Cigarette smoking status alters dysbiotic gut microbes in hypertensive patients.
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ABSTRACT:
SUBMITTER: Wang P
PROVIDER: S-EPMC8678690 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundAccumulating studies have suggested that gut microbiota (GM) dysbiosis and vitamin D3 deficiency each play an important role during the progression of hypertension (HTN). However, few studies have characterized the underlying interaction between GM shift and vitamin D3 deficiency in HTN patients.HypothesisThis study aimed to evaluate the possible crosstalk between GM dysbiosis and vitamin D deficiency in the pathogenesis of HTN.MethodsIn a cohort of 34 HTN patients and 15 healthy controls, we analyzed the fecal microbiota products, GM composition, and the interaction between GM and vitamin D3.ResultsVitamin D3 was significantly decreased in feces of HTN patients (P = .006, vs controls) and was correlated with altered GM, including decreased Shannon index (R2 = 0.1296, P = .0111) and Pielou evenness (R2 = 0.1509, P = .0058). Moreover, vitamin D3 positively correlated with HTN-reduced bacterial genera, including Subdoligranulum (R2 = 0.181, P = .0023), Ruminiclostridium (R2 = 0.1217, P = .014), Intestinimonas (R2 = 0.2036, P = .0011), Pseudoflavonifractor (R2 = 0.1014, P = .0257), Paenibacillus (R2 = 0.089, P = .0373), and Marvinbryantia (R2 = 0.08173, P = .0464). Partial least squares structural equation modeling showed that 27.7% of the total effect of gut microbiome on HTN was mediated by limiting vitamin D production. Finally, receiver operating characteristic curve analysis revealed the predictive capacity of differential gut microbiome signatures and decreased vitamin D3 to distinguish HTN patients (AUC = 0.749, P = .006).ConclusionsOur findings suggest that the GM dysbiosis contributing to the development of HTN might be partially mediated by vitamin D3 deficiency. Future studies involving the underlying mechanism and intervention strategies targeting microbiome composition and vitamin D3 to counteract the progression of HTN are warranted.
| S-EPMC6672427 | biostudies-literature
Project description:Numerous health consequences of tobacco smoke exposure have been characterized, and the effects of smoking on traditional measures of male fertility are well described. However, a growing body of data indicates that pre‐conception paternal smoking also confers increased risk for a number of morbidities on offspring. The mechanism for this increased risk has not been elucidated, but it is likely mediated, at least in part, through epigenetic modifications transmitted through spermatozoa. In this study, we investigated the impact of cigarette smoke exposure on sperm DNA methylation patterns in 78 men who smoke and 78 never‐smokers using the Infinium Human Methylation 450 beadchip. We investigated two models of DNA methylation alterations: (i) consistently altered methylation at specific CpGs or within specific genomic regions and (ii) stochastic DNA methylation alterations manifest as increased variability in genome‐wide methylation patterns in men who smoke. We identified 141 significantly differentially methylated CpGs associated with smoking. In addition, we identified a trend toward increased variance in methylation patterns genome‐wide in sperm DNA from men who smoke compared with never‐smokers. These findings of widespread DNA methylation alterations are consistent with the broad range of offspring heath disparities associated with pre‐conception paternal smoke exposure and warrant further investigation to identify the specific mechanism by which sperm DNA methylation perturbation confers risk to offspring health and whether these changes can be transmitted to offspring and transgenerationally.
2018-05-23 | GSE114753 | GEO
Project description:Numerous health consequences of tobacco smoke exposure have been characterized, and the effects of smoking on traditional measures of male fertility are well described. However, a growing body of data indicates that pre-conception paternal smoking also confers increased risk for a number of morbidities on offspring. The mechanism for this increased risk has not been elucidated, but it is likely mediated, at least in part, through epigenetic modifications transmitted through spermatozoa. In this study, we investigated the impact of cigarette smoke exposure on sperm DNA methylation patterns in 78 men who smoke and 78 never-smokers using the Infinium Human Methylation 450 beadchip. We investigated two models of DNA methylation alterations: (i) consistently altered methylation at specific CpGs or within specific genomic regions and (ii) stochastic DNA methylation alterations manifest as increased variability in genome-wide methylation patterns in men who smoke. We identified 141 significantly differentially methylated CpGs associated with smoking. In addition, we identified a trend toward increased variance in methylation patterns genome-wide in sperm DNA from men who smoke compared with never-smokers. These findings of widespread DNA methylation alterations are consistent with the broad range of offspring heath disparities associated with pre-conception paternal smoke exposure and warrant further investigation to identify the specific mechanism by which sperm DNA methylation perturbation confers risk to offspring health and whether these changes can be transmitted to offspring and transgenerationally.
| S-EPMC5679018 | biostudies-literature
Project description:There have been few large-scale studies on the relationship between smoking and gut microbiota. We investigated the relationship between smoking status and the composition of gut microbiota. This was a population-based cross-sectional study using Healthcare Screening Center cohort data. A total of 758 men were selected and divided into three groups: never (n = 288), former (n = 267), and current smokers (n = 203). Among the three groups, there was no difference in alpha diversity, however, Jaccard-based beta diversity showed significant difference (p = 0.015). Pairwise permutational multivariate analysis of variance (PERMANOVA) tests between never and former smokers did not show a difference; however, there was significant difference between never and current smokers (p = 0.017) and between former and current smokers (p = 0.011). Weighted UniFrac-based beta diversity also showed significant difference among the three groups (p = 0.038), and pairwise PERMANOVA analysis of never and current smokers showed significant difference (p = 0.01). In the analysis of bacterial composition, current smokers had an increased proportion of the phylum Bacteroidetes with decreased Firmicutes and Proteobacteria compared with never smokers, whereas there were no differences between former and never smokers. In conclusion, gut microbiota composition of current smokers was significantly different from that of never smokers. Additionally, there was no difference in gut microbiota composition between never and former smokers.
| S-EPMC6162563 | biostudies-literature
Project description:Alveolar macrophages from never smokers and active smokers were isolated by bronchoalveolar lavage and gene expression was measured. Chronic cigarette smoke exposure, as occurs in smoker's lungs, leads to significant changes in gene expression. Of note, RNA was isolated immediately following bronchoscopy. Alveolar macrophage levels were >95%.
2012-10-02 | GSE34517 | GEO
Project description:Alveolar macrophages from never smokers and active smokers were isolated by bronchoalveolar lavage and gene expression was measured. Chronic cigarette smoke exposure, as occurs in smoker's lungs, leads to significant changes in gene expression. Of note, RNA was isolated immediately following bronchoscopy. Alveolar macrophage levels were >95%. 4 never smokers and 4 active smokers were recruited for the study. After bronchoalveolar lavage and RNA isolation, gene expression was measured using Affymetrix Human Exon 1.0 ST arrays.
2012-10-02 | E-GEOD-34517 | biostudies-arrayexpress
Project description:Introduction:Although socioeconomic status (SES) resources influence population and individual health behaviors, socially marginalized groups gain significantly less health from their SES indicators, such as education and income, compared to the socially privileged groups. This pattern is called marginalization-related diminished returns (MDRs). However, most of the MDRs literature is derived from studies that have defined marginalization based on race and ethnicity. As a result, more research is needed on MDRs due to immigration. To extend what is known about MDRs due to immigration, the current study compared a national sample of immigrants and non-immigrants for the effects of education and income on current cigarette smoking of adults in the United States. Methods:This is a cross-sectional study. The 2015 National Health Interview Survey (NHIS) enrolled 14,149 individuals who were either immigrants (n=1977; 14.0%) or non-immigrants (n=12,166; 86.0%). The independent variables (IV) were education and income that were treated as categorical variables. The dependent variable was current cigarette smoking. Age, gender, race, ethnicity, marital status, employment, and region were confounders. Immigration was the moderator. Logistic regression was used for data analysis. Results:High education and income were associated with lower odds of current cigarette smoking. However, immigration showed significant statistical interactions with both education and income. These interactions were suggestive of smaller protective effects of high education and income on current cigarette smoking for immigrant than non-immigrant adults. Conclusion:In line with the MDRs, the effects of education and income on tobacco use is weaker for immigrant than non-immigrant adults.
| S-EPMC7351318 | biostudies-literature
Project description:Objectives Substance use during pregnancy is a significant public health issue. Prenatal substance use increased in the past decade while prenatal cigarette smoking has remained stable. Co-use of tobacco and other drugs is a concern because of potential additive risks. This study aims to describe the prevalence rates of substance use among pregnant women and examine the association between smoking status (nonsmoker, recent quitter and current smoker) and other drug use. Methods In this cross-sectional study, pregnant women (n?=?500) were recruited from two obstetric practices to complete three substance use screeners and have their urine tested for 12 different drug classes, including cannabis, opioids and cocaine. Participants were divided into three groups based on survey responses: nonsmokers, recent quitters (smoked in the month prior to pregnancy but not past month) and current smokers (past-month). Results Approximately 29% of participants reported smoking in the month before pregnancy. During pregnancy, 17, 12 and 71% were current smokers, recent quitters and nonsmokers respectively. Overall prevalence of illicit or prescription drug use in pregnancy was 27%. Cannabis was the most common drug used in pregnancy with prevalence of 22%, followed by opioids (4%), cocaine (1%), tricyclic antidepressants (TCAs) (1%), amphetamines (1%), and benzodiazepines (1%). On multivariable logistic regression, smoking in pregnancy was associated with a positive urine drug screen; with adjusted odds ratio (aOR) 4.7 (95% CI 2.6-8.3) for current smokers and 1.6 (95% CI 0.8-3.3) for recent quitters. Factors negatively associated with positive drug screen were second and third trimester pregnancies, 0.5 (0.3-0.9) and 0.3 (0.2-0.6) respectively; and employment, 0.5 (0.3-0.8). Conclusions for Practice Co-use of tobacco and illicit drugs, particularly cannabis, is relatively high during pregnancy. Additional research is needed to understand the health implications of co-use versus use of tobacco only. Given the strong association between smoking and other drug use, clinicians should routinely assess for illicit drug use in women who smoke during pregnancy.
| S-EPMC6430977 | biostudies-literature
Project description:Background: Cigarette smoking has been considered a modifiable risk factor for coronary artery disease (CAD). Changes in gut microbiota and microbe-derived metabolites have been shown to influence atherosclerotic pathogenesis. However, the effect of cigarette smoking on the gut microbiome and serum metabolites in CAD remains unclear. Method: We profiled the gut microbiota and serum metabolites of 113 male participants with diagnosed CAD including 46 current smokers, 34 former smokers, and 33 never smokers by 16S ribosomal RNA (rRNA) gene sequencing and untargeted metabolomics study. A follow-up study was conducted. PICRUSt2 was used for metagenomic functional prediction of important bacterial taxa. Results: In the analysis of the microbial composition, the current smokers were characterized with depleted Bifidobacterium catenulatum, Akkermansia muciniphila, and enriched Enterococcus faecium, Haemophilus parainfluenzae compared with the former and never smokers. In the untargeted serum metabolomic study, we observed and annotated 304 discriminant metabolites, uniquely including ceramides, acyl carnitines, and glycerophospholipids. Pathway analysis revealed a significantly changed sphingolipids metabolism related to cigarette smoking. However, the change of the majority of the discriminant metabolites is possibly reversible after smoking cessation. While performing PICRUSt2 metagenomic prediction, several key enzymes (wbpA, nadM) were identified to possibly explain the cross talk between gut microbiota and metabolomic changes associated with smoking. Moreover, the multi-omics analysis revealed that specific changes in bacterial taxa were associated with disease severity or outcomes by mediating metabolites such as glycerophospholipids. Conclusions: Our results indicated that both the gut microbiota composition and metabolomic profile of current smokers are different from that of never smokers. The present study may provide new insights into understanding the heterogenic influences of cigarette smoking on atherosclerotic pathogenesis by modulating gut microbiota as well as circulating metabolites.
| S-EPMC8581230 | biostudies-literature
Project description:BackgroundThe effect of oral microbiota on the intestinal microbiota has garnered growing attention as a mechanism linking periodontal diseases to systemic diseases. However, the salivary microbiota is diverse and comprises numerous bacteria with a largely similar composition in healthy individuals and periodontitis patients.AimWe explored how health-associated and periodontitis-associated salivary microbiota differently colonized the intestine and their subsequent systemic effects.MethodsThe salivary microbiota was collected from a healthy individual and a periodontitis patient and gavaged into C57BL/6NJcl[GF] mice. Gut microbial communities, hepatic gene expression profiles, and serum metabolites were analyzed.ResultsThe gut microbial composition was significantly different between periodontitis-associated microbiota-administered (PAO) and health-associated oral microbiota-administered (HAO) mice. The hepatic gene expression profile demonstrated a distinct pattern between the two groups, with higher expression of lipid and glucose metabolism-related genes. Disease-associated metabolites such as 2-hydroxyisobutyric acid and hydroxybenzoic acid were elevated in PAO mice. These metabolites were significantly correlated with characteristic gut microbial taxa in PAO mice. Conversely, health-associated oral microbiota were associated with higher levels of beneficial serum metabolites in HAO mice.ConclusionThe multi-omics approach used in this study revealed that periodontitis-associated oral microbiota is associated with the induction of disease phenotype when they colonized the gut of germ-free mice.
| S-EPMC9373767 | biostudies-literature