On Burkholderiales order microorganisms and cystic fibrosis in Russia

Voronina, Olga L.; Kunda, Marina S.; Ryzhova, N. N.; Aksenova, Ekaterina I.; Sharapova, N. E.; Semenov, Andrey N.; Amelina, E.; Чучалин, А. Г.; Gintsburg, A. L.

doi:10.1186/s12864-018-4472-9

Cited by 19 publications

(10 citation statements)

References 60 publications

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“…S2). The most interesting finding was an increase in Burkholderiales, an order of pathogenic bacteria commonly found in hospital-borne infections, in the colon of MSD/sham-irradiated mice, while the levels of Burkholderiales in the colon of MAD/sham irradiated was mice was negligible (69). Furthermore, only minor increases in Burkholderiales were observed in the colon of MAD mice exposed to 3-Gy TBI, whereas more robust increases were observed in 8.5-GyϩMAD and 3-and 8.5-GyϩMSD mice, the treatment regimens strongly associated with severe RIGIS and mortality (Fig.…”

Section: Resultsmentioning

confidence: 98%

Methionine dietary supplementation potentiates ionizing radiation-induced gastrointestinal syndrome

Miousse

Ewing

Skinner

et al. 2020

American Journal of Physiology-Gastrointestinal and Liver Physi

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Methionine is an essential amino acid needed for a variety of processes in living organisms. Ionizing radiation depletes tissue methionine concentrations and leads to the loss of DNA methylation and decreased synthesis of glutathione. In this study, we aimed to investigate the effects of methionine dietary supplementation in CBA/CaJ mice after exposure to doses ranging from 3 to 8.5 Gy of 137Cs of total body irradiation. We report that mice fed a methionine-supplemented diet (MSD; 19.5 vs. 6.5 mg/kg in a methionine-adequate diet, MAD) developed acute radiation toxicity at doses as low as 3 Gy. Partial body irradiation performed with hindlimb shielding resulted in a 50% mortality rate in MSD-fed mice exposed to 8.5 Gy, suggesting prevalence of radiation-induced gastrointestinal syndrome in the development of acute radiation toxicity. Analysis of the intestinal microbiome demonstrated shifts in the gut ecology, observed along with the development of leaky gut syndrome and bacterial translocation into the liver. Normal gut physiology impairment was facilitated by alterations in the one-carbon metabolism pathway and was exhibited as decreases in circulating citrulline levels mirrored by decreased intestinal mucosal surface area and the number of surviving crypts. In conclusion, we demonstrate that a relevant excess of methionine dietary intake exacerbates the detrimental effects of exposure to ionizing radiation in the small intestine. NEW & NOTEWORTHY Methionine supplementation, instead of an anticipated health-promoting effect, sensitizes mice to gastrointestinal radiation syndrome. Mechanistically, excess of methionine negatively affects intestinal ecology, leading to a cascade of physiological, biochemical, and molecular alterations that impair normal gut response to a clinically relevant genotoxic stressor. These findings speak toward increasing the role of registered dietitians during cancer therapy and the necessity of a solid scientific background behind the sales of dietary supplements and claims regarding their benefits.

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Section: Resultsmentioning

confidence: 98%

Methionine dietary supplementation potentiates ionizing radiation-induced gastrointestinal syndrome

Miousse

Ewing

Skinner

et al. 2020

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…We also found the order Burkholderiales to be more significantly enriched in the NiO NPs-exposed groups based on LEfSe analysis at 1 day after instillation. Burkholderiales are clinically associated with the exacerbation of patients with cystic fibrosis and abundantly found in patients with lung transplantation [ 44 , 48 , 49 ]. Previous studies have shown that burkholdeira spp., included in the order Burkholderiales , exert proinflammatory effects on the lung by inducing respiratory epithelial cells to secrete cytokines such as IL-1β, IL-6, IL-8, TNF-α, MCP-1, and chemokine ligand 20 (CCL20) in humans [ 50 , 51 , 52 ].…”

Section: Discussionmentioning

confidence: 99%

Exposure to Nickel Oxide Nanoparticles Induces Acute and Chronic Inflammatory Responses in Rat Lungs and Perturbs the Lung Microbiome

Jeong

Jeon

et al. 2022

IJERPH

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Nickel oxide nanoparticles (NiO NPs) are highly redox active nanoparticles. They can cause acute and chronic inflammation in rat lungs. Unlike the gut microbiome, the association between the lung microbiome’s role and pulmonary inflammatory response to inhaled nanoparticles remains largely unexplored. We aimed to explore the interaction between the lung microbiome and inflammatory responses in rats exposed to NiO NPs. Thirty female Wistar rats were randomly categorized into control and low- (50 cm2/rat), and high- (150 cm2/rat) dose NiO NPs exposure groups. NiO NPs were intratracheally instilled, and cytological, biochemical, proinflammatory cytokine, and lung microbiome analyses of bronchoalveolar lavage fluid were performed at 1 day and 4 weeks after instillation. NiO NPs caused a neutrophilic and lymphocytic inflammatory response in rat lung. We demonstrated that exposure to NiO NPs can alter the lung microbial composition in rats. In particular, we found that more Burkholderiales are present in the NiO NPs exposure groups than in the control group at 1 day after instillation. Dysbiosis in the lung microbiome is thought to be associated with acute lung inflammation. We also suggested that Burkholderiales may be a key biomarker associated with lung neutrophilic inflammation after NiO NPs exposure.

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“…Ziganshina and colleagues (2016) found that the order Burkholderiales and the genus Curvibacter were elevated in patients' atherosclerotic plaque samples [15]. Voronina et al showed that Burkholderiales and other members of Ralstonia and Propionibacterium represented the most elevated taxa within atherosclerotic plaques [16]. Some bacteria founded in plaques were also associated with several clinical traits, such as alanine aminotransferase, total cholesterol, and fibrinogen levels [18].…”

Section: Gut Dysbiosis In Acvdmentioning

confidence: 99%

The Gut Dysbiosis and Immune System in Atherosclerotic Cardiovascular Disease (ACVD)

Yoo¹,

Sniffen²,

Percy³

et al. 2021

Preprint

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Atherosclerosis is a leading cause of cardiovascular disease and mortality worldwide. Alterations in the gut microbiota composition, known as gut dysbiosis, have been shown to contribute to atherosclerotic cardiovascular disease (ACVD) development through several pathways. Disruptions in gut homeostasis are associated with activation of immune processes and systemic inflammation. The gut microbiota produces several metabolic products, namely trimethylamine (TMA), which is used to produce the proatherogenic metabolite trimethylamine-N-oxide (TMAO). Short chain fatty acids (SCFAs), including acetate, butyrate, and propionate, and certain bile acids (BAs) produced by the gut microbiota lead to inflammation resolution and decrease atherogenesis. Chronic low-grade inflammation is associated to common risk factors for atherosclerosis, including metabolic syndrome, type 2 diabetes mellitus (T2DM), and obesity. Novel strategies for reducing ACVD include the use of nutraceuticals such as resveratrol, modification of glucagon-like peptide 1 (GLP-1) levels, supplementation with probiotics, and administration of prebiotic SCFAs and BAs. Investigation into the relationship between the gut microbiota and its metabolites, and the host immune system could reveal promising insight into ACVD development, prognostic factors, and treatments.

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On Burkholderiales order microorganisms and cystic fibrosis in Russia

Cited by 19 publications

References 60 publications

Methionine dietary supplementation potentiates ionizing radiation-induced gastrointestinal syndrome

Methionine dietary supplementation potentiates ionizing radiation-induced gastrointestinal syndrome

Exposure to Nickel Oxide Nanoparticles Induces Acute and Chronic Inflammatory Responses in Rat Lungs and Perturbs the Lung Microbiome

The Gut Dysbiosis and Immune System in Atherosclerotic Cardiovascular Disease (ACVD)

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