Low-dose penicillin in early life induces long-term changes in murine gut microbiota, brain cytokines and behavior

Changes in the gut microbiome have already been associated with postoperative complications in major abdominal surgery. However, it is still unclear whether these changes are transient or a long-lasting effect. Therefore, the aim of this prospective clinical pilot study was to examine long-term changes in the gut microbiota and to correlate these changes with the clinical course of the patient. Methods: In total, stool samples of 62 newly diagnosed colorectal cancer patients undergoing primary tumor resection were analyzed by 16S-rDNA next-generation sequencing. Stool samples were collected preoperatively in order to determine the gut microbiome at baseline as well as at 6, 12, and 24 months thereafter to observe longitudinal changes. Postoperatively, the study patients were separated into two groups—patients who suffered from postoperative complications (n = 30) and those without complication (n = 32). Patients with postoperative complications showed a significantly stronger reduction in the alpha diversity starting 6 months after operation, which does not resolve, even after 24 months. The structure of the microbiome was also significantly altered from baseline at six-month follow-up in patients with complications (p = 0.006). This was associated with a long-lasting decrease of a large number of species in the gut microbiota indicating an impact in the commensal microbiota and a long-lasting increase of Fusobacterium ulcerans. The microbial composition of the gut microbiome shows significant changes in patients with postoperative complications up to 24 months after surgery.

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IgA dysfunction induced by the early-lifetime disruption of gut microbiota aggravates diet–induced metabolic syndrome in mice

10.21203/rs.3.rs-40336/v2 ◽

2021 ◽

Author(s):

Jielong Guo ◽

Xue Han ◽

Yilin You ◽

Weidong Huang ◽

Zhan Jicheng

Keyword(s):

Metabolic Syndrome ◽

Gut Microbiota ◽

Early Life ◽

Low Dose ◽

Dependent Manner ◽

Wild Type ◽

Bacterial Composition ◽

Germ Free ◽

Iga Response ◽

Intestinal Iga

Abstract BackgroundLow-dose antibiotic contamination in animal food is still a severe food safety problem worldwide. Penicillin is one of the main classes of antibiotics being detected in food. Previous studies have shown that transient exposure of low-dose penicillin (LDP) during early life resulted in metabolic syndrome (MetS) in mice. However, the underlying mechanism(s) and efficient approaches to counteracting this are largely unknown.MethodsWild-type (WT) or secretory IgA (SIgA)-deficient (Pigr-/-) C57BL/6 mice were exposed to LDP or not from several days before birth to 30 d of age. Five times of FMT or probiotics (a mixture of Lactobacillus bulgaricus and L. rhamnosus GG) treatments were applied to parts of these LDP-treated mice from 12 d to 28 d of life. Bacterial composition from different regions (mucosa and lumen) of the colon and ileum were analyzed through 16S rDNA sequencing. Intestinal IgA response was analyzed. Multiple parameters related to MetS were also determined. In addition, germ-free animals and in vitro tissue culture were also used to determine the correlations between LDP, gut microbiota (GM) and intestinal IgA response.ResultsLDP disturbed the intestinal bacterial composition, especially for ileal mucosa, the main inductive and effective sites of IgA response, in 30-d-old mice. The alteration of early GM resulted in a persistent inhibition of the intestinal IgA response, leading to a constant reduction of fecal and caecal SIgA levels throughout the 25-week experiment, which is early life-dependent, as transfer of LDP-GM to 30 d germ-free mice only resulted in a transient reduction in fecal SIgA. LDP-induced reduction in SIgA led to a decrease in IgA+ bacteria and a dysbiosis in the ileal mucosal samples of 25 week wild-type but not Pigr-/- mice. Moreover, LDP also resulted in increases in ileal bacterial encroachment and adipose inflammation, along with an enhancement of diet-induced MetS in an intestinal SIgA-dependent manner. Furthermore, several times of FMT or probiotic treatments during LDP treatment are efficient to fully (for FMT) or partially (for probiotics) counteract the LDP-effect on both GM and metabolism.ConclusionsEarly-life LDP-induced enhancement of diet-induced MetS is mediated by intestinal SIgA, which could be (partially) restored by FMT or probiotics treatment.

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The Dysbiosis of Gut Microbiota Caused by Low-Dose Cadmium Aggravate the Injury of Mice Liver through Increasing Intestinal Permeability

Microorganisms ◽

10.3390/microorganisms8020211 ◽

2020 ◽

Vol 8 (2) ◽

pp. 211 ◽

Cited By ~ 3

Author(s):

Yehao Liu ◽

Yuhui Li ◽

Yuhong Xia ◽

Kaiyong Liu ◽

Lingling Ren ◽

...

Keyword(s):

Gut Microbiota ◽

Intestinal Permeability ◽

Health Risks ◽

Low Dose ◽

Underlying Mechanism ◽

Mice Liver ◽

Hepatic Transcriptome ◽

Cd Exposure ◽

Gut Microbiota Composition

Cadmium (Cd), widely present in food and drinking water at low doses, can cause health risks. However, the mechanistic effects of long-term Cd exposure at low dose through dietary intake is poorly studied. The aim of this study is to elucidate whether the dysbiosis of gut microbiota caused by Cd at an environmental low dose can aggravate the injury of mice liver, and the possible mechanism is investigated. In order to explore the potential underlying mechanism, the analyses of the variation of gut microbiota composition, intestinal permeability, and hepatic transcriptome were conducted. Our results showed that gut microbiota was disturbed. The rise of intestinal permeability induced by the dysbiosis of gut microbiota resulted in more Cd ions accumulating in mice liver, but it could be restored partly through depleting gut microbiota by antibiotics cocktail. Transcriptomic analyses indicated that 162 genes were significantly differentially expressed including 59 up-regulated and 103 down-regulated in Cd treatment. These genes were involved in several important pathways. Our findings provide a better understanding about the health risks of cadmium in the environment.

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Long‐term changes in the gut microbiota after 14‐day bismuth quadruple therapy in penicillin‐allergic children

Helicobacter ◽

10.1111/hel.12721 ◽

2020 ◽

Vol 25 (5) ◽

Cited By ~ 1

Author(s):

Ying Zhou ◽

Ziqing Ye ◽

Junping Lu ◽

Shijian Miao ◽

Xiaolan Lu ◽

...

Keyword(s):

Gut Microbiota ◽

Quadruple Therapy ◽

Long Term Changes

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Low-Dose Sarin Exposure Produces Long Term Changes in Brain Neurochemistry of Mice

Neurochemical Research ◽

10.1007/s11064-012-0896-9 ◽

2012 ◽

Vol 38 (1) ◽

pp. 108-116 ◽

Cited By ~ 13

Author(s):

Dhawal P. Oswal ◽

Teresa L. Garrett ◽

Mariana Morris ◽

James B. Lucot

Keyword(s):

Low Dose ◽

Long Term Changes

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Prevention of Progression in Myopia: A Systematic Review

Diseases ◽

10.3390/diseases6040092 ◽

2018 ◽

Vol 6 (4) ◽

pp. 92 ◽

Cited By ~ 7

Author(s):

Aldo Vagge ◽

Lorenzo Ferro Desideri ◽

Paolo Nucci ◽

Massimiliano Serafino ◽

Giuseppe Giannaccare ◽

...

Keyword(s):

Low Dose ◽

Contact Lenses ◽

Rebound Effect ◽

Infectious Keratitis ◽

First Line ◽

Outdoor Activities ◽

Effect Of Treatment ◽

And Behavior ◽

Near Work

The prevalence of myopia has increased worldwide in recent decades and now is endemic over the entire industrial world. This increase is mainly caused by changes in lifestyle and behavior. In particular, the amount of outdoor activities and near work would display an important role in the pathogenesis of the disease. Several strategies have been reported as effective. Spectacles and contact lenses have shown only slight results in the prevention of myopia and similarly ortokerathology should not be considered as a first-line strategy, given the high risk of infectious keratitis and the relatively low compliance for the patients. Thus, to date, atropine ophthalmic drops seem to be the most effective treatment for slowing the progression of myopia, although the exact mechanism of the effect of treatment is still uncertain. In particular, low-dose atropine (0.01%) was proven to be an effective and safe treatment in the long term due to the lowest rebound effect with negligible side effects.

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Long-term changes of gut microbiota, antibiotic resistance, and metabolic parameters after Helicobacter pylori eradication: a multicentre, open-label, randomised trial

The Lancet Infectious Diseases ◽

10.1016/s1473-3099(19)30272-5 ◽

2019 ◽

Vol 19 (10) ◽

pp. 1109-1120 ◽

Cited By ~ 20

Author(s):

Jyh-Ming Liou ◽

Chieh-Chang Chen ◽

Chih-Min Chang ◽

Yu-Jen Fang ◽

Ming-Jong Bair ◽

...

Keyword(s):

Helicobacter Pylori ◽

Antibiotic Resistance ◽

Gut Microbiota ◽

Randomised Trial ◽

Metabolic Parameters ◽

Open Label ◽

Helicobacter Pylori Eradication ◽

Long Term Changes

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Low-dose penicillin exposure in early life decreases Th17 and the susceptibility to DSS colitis in mice through gut microbiota modification

Scientific Reports ◽

10.1038/srep43662 ◽

2017 ◽

Vol 7 (1) ◽

Cited By ~ 24

Author(s):

Shuang Jin ◽

Di Zhao ◽

Chenwen Cai ◽

Dongjuan Song ◽

Jun Shen ◽

...

Keyword(s):

Gut Microbiota ◽

Early Life ◽

Low Dose ◽

Dss Colitis

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Long-Term Changes in Neurocognition and Behavior Following Treatment of Sleep Disordered Breathing in School-Aged Children

SLEEP ◽

10.5665/sleep.3312 ◽

2014 ◽

Vol 37 (1) ◽

pp. 77-84 ◽

Cited By ~ 69

Author(s):

Sarah N. Biggs ◽

Anna Vlahandonis ◽

Vicki Anderson ◽

Robert Bourke ◽

Gillian M. Nixon ◽

...

Keyword(s):

Sleep Disordered Breathing ◽

School Aged Children ◽

Long Term Changes ◽

And Behavior ◽

Disordered Breathing

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Early-Life Exposure to Low-Dose Cadmium Accelerates Diethylnitrosamine and Diet-Induced Liver Cancer

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/1427787 ◽

2021 ◽

Vol 2021 ◽

pp. 1-15

Author(s):

Hongbo Men ◽

Jamie L. Young ◽

Wenqian Zhou ◽

Haina Zhang ◽

Xiang Wang ◽

...

Keyword(s):

Liver Cancer ◽

Early Life ◽

Low Dose ◽

Liver Tumors ◽

Cadmium Exposure ◽

Male Mice ◽

Nonalcoholic Fatty Liver ◽

Early Life Exposure ◽

The Impact

Maternal exposure to cadmium causes obesity and metabolic changes in the offspring, including nonalcoholic fatty liver disease-like pathology. However, whether maternal cadmium exposure accelerates liver cancer in the offspring is unknown. This study investigated the impact of early-life exposure to cadmium on the incidence and potential mechanisms of hepatocellular carcinoma (HCC) in offspring subjected to postweaning HCC induction. HCC in C57BL/6J mice was induced by diethylnitrosamine (DEN) injection at weaning, followed by a long-term high-fat choline-deficient (HFCD) diet. Before weaning, liver cadmium levels were significantly higher in mice with early-life cadmium exposure than in those without cadmium exposure. However, by 26 and 29 weeks of age, hepatic cadmium fell to control levels, while a significant decrease was observed in copper and iron in the liver. Both male and female cadmium-exposed mice showed increased body weight compared to non-cadmium-treated mice. For females, early-life cadmium exposure also worsened insulin intolerance but did not significantly promote DEN/HFCD diet-induced liver tumors. In contrast, in male mice, early-life cadmium exposure enhanced liver cancer induction by DEN/HFCD with high incidence and larger liver tumors. The liver peritumor tissue of early-life cadmium-exposed mice exhibited greater inflammation and disruption of fatty acid metabolism, accompanied by higher malondialdehyde and lower esterified triglyceride levels compared to mice without cadmium exposure. These findings suggest that early-life exposure to low-dose cadmium accelerates liver cancer development induced by a DEN/HFCD in male mice, probably due to chronic lipotoxicity and inflammation caused by increased uptake but decreased consumption of fatty acids.

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