellular survival/replication phenotypes do contribute to murine intestinal inflammation, suggesting that the AIEC overgrowth observed in human IBD makes a causal contribution to disease. The ability to differentiate pathologically-relevant AIEC phenotypes from those that are not provides an important foundation for developing strategies to predict, diagnose and treat human IBD through characterizing and modulating patient E. coli populations.

microbiology