Perioperative neurocognitive disorder (PND) is one of the common perioperative complications in surgical patients, which has been concerned by most researchers. With the gradual increase of the elderly population in China, the complexity of individual diseases and the risk of PND is more and more severe. In recent years, a large number of studies have confirmed the close relationship between intestinal flora and neurological diseases and various studies have also proved that gut microbiota may contribute to the occurrence and development of PND. Based on the current studies, this article summarizes the effects of gut microbiota on PND, including possible mechanisms and intervention measures, providing some ideas for researchers and treatment of PND.
ObjectiveTo establisht a gut microbiota mice model for chronic obstructive pulmonary disease (COPD) with fecal microbiota transplantation (FMT) and its evaluation.MethodsThe mice received FMT from healthy individuals, COPD Ⅰ-Ⅱ subjects, or COPD Ⅲ–Ⅳ subjects. After microbiota depletion, the FMT was performed by a single oral administration of 100 μL per mouse every other day, for a total of 14 times in 28 days. On the 29th day, the peripheral blood mononuclear cells were analyzed, the gut microbiota of mice before and after FMT was analyzed by 16S rRNA sequencing, and the mice model were evaluated.ResultsThe operational taxonomic units, Chao 1 and Shannon indexes of mice all decreased significantly after antibiotic treatment (P<0.001), but increased significantly after FMT from healthy individuals, COPD Ⅰ-Ⅱ subjects, or COPD Ⅲ–Ⅳ subjects (P<0.05 or P<0.01). The abundance of Firmicutes, Proteobacteria and Actinobacteria in the guts of the mice in the healthy human FMT group, COPD Ⅰ-Ⅱ FMT group and COPD Ⅲ-Ⅳ FMT group were significantly different from those of the control group who only received phosphate buffer saline instead of FMT (P<0.05 or P<0.01). The auxiliary T lymphocytes and cytotoxic T lymphocytes were higher, but B lymphocytes decreased in the peripheral blood of the mice in the COPD Ⅰ-Ⅱ FMT group and COPD Ⅲ-Ⅳ FMT group (P<0.05 or P<0.01).ConclusionFMT can successfully establish a COPD gut microbiota research model.
ObjectiveTo systematically review the intestinal flora diversity profile of pancreatic cancer patients. MethodsThe Cochrane Library, PubMed, Web of Science, EMbase, CNKI, CBM, WanFang Data and VIP databases were electronically searched to collect cross-sectional studies on the intestinal flora diversity profile of pancreatic cancer patients from inception to December 31, 2021. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies; then, meta-analysis was performed by using RevMan 5.3 software. ResultsA total of 7 cross-sectional studies involving 250 pancreatic cancer patients and 166 healthy controls were included. The results of meta-analysis showed that: compared with the healthy control group, the intestinal flora of patients with pancreatic cancer α reduced diversity with the Shannon index. High-throughput sequencing found that Proteobacteria and Prevotella were more abundant in pancreatic cancer patients, Firmicutes, Faecalbacterium, Bifidobacterium and Clostridium in pancreatic cancer patients was lower. ConclusionCurrent evidence shows that the intestinal flora of pancreatic cancer patients has certain characteristics. Proteobacteria and Prevotella are relatively abundant in pancreatic cancer patients. Due to limited quality and quantity of the included studies, more high-quality studies are needed to verify above conclusion.
The concept of “Microbe-gut-eye axis” holds that metabolites of the gut microbiota are involved in the pathogenesis of various eye diseases. The composition and diversity of gut microbiota in diabetic retinopathy (DR) patients are significantly different from those in non-DR patients. Metabolites of the gut microbiota such as lipopolysaccharide, short-chain fatty acid, bile acids and branched-chain amino acid aggravate or attenuate the progression of DR by regulating the release of inflammatory cytokines, mitochondrial function, insulin sensitivity, immune response, and autophagy of retinal cells. Therefore, gut microbiota and their metabolites play a role in the occurrence and development of DR through multiple pathways. The participation of gut microbiota may open up a new way to prevent and treat DR in the future.
Gut microbiota and its metabolites in various human diseases have gradually become a research hotspot in the current medical community. And coronary artery disease is currently one of the most threatening clinical cardiovascular diseases in the world, so the use of gut microbiota and its metabolites in the development of its pathophysiology has also received more and more attention. Therefore, this paper reviews the effects of gut microbiota and its metabolites on coronary artery disease, as well as the research progress of intervening gut microbiota and its metabolites as therapeutic targets, hoping to expand the future research direction in this field and provide new ideas with treating coronary artery disease.
The human gut microbiota regulates many host pathophysiological processes including metabolic, inflammatory, immune and cellular responses. In recent years, the incidence and mortality of lung cancer have increased rapidly, which is one of the biggest challenges in the field of cancer treatment today, especially in non-small cell lung cancer. Animal models and clinical studies have found that the gut microbiota of non-small cell lung cancer patients is significantly changed compared with the healthy people. The gut microbiota and metabolites can not only play a pro-cancer or tumor suppressor role by regulating immune, inflammatory responses and so on, but also be related with radiotherapy and chemotherapy of non-small cell lung cancer and the resistance of immunotherapy. Therefore, gut microbiota and related metabolites can be both potential markers for early diagnosis and prognosis in patients with non-small cell lung cancer and novel therapeutic targets for targeted drugs. This study will review the latest research progress of effect of gut microbiota on non-small cell lung cancer, and provide a new diagnosis and treatment ideas for non-small cell lung cancer.
Diabetic neuropathic pain (DNP) is one of the most common and complex complications of diabetes. In recent years, studies have shown that gut microbiota can regulate inflammatory response, intestinal permeability, glucose metabolism, and fatty acid oxidation, synthesis, and energy consumption by regulating factors such as lipopolysaccharides, short chain fatty acids, bile acids, and branched chain amino acids, achieving the goal of treating DNP. This paper summarizes the relevant mechanisms of gut microbiota in the treatment of DNP, the relevant intervention measures of traditional Chinese and western medicine, in order to provide new ideas for clinical treatment of DNP.
ObjectiveTo explore the composition of intestinal microbiota between patients with fixed airflow obstruction asthma, reversible airflow obstruction asthma, and healthy control, and analyze the correlation between key differential bacterial distribution and clinical characteristics. MethodsFifteen patients with fixed airflow obstruction asthma (FAO) and 13 patients with reversible airflow obstruction asthma (RAO) were included, along with 11 matched healthy control subjects. Clinical data were collected, and lung function tests and induced sputum examination were performed. Blood and stool samples were tested to compare the gut microbiota status among the groups, and analyze the relationship between gut microbiota abundance and patients' blood routine, IgE levels, lung function, and induced sputum. Results The dominant bacterial compositions were similar in the three groups, but there were differences in the abundance of some species. Compared to the RAO group, the FAO group showed a significant increase in the genera of Bacteroides and Escherichia coli, while Pseudomonas was significantly decreased. The phylum Firmicutes was negatively correlated with the course of asthma, while the phylum Bacteroidetes and genus Bacteroides were positively correlated with the asthma course. Bacteroidetes was negatively correlated with Pre-BD FEV1/FVC, Pseudomonas was positively correlated with Pre-BD FEV1, Escherichia coli was negatively correlated with Post-BD FEV1/FVC, and Bacteroides was negatively correlated with Post-BD MMEF. The class Actinobacteria and the order Actinomycetales were negatively correlated with peripheral blood EOS%, while the order Enterobacteriales and the family Enterobacteriaceae were positively correlated with peripheral blood IgE levels. Furthermore, Actinobacteria and Actinomycetales were negatively correlated with induced sputum EOS%. Conclusions There are differences in the gut microbiota among patients with fixed airflow obstruction asthma, reversible airflow obstruction asthma, and healthy individuals. Bacteroides and Escherichia coli are enriched in the fixed airflow obstruction asthma group, while the Firmicutes are increased in the reversible airflow obstruction asthma group. These three microbiota may act together on Th2 cell-mediated inflammatory responses, influencing the process of airway remodeling, and thereby interfering with the occurrence of fixed airflow obstruction in asthma.
ObjectiveTo investigate the causal relationship between gut microbiota and idiopathic pulmonary fibrosis (IPF). MethodsGenome-wide association studies (GWAS) data of gut microbiota and IPF were obtained from MiBioGen and Finngen databases, respectively. Instrumental variables were screened by means of significance, linkage disequilibrium, weak instrumental variable screening, and removal of confounding factors (genetics, smoking, host characteristics). Inverse variance weighted (IVW) was used as the main Mendelian randomization (MR) analysis method, and the weighted median, simple mode, MR-Egger, and weighted mode were used to perform MR to reveal the causal effect of gut microbiota and IPF. The Cochrane's Q, leave-one-out, MR-Egger-intercept, and Mendelian randomization pleiotropy residual sum and outlier (MR-PRESSO) and Steiger tests were used to analyze the heterogeneity, horizontal pleiotropy, outliers, and directionality, respectively. ResultsIVW analysis results showed that Actinomycetes [OR=1.773, 95%CI (1.323, 2.377), P<0.001], Erysipelatoclostridium [OR=2.077, 95%CI (1.107, 3.896), P=0.023], and Streptococcus [OR=1.35, 95%CI (1.100, 1.657), P=0.004] could increase the risk of IPF. Bifidobacterium [OR=0.668, 95%CI (0.620, 0.720), P<0.001], Ruminococcus [OR=0.434, 95%CI (0.222,0.848), P=0.015], and Tyzzerella [OR=0.479, 95%CI (0.304, 0.755), P=0.001] could reduce the risk of IPF. No significant heterogeneity, horizontal pleiotropy, outliers, and reverse causality were found. ConclusionActinobacteria, Erysipelatoclostridium and Streptococcus may increase the risk of IPF, while Bifidobacterium, Ruminococcus and Tyzzerella may reduce the risk of IPF. Regulation of the above gut microbiota may become a new direction in the study of the pathogenesis of IPF.
Vagus nerve stimulation was first used in the treatment of refractory epilepsy and depression, and its indications have expanded in recent years. The brain-gut axis is a bidirectional communication network pathway connecting the gut to the brain, maintaining homeostatic balance of the gut microbiota and shaping brain function. The vagus nerve plays an important role in brain-gut axis mechanisms in neurological disorders, which may be an important rationale for vagus nerve stimulation in the treatment of related diseases. Recent studies have shown that vagus nerve stimulation modulates the intestinal microenvironment and the intestinal microbiota, but the specific mechanisms of this alteration need further investigation. Fecal transplants or oral probiotics combined with vagus nerve stimulation may become an important therapeutic tool in the future, especially to improve the efficacy of vagus nerve stimulation for epilepsy; the gut microbiota may also be a predictive target for the efficacy of vagus nerve stimulation for epilepsy.