Lactational delivery of Triclosan promotes non-alcoholic fatty liver disease in newborn mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE200705 | GEO | 2022/04/15
REPOSITORIES: GEO
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Project description:Lactational delivery of Triclosan promotes non-alcoholic fatty liver disease in newborn mice
| PRJNA826106 | ENA
Project description:Here we show that Triclosan (TCS), a high-volume antimicrobial additive that has been detected in human breastmilk, can be efficiently transferred by lactation to newborn mice, causing significant fatty liver (FL) during the suckling period. These findings are relevant since pediatric non-alcoholic fatty liver disease (NAFLD) is escalating in the United States, with a limited mechanistic understanding. Lactational delivery stimulated hepatosteatosis, triglyceride accumulation, endoplasmic reticulum (ER) stress, signs of inflammation, and liver fibrosis. De novo lipogenesis (DNL) induced by lactational TCS exposure is shown to be mediated in a PERK-eIF2α-ATF4-PPARα cascade. The administration of obeticholic acid (OCA), a potent FXR agonist, as well as activation of intestinal mucosal-regenerative gp130 signaling, led to reduced liver ATF4 expression, PPARα signaling, and DNL when neonates were exposed to TCS. It is yet to be investigated but mother to child transmission of TCS or similar toxicants may underlie the recent increases in pediatric NAFLD.
| S-EPMC9329322 | biostudies-literature
Project description:Triclosan is a biocidal active agent commonly found in domestic cleaning products, hand sanitizers, cosmetics and personal care products. It is used to control microbial contamination and has a broad-spectrum of activity against many Gram-positive and Gram-negative bacteria. The development of triclosan tolerance with potential cross resistance to clinically relevant antibiotics in zoonotic pathogens is of concern given the widespread use of this active agent in clinical, food processing and domestic environments. Some studies have proposed that an over-dependence on triclosan-containing products could lead to the emergence of clinically important pathogens that are highly tolerant to both biocides and antibiotics. Currently, there is limited understanding of the mechanisms contributing to the emergence of triclosan tolerance in foodborne pathogens at a genetic level. We used microarray analysis to compare gene expression between a wildtype E. coli O157:H19 isolate (WT) with a minimum inhibitory concentration (MIC) to triclosan of 6.25 ug/ml and its laboratory generated triclosan tolerant mutant (M) with a MIC of >8000 ug/ml.
2013-10-15 | GSE39343 | GEO
Project description:Triclosan is a biocidal active agent commonly found in domestic cleaning products, hand sanitizers, cosmetics and personal care products. It is used to control microbial contamination and has a broad-spectrum of activity against many Gram-positive and Gram-negative bacteria. The development of triclosan tolerance with potential cross resistance to clinically relevant antibiotics in zoonotic pathogens is of concern given the widespread use of this active agent in clinical, food processing and domestic environments. Some studies have proposed that an over-dependence on triclosan-containing products could lead to the emergence of clinically important pathogens that are highly tolerant to both biocides and antibiotics. Currently, there is limited understanding of the mechanisms contributing to the emergence of triclosan tolerance in foodborne pathogens at a genetic level. We used microarray analysis to compare gene expression between a wildtype E. coli O157:H19 isolate (WT) with a minimum inhibitory concentration (MIC) to triclosan of 6.25 ug/ml and its laboratory generated triclosan tolerant mutant (M) with a MIC of >8000 ug/ml. Gene expression profiling was performed on untreated E. coli O157:H19 wildtype (WTu) and mutant (Mu), and on the wildtype and mutant treated with 6 ug/ml triclosan for 30 minutes (WTt and Mt respectively). RNA was extracted from three independent biological replicates for WTu, Mu, WTt & Mt for hybridization on Affymetrix GeneChip E. coli Genome 2.0 Arrays. Micorarray analysis including pre-processing, normalisation and statistical analysis were performed using R (R, 2007) version 2.6 and Bioconductor (Gentleman et al. 2004, Genome Biol. 5:R80) version 2.1 as previously described by Morris et al.(2009, Physiol. Genomics 39:28-37).
2013-10-15 | E-GEOD-39343 | biostudies-arrayexpress
Project description:The goal was to study the long term metabolic programming effects of exposure of offspring to a dam eating 60% high fat diet during the lactation period only. We previously showed that offspring from dams given lactational high fat diet (HFD) are predisposed to obesity, glucose intolerance and inflammation. The purpose of these studies was to understand the programming implications of lactational HFD on offspring metabolic liver disease risk. Dams were fed a 60% lard-based HFD from the day of delivery through the 21 day lactation period. Starting at weaning offspring were fed normal fat diet until 3 months of age at which point a subset were challenged with an additional HFD stressor. Lactational HFD fed male offspring developed hepatic insulin resistance. Postweaning HFD challenge led male offspring progressing to NAFLD with more severe outcomes in the lactational HFD challenged offspring.
2021-08-14 | GSE182071 | GEO
Project description:[Original title] In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces disruption of the prostate glands and fibrosis in rhesus monkeys. We investigated the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure on the prostate in rhesus monkey offspring. Dams received 0, 30 or 300 ng/kg TCDD subcutaneously on Day 20 of gestation, and then 5% of the initial dose was injected every 30 days until Day 90 after delivery. The offspring were maintained until reaching sexual maturity, and examined histopathologically. Dose-dependent decreases in the prostate glands and widespread fibrosis were observed in offspring. It is noteworthy that 7 years from the final lactational TCDD exposure, inflammatory cell infiltration and disruption of the prostate glands were also observed. Differential mRNA expression associated with fibrosis, inflammatory response and disruption of cell components were demonstrated by microarray analysis, and up-regulation of TGM4, TGFB1, COL1A1 and MMP2 was confirmed with Real-time PCR. In conclusion, in utero and lactational exposure to TCDD induced dose-proportional prostatic fibrosis, indicating prostatic dysfunction and inducible semen quality reduction in second-generation rhesus monkeys. Dam received 0, 30 or 300 ng/kg TCDD subcutaneously on Day 20 of gestation, and then 5% of the initial dose was injected every 30 days until Day 90 after delivery. The offspring were maintained until reaching sexual maturity, and the prostates from 3 offspring in each group were evalutated by histopathological examination, microarray analysis and Real-time quantitative PCR. Supplementary file: Fold_change comparison results of 'control group vs 30 ng/kg group' and 'control group vs 300 ng/kg group'.
2010-01-27 | E-GEOD-20043 | biostudies-arrayexpress
Project description:Global gene expression analysis of Mycobacterium bovis BCG following Triclosan treatment using Affymetrix GeneChip arrays. Results from this study provide insight into the molecular mechanisms underlying the cellular response of Mycobacterium bovis BCG to Triclosan
2012-12-25 | GSE33800 | GEO
Project description:Global gene expression analysis of Mycobacterium bovis BCG following Triclosan treatment using Affymetrix GeneChip arrays. Results from this study provide insight into the molecular mechanisms underlying the cellular response of Mycobacterium bovis BCG to Triclosan We conducted three independent microarray experiments (biological replicates) in the absence (control) and the presence (experimental) of triclosan. Fold change was calculated as a ration between the signal averages of three untreated (control) and three triclosan-treated (experimental) cultures for 0, 10 and 60min exposures.
2012-12-25 | E-GEOD-33800 | biostudies-arrayexpress