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Biology subjects

Engdahl, E.

Publications and source records attributed to Engdahl, E..

2 recordsLinked to original sources

A mixture of endocrine disrupting chemicals linked to lower birth weight induces adipogenesis and transcriptional changes related to birth weight alterations and diabetes

There is increasing evidence that endocrine disrupting chemicals (EDCs) are contributing to the rise in metabolic disorders and obesity. Humans are constantly exposed to numerous EDCs, thus human exposure entails complex EDC mixtures. In this study, we examined the effects of an EDC mixture, mixture G, composed of four phthalate esters, triclosan, and three poly- och perfluorinated alkyl substances. Mixture G had previously been defined based on its association with lower birth weight in a pregnancy cohort, where low birth weight is an early risk factor for metabolic morbidities later in life. Here, we studied its effects on adipogenesis and uncovered their underlying transcriptional changes. Human mesenchymal stem cells (hMSCs) were exposed to mixture G in concentrations and mixing ratios that reflect those measured in human serum. Mixture G induced adipogenesis in hMSCs, as evidenced by a dose-dependent increase in lipid droplet accumulation after 14-21 days. Notably, significant adipogenic effects were observed at concentrations comparable to those detected in humans. RNA-sequencing upon exposure for 48 h revealed dose-dependent transcriptional changes in over 1000 genes. Mixture G-induced differentially expressed genes (DEGs) showed significant overlap with genes involved in osteogenesis, with glucocorticoid-regulated genes, and with genes associated with birth weight alterations and diabetes type II. These results indicate that exposure to an environmentally relevant EDC mixture induces adipogenesis and leads to transcriptional alterations that might change the balance between adipogenic and osteogenic differentiation as well as the functionality of MSCs, possibly via interference with glucocorticoid signalling. Thus our findings underscore the role of EDCs as metabolic disruptors and shed light on the molecular mechanisms underlying their potential contribution to the development of metabolic disorders. HighlightsO_LIAn endocrine disruptor mixture linked to lower birth weight increases adipogenesis C_LIO_LIThe mixture induced transcriptomic changes at low doses C_LIO_LIAffected genes are associated with birth weight and diabetes type II C_LI Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=78 SRC="FIGDIR/small/638050v1_ufig1.gif" ALT="Figure 1"> View larger version (17K): org.highwire.dtl.DTLVardef@12428bforg.highwire.dtl.DTLVardef@ef28b3org.highwire.dtl.DTLVardef@159024corg.highwire.dtl.DTLVardef@a605b7_HPS_FORMAT_FIGEXP M_FIG C_FIG

pharmacology and toxicology↗

Increased serological response against human herpesvirus 6A is associated with risk for multiple sclerosis

Human herpesvirus (HHV)-6A or HHV-6B involvement in multiple sclerosis (MS) etiology has remained controversial mainly due to the lack of serological methods that can distinguish the two viruses.\n\nA novel multiplex serological assay measuring IgG reactivity against the immediate-early protein 1 from HHV-6A (IE1A) and HHV-6B (IE1B) was used in a MS cohort (8742 persons with MS and 7215 matched controls), and a pre-MS cohort (478 individuals and 476 matched controls) to investigate this further.\n\nThe IgG response against IE1A was positively associated with MS (OR = 1.55, p = 9x10-22), and increased risk of future MS (OR = 2.22, p = 2x10-5). An interaction was observed between IE1A and Epstein-Barr virus (EBV) antibody responses for MS risk (attributable proportion = 0.24, p = 6x10-6). In contrast, the IgG response against IE1B was negatively associated with MS (OR = 0.74, p = 6x10-11). The association did not differ between MS subtypes or vary with severity of disease. The genetic control of HHV-6A/B antibody responses were located to the Human Leukocyte Antigen (HLA) region and the strongest association for IE1A was the DRB1*13:01-DQA1*01:03-DQB1*06:03 haplotype while the main association for IE1B was DRB1*13:02-DQA1*01:02-DQB1*06:04.\n\nIn conclusion a role for HHV-6A in MS etiology is supported by an increased serological response against HHV-6A IE1 protein, an interaction with EBV, and an association to HLA genes.

immunology↗