The gut microbiome and elevated cardiovascular risk in obesity and autoimmunity

Kasselman, Lora J.; Vernice, Nicholas A.; DeLeon, Joshua; Reiss, Allison B.

doi:10.1016/j.atherosclerosis.2018.02.036

Cited by 135 publications

(94 citation statements)

References 104 publications

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“…An increased level of Prevotella histicola bacteria can increase the LPS concentration, which activates toll‐like receptor‐4 (TLR4). TLR4 activation is associated with the secretion of interleukin‐4 (IL‐4) and the failure of T cells to properly differentiate, both of which contribute to the chronic inflammatory state that is characteristic of patients with CVD and RA . Many disease‐modifying antirheumatic drugs can reverse the dysbiosis associated with RA …”

Section: Discussionmentioning

confidence: 99%

“…RA is also associated with chronic inflammation and significant alterations in the composition of intestinal microbiota. The abnormal changes of gut microbiota may correlate with chronic inflammation, and together increase the risk of CVD . One study indicated that gut microbiota can metabolize dietary L ‐carnitine into trimethylamine N‐oxide (TMAO), and this can accelerate atherosclerosis .…”

Section: Introductionmentioning

confidence: 99%

“…One study indicated that gut microbiota can metabolize dietary L ‐carnitine into trimethylamine N‐oxide (TMAO), and this can accelerate atherosclerosis . Treatment of RA patients with probiotics may help to restore intestinal health, reduce inflammation, and decrease the incidence of CVD . An appropriate animal model could help scientists to better understand the relationships of inflammatory arthritis and atherosclerosis in RA.…”

Section: Introductionmentioning

confidence: 99%

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Protective effect of hydroxychloroquine on rheumatoid arthritis‐associated atherosclerosis

Shi

Zhang

Silverman

et al. 2019

Anim Models and Exp Med

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Background Patients with rheumatoid arthritis (RA) have an increased risk for cardiovascular disease. We examined the effect of gut microbiota in a mouse model of RA that develops atherosclerosis. Methods We created three groups of K/BxN female mice that were positive for the anti‐glucose‐6‐phosphate isomerase (GPI) antibody: control diet (CD), high fat diet (HFD), and HFD with hydroxychloroquine (HFD + HCQ). Serological tests were used to detect the serum levels of total cholesterol (TCHO), low‐density lipoprotein cholesterol (LDL‐C), triglyceride (TG), high‐density lipoprotein cholesterol (HDL‐C), anti‐GPI antibody titers, and serum cytokines. Atherosclerotic plaque was determined by histological analysis, and gut microbiota were determined by 16sV4 sequencing. Results Relative to mice given the CD, those receiving the HFD had increased serum levels of LDL‐C, TCHO, and TG, decreased serum levels of HDL‐C, increased atherosclerotic lesions in the aortic root, and altered gut microbiota. Addition of HCQ to HFD decreased the serum levels of LDL‐C, TCHO, and TG, increased serum levels of HDL‐C, and decreased the atherosclerotic lesions in the aortic root. Mice receiving HFD + HCQ also had the greatest bacterial diversity among the three experimental groups. Moreover, HCQ treatment significantly increased the abundance of Akkermansia and Parabacteroides , and decreased the abundance of Clostridium sensu stricto cluster 1, and therefore may be responsible for the reduced RA‐associated atherosclerosis and dyslipidemia. Conclusion Our mouse model of RA indicated that HFD increased ankle width and aggravated atherosclerosis and dyslipidemia, and that HCQ alleviated the dyslipidemia and atherosclerosis, but had no effect on ankle width.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Protective effect of hydroxychloroquine on rheumatoid arthritis‐associated atherosclerosis

Shi

Zhang

Silverman

et al. 2019

Anim Models and Exp Med

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“…Dysbiosis plays a main role in increasing intestinal permeability, which permits passage of bacteria‐derived products such as LPS into the portal circulation. In addition to IBD, dysbiosis, intestinal permeability and the ensuing inflammation, has been associated with numerous diseases including NEC, allergies, nonalcoholic fatty liver disease (NAFLD), cardiovascular disease, rheumatoid arthritis, and numerous neurological disorders such as bipolar, schizophrenia, autism, and Parkinson's . Systemic inflammation was assessed using an inflammatory cytokine protein array that detects 40 different inflammatory cytokines.…”

Section: Resultsmentioning

confidence: 99%

Excess Dietary Zinc Intake in Neonatal Mice Causes Oxidative Stress and Alters Intestinal Host–Microbe Interactions

Podany

Rauchut

et al. 2018

Molecular Nutrition Food Res

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Scope Greater than 68% of young infants are exposed to dietary zinc (Zn) levels that are higher than the Tolerable Upper Intake Limit. However, the consequences of excess dietary Zn during early life on intestinal function and host–microbe interactions are unknown. Methods and Results Neonatal mice are gavaged with 100 Zn µg d–1 from postnatal day (PN) 2 through PN10 and indices of intestinal function and host–microbe interactions are compared to unsupplemented mice. Excess dietary Zn causes oxidative stress, increases goblet cell number and mucus production, and are associated with increased intestinal permeability and systemic inflammation. Over 900 genes are differentially expressed; 413 genes display a fold‐change >1.60. The Gene Ontology Biological processes most significantly affected include biological adhesion, the immune system, metabolic processes, and response to stimulus. Key genes most highly and significantly upregulated include ALDH2, MT1, TMEM6, CDK20, and COX62b, while CALU, ST3GAL4, CRTC2, SLC28A2, and COMMA1 are downregulated. These changes are associated with a microbiome enriched in pathogenic taxa including Pseudomonadales and Campylobacter, and greater expression of bacterial stress response genes. Conclusion Excess dietary Zn may have unforeseen influences on epithelial signaling pathways, barrier function, and luminal ecology in the intestine that may have long‐term consequences on intestinal health.

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“…When homeostasis becomes unbalanced and microbial populations and functions are altered, the phenomenon is called dysbiosis. It has been directly associated [149][150][151] with the onset, progression and therapeutic response of multiple health conditions, including lung-associated disorders [152,153], obesity [154,155], diabetes [156,157], cardiovascular disease and atherosclerosis [158][159][160][161], chronic kidney disease [162][163][164], cancer [165][166][167], neurological and neuropsychiatric disorders [168][169][170][171], and, in the spirit of this review, IBD [172][173][174].…”

Section: Microbiome In Ibd: the Meta-paradigmmentioning

confidence: 96%

Systems biology in inflammatory bowel diseases: on the way to precision medicine

Dovrolis

Filidou

Kolios

2019

aog

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Inflammatory bowel diseases (IBD) are chronic and recurrent inflammatory disorders of the gastrointestinal tract. The elucidation of their etiopathology requires complex and multiple approaches. Systems biology has come to fulfill this need in approaching the pathogenetic mechanisms of IBD and its etiopathology, in a comprehensive way, by combining data from different scientific sources. In combination with bioinformatics and network medicine, it uses principles from computer science, mathematics, physics, chemistry, biology, medicine and computational tools to achieve its purposes. Systems biology utilizes scientific sources that provide data from omics studies (e.g., genomics, transcriptomics, etc.) and clinical observations, whose combined analysis leads to network formation and ultimately to a more integrative image of disease etiopathogenesis. In this review, we analyze the current literature on the methods and the tools utilized by systems biology in order to cover an innovative and exciting field: IBD-omics.

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The gut microbiome and elevated cardiovascular risk in obesity and autoimmunity

Cited by 135 publications

References 104 publications

Protective effect of hydroxychloroquine on rheumatoid arthritis‐associated atherosclerosis

Protective effect of hydroxychloroquine on rheumatoid arthritis‐associated atherosclerosis

Excess Dietary Zinc Intake in Neonatal Mice Causes Oxidative Stress and Alters Intestinal Host–Microbe Interactions

Systems biology in inflammatory bowel diseases: on the way to precision medicine

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