Background: A growing body of evidence highlights the role of the intestine in the development of various alcohol use disorder (AUD) complications. The intestinal microbiome has been proposed as an essential factor in mediating the development of AUD complications such as alcoholic liver disease. Objectives: To provide a comprehensive description of alcohol-induced intestinal microbiome alterations. Methods: We conducted a systematic review of studies investigating the effect of alcohol on the intestinal microbiome using the PRISMA checklist. We searched the Medline database on the PubMed platform for studies determining the effect of alcohol on microbiota in individuals with AUD. The manual search included references of retrieved articles. Only human studies examining the intestinal bacterial microbiome using 16S ribosomal RNA sequencing were included. Data comparing relative abundances of bacteria comprising intestinal microbiota was extracted. Results: We retrieved 17 studies investigating intestinal microbiome alterations in individuals with AUD. Intestinal microbiome alterations in individuals with AUD included depletion of Akkermansia muciniphila and Faecalibacterium prausnitzii and an increase of Enterobacteriaceae. At the phylum level, a higher abundance of Proteobacteria and lower of Bacteroidetes were found. Mixed results regarding Bifidobacterium were obtained. Several species of short-chain fatty acids producing bacteria had a lower abundance in individuals with alcohol use disorder. Conclusion: Intestinal microbiome alterations associated with dysbiosis in individuals with AUD are generally consistent across studies, making it a promising target in potential AUD complications treatment. ARTICLE HISTORY
Norepinephrine (NE), the stress hormone, stimulates many bacterial species' growth and virulence, including Escherichia coli. However, the hormone's impact on the adherent-invasive E. coli (AIEC) implicated in Crohn's disease is poorly understood. In the study, we have investigated the effect of NE on the interaction of six AIEC strains isolated from an intestinal biopsy from 6 children with Crohn's disease with Caco-2 cells. Our study focused on type 1 fimbria and CEACAM6 molecules serving as docking sites for these adhesins. The study results demonstrated that the hormone significantly increased the adherence and invasion of AIEC to Caco-2 cells in vitro. However, the effect was not associated with the impact of NE on the increased proliferation rate of AIEC or the fimA gene expression vital for their interaction with intestinal epithelial cells. Instead, the carcinoembryonic antigen-related cell-adhesion-molecule-6 (CEACAM6) level was increased significantly in NE-treated Caco-2 cells infected with AIEC in contrast to control uninfected NE-treated cells. These results indicated that NE influenced the interaction of AIEC with intestinal epithelium by increasing the level of CEACAM6 in epithelial cells, strengthening their adherence and invasion.
Several concerns regarding the safety of face masks use have been propounded in public opinion. The objective of this review is to examine if these concerns find support in the literature by providing a comprehensive overview of physiological responses to the use of face masks. We have performed a systematic review, pairwise and network meta-analyses to investigate physiological responses to the use of face masks. The study has been registered with PROSPERO (C RD42020224791). Obtained results were screened using our exclusion and inclusion criteria. Meta-analyses were performed using the GeMTC and meta R packages. We have identified 26 studies meeting our inclusion and exclusion criteria, encompassing 751 participants. The use of face masks was not associated with significant changes in pulsoxymetrically measured oxygen saturation, even during maximal-effort exercises. The only significant physiological responses to the use of face masks during low-intensity activities were a slight increase in heart rate, mildly elevated partial pressure of carbon dioxide (not meeting criteria for hypercarbia), increased temperature of facial skin covered by the mask, and subsequent increase of the score in the rating of heat perception, with N95 filtering facepiece respirators having a greater effect than surgical masks. In high-intensity conditions, the use of face masks was associated with decreased oxygen uptake, ventilation, and RR. Face masks are safe to use and do not cause significant alterations in human physiology. The increase in heart rate stems most likely from increased respiratory work required to overcome breathing resistance. The increase in carbon dioxide is too small to be clinically relevant. An increased rating of heat perception when using face masks results from higher temperature of facial skin covered by the mask.
In recent years, the importance of the gut microbiome in human health and disease has increased. Growing evidence suggests that gut dysbiosis might be a crucial risk factor for coronary artery disease (CAD). Therefore, we conducted a systematic review and meta-analysis to determine whether or not CAD is associated with specific changes in the gut microbiome. The V3–V4 regions of the 16S rDNA from fecal samples were analyzed to compare the gut microbiome composition between CAD patients and controls. Our search yielded 1181 articles, of which 21 met inclusion criteria for systematic review and 7 for meta-analysis. The alpha-diversity, including observed OTUs, Shannon and Simpson indices, was significantly decreased in CAD, indicating the reduced richness of the gut microbiome. The most consistent results in a systematic review and meta-analysis pointed out the reduced abundance of Bacteroidetes and Lachnospiraceae in CAD patients. Moreover, Enterobacteriaceae, Lactobacillus, and Streptococcus taxa demonstrated an increased trend in CAD patients. The alterations in the gut microbiota composition are associated with qualitative and quantitative changes in bacterial metabolites, many of which have pro-atherogenic effects on endothelial cells, increasing the risk of developing and progressing CAD.
Gut dysbiosis, alongside a high-fat diet and cigarette smoking, is considered one of the factors promoting coronary arterial disease (CAD) development. The present study aimed to research whether gut dysbiosis can increase bacterial metabolites concentration in the blood of CAD patients and what impact these metabolites can exert on endothelial cells. The gut microbiomes of 15 age-matched CAD patients and healthy controls were analyzed by 16S rRNA sequencing analysis. The in vitro impact of LPS and indoxyl sulfate at concentrations present in patients’ sera on endothelial cells was investigated. 16S rRNA sequencing analysis revealed gut dysbiosis in CAD patients, further confirmed by elevated LPS and indoxyl sulfate levels in patients’ sera. CAD was associated with depletion of Bacteroidetes and Alistipes. LPS and indoxyl sulfate demonstrated co-toxicity to endothelial cells inducing reactive oxygen species, E-selectin, and monocyte chemoattractant protein-1 (MCP-1) production. Moreover, both of these metabolites promoted thrombogenicity of endothelial cells confirmed by monocyte adherence. The co-toxicity of LPS and indoxyl sulfate was associated with harmful effects on endothelial cells, strongly suggesting that gut dysbiosis-associated increased intestinal permeability can initiate or promote endothelial inflammation and atherosclerosis progression.
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