23 November 2022 In Cancer

The relationship between alcohol consumption and cancer has no consistent results both in epidemiological studies and animal models. The inaccuracy of alcohol consumption dosage in the experimental design maybe leads to inconsistent results and makes the researchers ignore the effect of very-light alcohol consumption on cancer. To determine the effects of very-light alcohol consumption on cancer, in this study, the manner of gavage was used to control the alcohol consumption accurately. The impacts of age and time of drinking on cancer progression were also evaluated in this study. Here, we find that a certain range of alcohol consumption (from 0.5% w/v to 2.0% w/v) can suppress tumor development in the breast metastasis mouse model by controlling the alcohol consumption dosage accurately. RNA sequencing analyses were performed in primary tumors and related metastases from the NC group and 1.0% w/v group. The results of primary tumors and related metastases indicated that chronic very-light alcohol consumption downregulates breast tumor-associated oncogenes in primary tumors and regulates the immune system and metabolic system in metastatic carcinoma. To provide the public with drinking recommendations, eight commercial alcohol types were investigated at a dosage of 1.0% w/v. Two types of commercial alcohol, red wine (made in France, brand 1) and baijiu (made in China, brand 1), exerted excellent primary tumor and metastasis inhibitory effects. The untargeted metabolomic analysis of commercial alcohol by liquid chromatography-tandem mass spectrometry indicated that baijiu (brand 1) and baijiu (brand 2) exhibited a difference in compositions that can lead to their different anti-cancer effects. These results indicated that a certain range of very light alcohol dosages might have a potential human-cancer inhibition effect.

25 August 2020 In General Health

The microbiota is known to modulate the host response to influenza infection through as-yet-unclear mechanisms. We hypothesized that components of the microbiota exert effects through type I interferon (IFN), a hypothesis supported by analysis of influenza in a gain-of-function genetic mouse model.

Here we show that a microbially associated metabolite, desaminotyrosine (DAT), protects from influenza through augmentation of type I IFN signaling and diminution of lung immunopathology. A specific human-associated gut microbe, Clostridium orbiscindens, produced DAT and rescued antibiotic-treated influenza-infected mice. DAT protected the host by priming the amplification loop of type I IFN signaling.

These findings show that specific components of the enteric microbiota have distal effects on responses to lethal infections through modulation of type I IFN.

27 March 2020 In General Health

The microbiota is known to modulate the host response to influenza infection through as-yet-unclear mechanisms. We hypothesized that components of the microbiota exert effects through type I interferon (IFN), a hypothesis supported by analysis of influenza in a gain-of-function genetic mouse model. Here we show that a microbially associated metabolite, desaminotyrosine (DAT), protects from influenza through augmentation of type I IFN signaling and diminution of lung immunopathology. A specific human-associated gut microbe, Clostridium orbiscindens, produced DAT and rescued antibiotic-treated influenza-infected mice. DAT protected the host by priming the amplification loop of type I IFN signaling. These findings show that specific components of the enteric microbiota have distal effects on responses to lethal infections through modulation of type I IFN.

01 February 2017 In Liver Disease

BACKGROUND: Liver damage is a serious and sometimes fatal consequence of long-term alcohol intake, which progresses from early-stage fatty liver (steatosis) to later-stage steatohepatitis with inflammation and fibrosis/necrosis. However, very little is known about earlier stages of liver disruption that may occur in problem drinkers, those who drink excessively but are not dependent on alcohol.

METHODS: We examined how repeated binge-like alcohol drinking in C57BL/6 mice altered liver function, as compared with a single binge-intake session and with repeated moderate alcohol consumption. We measured a number of markers associated with early- and later-stage liver disruption, including liver steatosis, measures of liver cytochrome P4502E1 (CYP2E1) and alcohol dehydrogenase (ADH), alcohol metabolism, expression of cytokine mRNA, accumulation of 4-hydroxynonenal (4-HNE) as an indicator of oxidative stress, and alanine transaminase/aspartate transaminase as a measure of hepatocyte injury.

RESULTS: Importantly, repeated binge-like alcohol drinking increased triglyceride levels in the liver and plasma, and increased lipid droplets in the liver, indicators of steatosis. In contrast, a single binge-intake session or repeated moderate alcohol consumption did not alter triglyceride levels. In addition, alcohol exposure can increase rates of alcohol metabolism through CYP2E1 and ADH, which can potentially increase oxidative stress and liver dysfunction. Intermittent, excessive alcohol intake increased liver CYP2E1 mRNA, protein, and activity, as well as ADH mRNA and activity. Furthermore, repeated, binge-like drinking, but not a single binge or moderate drinking, increased alcohol metabolism. Finally, repeated, excessive intake transiently elevated mRNA for the proinflammatory cytokine IL-1B and 4-HNE levels, but did not alter markers of later-stage liver hepatocyte injury.

CONCLUSIONS: Together, we provide data suggesting that even relatively limited binge-like alcohol drinking can lead to disruptions in liver function, which might facilitate the transition to more severe forms of liver damage.

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