From the emerging studies, the more diverse the microbial population in the gut, the healthier the gut. Health benefits are associated with the functional characteristics of these diverse microbial genes. Extrinsic factors causing dysbiosis are extensively studied however, linking the varying degree of consequences to the respective factors and therapeutic possibilities are not explored at length. This review aims to examine from previous studies and put forward the types of dysbiosis, the immediate consequences and the scientific approaches to restore disrupted microbiota. Dietary supplements are found to be one of the factors contributing profoundly to the alteration of gut microbiota. While diet rich in fibre and fermented food established a diverse microbiome and produce vital metabolites, high fat, animal proteins and high caloric carbohydrate are as well relative to dysbiosis among infants, adult or diseases individuals. The intermittent fasting, feeding methods, the pH and water quality are among the factors associated with dysbiosis. Prebiotics and Probiotics maintain and restore gut homeostasis. Antibiotic-induced dysbiosis are relatively on the spectrum of activity, the pharmacokinetics properties, the dose taken during the treatment route of administration and the duration of drug therapy. The higher the altitude, the lesser the diversity. Extreme temperatures as well are related to reduced microbial activity and metabolism. Delivery through caserium-section deprived the newborn from restoring valuable vaginal bacterial species and the baby will instead assumed intestinal microbiota-like. While exercise and oxidative stress contribute even though moderately, fecal microbial transfer (FMT) also influence gut microbiota.
Background: The intestinal flora can influence behavior through the microbiota-gut-brain axis and is closely related to the occurrence and development of nervous system diseases such as depression. Probiotics like Lactobacillus may regulate the balance of the intestinal flora and play an active role in preventing and treating depression.Methods: Eight-week-old C57BL/6J mice (n=32) were randomly and equally divided into a normal control group, a control + Lac group, a model group, and a model + Lac group. The model and model + Lac groups were intraperitoneally injected with 1.2 mg/kg lipopolysaccharide for 7 days, and the behavior of the mice was assessed 24 hours later. The normal and model groups received intragastric administration of saline daily, while the control + Lac and model + Lac groups were given 10 9 cfu Lac intragastrically daily for 7 days. The inhibitory effect of Lac and its fermentation products on depression-related bacteria were examined in vitro.Results: Lac effectively inhibited the production of depression-like behaviors in mice. The expression levels of zonula occludens-1 (ZO-1) and E-cadherin in the small intestine in the model group were significantly decreased, but Lac abrogated this effect. Overactivation of microglia and decreased expression of dopamine transporter (DAT) in brain tissues, which are closely related to depression, were also abrogated by Lac treatment. Furthermore, the expression of toll-like receptor 4 (TLR4) and nod-like receptor protein-3 (NLRP3), as well as the level of interleukin-1 beta (IL-1β) in the intestine and brain, were all significantly increased; however, these effects were subsequently abrogated by Lac. Moreover, Lac inhibited dysbiosis through its metabolites.Conclusions: Lac has a remarkable antidepressant function, which it performs through the inhibition of dysbiosis (via its metabolites) and pattern recognition receptor TLR4 signaling.
Studies have shown that metabolic diseases, such as obesity, are significantly associated with intestinal flora imbalance. The amplification of opportunistic pathogens induced by the glyoxylic acid cycle contributes to intestinal flora imbalance. Promising, though, is that saturated hydrogen can effectively improve the occurrence and development of metabolic diseases, such as obesity. However, the specific mechanism of how saturated hydrogen operates is still not very clear. In this study, after a high-fat diet, the level of total cholesterol, total glyceride, and low-density lipoprotein in the peripheral blood of mice increased, and that of high-density lipoprotein decreased. Intestinal fatty acid metabolism-related gene Apolipoprotein E (ApoE), fatty acid synthase (FAS), intestinal fatty acid-binding protein (I-FAPB), acetyl-CoA carboxylase 1 (ACC1), peroxisome proliferator-activated receptor γ (PPARγ), and stearoyl-CoA desaturase 1 (SCD1) increased significantly. Bacteroides, Bifidobacteria, and Lactobacillus counts in feces decreased considerably, while Enterobacter cloacae increased. The activity of isocitrate lyase in feces increased markedly. Treatment of mice with saturated hydrogen led to decreased total cholesterol, total glyceride, and low-density lipoprotein and increased high-density lipoprotein in the peripheral blood. FAS and I-FAPB gene expression in the small intestine decreased. Bacteroides, Bifidobacteria, and Lactobacillus in feces increased significantly, whereas Enterobacter cloacae decreased. The activity of isocitrate lyase also diminished remarkably. These results suggest that saturated hydrogen could improve intestinal structural integrity and lipid metabolism disorders by inhibiting the glyoxylic acid cycle of the intestinal flora. Impact statement Past studies have shown that hydrogen can improve metabolic disorders, but its mechanism of action remains unclear. It is well known that metabolic diseases, such as obesity, are significantly associated with changes in the intestinal flora. The glyoxylic acid cycle is an essential metabolic pathway in prokaryotes, lower eukaryotes, and plants and could be the portal for mechanisms related to metabolic disorders. Many opportunistic pathogenic bacteria can recycle fatty acids to synthesize sugars and other pathogenic substances using the glyoxylic acid cycle. So, the glyoxylic acid cycle may be involved in intestinal dysbacteriosis under high-fat diet. This study, therefore, seeks to provide the mechanism of how hydrogen improves metabolic diseases and a new basis for the use of hydrogen in the treatment of metabolic disorders.
The lung-brain axis is an emerging area of study that got its basis from the gut-brain axis biological pathway. Using Respiratory Synctial Virus (RSV) as the model of respiratory viral pathogen, this study aims to establish some biological pathways. After establishing the mice model, the inflammation in lung and brain were assayed using Hematoxylin-eosin staining, indirect immunofluorescence (IFA), and quantitative reverse-transcription polymerase chain reaction. The biological pathways between lung and brain were detected through metabolomics analysis. In lung, RSV infection promoted epithelial shedding and infiltration of inflammatory cells. Also, RSV immunofluorescence and titerss were significantly increased. Moreover, interleukin (IL)-1, IL-6 and tumor necrosis factor-α (TNF-α) were also significantly increased after RSV infection.In brain, the cell structure of hippocampal CA1 area was loose and disordered.Inflammatory cytokines IL-6 and IL-1β expression in the brain also increased, however, TNF-α expression showed no differences among the control and RSV group. We observed an increased expression of microglia biomarker IBA-1 and decreased neuronal biomarker NeuN. In addition, RSV mRNA expression levels were also increased in the brains. 15 metabolites were found upregulated in the RSV group including nerve-injuring metabolite glutaric acid, hydroxyglutaric acid and Spermine. ɑ-Estradiol increased significantly while normorphine decreased significantly at Day 7 of infection among the RSV group. This study established a mouse model for exploring the pathological changes in lungs and brains. There are many biological pathways between lung and brain, including direct translocation of RSV and metabolite pathway.
Monkeypox has been spreading worldwide since May 2022, when the World Health Organization (WHO) declared the outbreak of a "Public health emergency of international concern". The spread of monkeypox has posed a serious threat to the health of people all over the world but few studies have been carried out on it, and the molecular mechanism of monkeypox after infection remains unclear. We therefore implemented a transcriptome analysis to identify signaling pathways and biomarkers in monkeypox-infected cells to help understand monkeypox-host cell interactions. In this study, the dataset GSE36854 and GSE11234 were obtained from GEO. Among them, 84 significantly different genes were identified in the dataset GSE36854, followed by KEGG, GO analysis protein-protein interaction (PPI) construction and Hub gene extraction. We also analyzed the expression regulation patterns of hub genes and screened the drugs targeting the hub genes. The results showed that monkeypox-infected cells significantly activated the cellular immune response, and induced inflammatory response. IER3, IFIT2, IL11, ZC3H12A, EREG, IER2, NFKBIE, FST, IFIT1 and AREG were the top 10 hub genes, in which anti-viral gene IFIT1 and IFIT2 were significantly suppressed. AP-26113 and itraconazole promoting the expression of IFIT1 and IFIT2 may be used as new candidates for the treatment of monkeypox viral infection. Our results provide a new entry point for understanding the mode of interaction between monkeypox virus and its host. Keywords: Monkeypox, transcriptome sequencing, protein-protein interaction, IFIT2
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