Vibrio cholerae causes cholera and can switch between planktonic and biofilm lifeforms, where biofilm formation enhances transmission, virulence, and antibiotic resistance. Due to antibiotic microbial resistance, new antimicrobials including silver nanoparticles (AgNPs) are being studied. Nevertheless, little is known about the metabolic changes exerted by AgNPs on both microbial lifeforms. Our objective was to evaluate the changes in the metabolomic profile of V. cholerae planktonic and biofilm cells in response to sublethal concentrations of AgNPs using MS2 untargeted metabolomics and chemoinformatics. A total of 690 metabolites were quantified among all groups. More metabolites were significantly modulated in planktonic cells (n = 71) compared to biofilm (n = 37) by the treatment. The chemical class profiles were distinct for both planktonic and biofilm, suggesting a phenotype-dependent metabolic response to the nanoparticles. Chemical enrichment analysis showed altered abundances of oxidized fatty acids (FA), saturated FA, phosphatidic acids, and saturated stearic acid in planktonic cells treated with AgNPs, which hints at a turnover of the membrane. In contrast, no chemical classes were enriched in the biofilm. In conclusion, this study suggests that the response of V. cholerae to silver nanoparticles is phenotype-dependent and that planktonic cells experience a lipid remodeling process, possibly related to an adaptive mechanism involving the cell membrane.

Breastmilk is essential for neonatal development, particularly in seeding the gut microbiota and modulating the immune system. This proof-of-concept study explores the systemic nature of colostrum and the influence of maternal obesity on co-occurrences of colostrum bioactives. Using 16S-rRNA sequencing, untargeted metabolomics, and cytokine quantification, we analyzed co-occurring elements in the colostrum of mothers with normal weight (18.5 < BMI < 25) or obesity (BMI > 30). We identified 5 different co-occurrence networks, characterized by positive correlations of taxonomically related bacteria. Our integrative analysis reveals that Aeromonadaceae, Xanthomonadaceae and Staphylococcaceae negatively correlate with pro-inflammatory cytokines TNF-α, IL-6, and IL-12p70 in the colostrum of mothers with obesity (WO). Additionally, lipid mediators, including 15-HEDE and LysoPC (16:00), were associated with cytokines IL-10 and IL-8 and microbiota taxa Burkholderiaceae, Beijerinckiaceae and Planococcaceae – first reported in the colostrum of mothers WO. Our findings suggest a pervasive regulation of bioactives in the colostrum of mothers WO. This may have implications for distinctive neonatal intestine development.

Coronary artery endothelial cells (CAEC) exert an important role in the development of cardiovascular disease. Dysfunction of CAEC is associated with cardiovascular disease in subjects with type 2 diabetes mellitus (T2DM). However, comprehensive studies of the effects that a diabetic environment exerts on this cellular type are scarce. The present study characterized the molecular perturbations occurring on cultured bovine CAEC subjected to a prolonged diabetic environment (high glucose and high insulin). Changes at the metabolite and peptide level were assessed by Liquid Chromatography–Mass Spectrometry (LC–MS²) and chemoinformatics. The results were integrated with published LC–MS²-based quantitative proteomics on the same in vitro model. Our findings were consistent with reports on other endothelial cell types and identified novel signatures of DNA/RNA, amino acid, peptide, and lipid metabolism in cells under a diabetic environment. Manual data inspection revealed disturbances on tryptophan catabolism and biosynthesis of phenylalanine-based, glutathione-based, and proline-based peptide metabolites. Fluorescence microscopy detected an increase in binucleation in cells under treatment that also occurred when human CAEC were used. This multi-omics study identified particular molecular perturbations in an induced diabetic environment that could help unravel the mechanisms underlying the development of cardiovascular disease in subjects with T2DM.

Coronary artery endothelial cells (CAEC) exert an important role in the development of cardiovascular disease. Dysfunction of CAEC is associated with cardiovascular disease in subjects with type 2 diabetes mellitus (T2DM). However, comprehensive studies of the effects that a diabetic environment exerts on this cellular type scarce. The present study characterized the molecular perturbations occurring on cultured bovine CAEC subjected to a prolonged diabetic environment (high glucose [HG] and high insulin [HI]). Changes at the metabolite and peptide level were assessed by untargeted metabolomics and chemoinformatics, and the results were integrated with proteomics data using published SWATH-based proteomics on the same in vitro model. Our findings were consistent with reports on other endothelial cell types, but also identified novel signatures of DNA/RNA, aminoacid, peptide, and lipid metabolism in cells under a diabetic environment. Manual data inspection revealed disturbances on tryptophan catabolism and biosynthesis of phenylalanine-based, glutathione-based, and proline-based peptide metabolites. Fluorescence microscopy detected an increase in binucleation in cells under treatment that also occurred when human CAEC were used. This multi-omics study identified particular molecular perturbations in an induced diabetic environment that could help unravel the mechanisms underlying the development of cardiovascular disease in subjects with T2DM.