ObjectiveUsing the whole genome association study (GWAS) data, Mendel randomization (MR) method was used to find the causal relationship between oral flora and type 2 diabetes (T2D) and myocardial infarction (MI). MethodsGenetic association data of oral microbiota were selected from the Chinese 4D-SZ cohort GWAS dataset, and T2D and MI outcome data were obtained from a large-scale cohort study in BioBank Japan. Four methods, including inverse variance weighting (IVW), were used to analyze the causal relationship between exposure and outcomes. Sensitivity analysis was conducted on significant MR results to further validate the robustness of the results. ResultsThe results showed a total of 24 species of dorsal tongue flora and 13 species of salivary flora with a potential causal relationship with T2D. There were 12 species each of dorsal tongue and salivary flora with a potential causal relationship with MI. A total of 8 oral flora were found on the dorsum of the tongue and saliva that could affect both T2D and MI, namely Saccharimonadaceae, Treponemataceae, Prevotella, Haemophilus, Lachnoanaerobaculum, Campylobacter_A, Neisseria, and Streptococcus. ConclusionWe identified 8 oral flora causally associated with both T2D and MI, suggesting that T2D may play a role in promoting the progression of MI by affecting the above oral flora.
End-stage renal disease is a late complication of chronic kidney disease (CKD) and one of the leading causes of high mortality worldwide. Over the years, the impacts of gut microbiota and their associated uremic toxins on kidney diseases through the intricate “gut-kidney axis” have been extensively studied. However, translation of microbiome-related omics results into specific mechanisms is still a significant challenge. In this paper, we review the interaction between gut microbiome and blood purification, as well as the current microbiota-based therapies in CKD. Additionally, the current sequencing technologies and progresses in the gut microbiome research are also discussed.
Childhood obesity is a global public health problem that seriously affects the normal growth and development of children. In recent years, a large number of studies have pointed out that the intestinal microbiome is closely related to childhood obesity, and the treatment strategies targeting the intestinal microbiome have a certain improvement effect on childhood obesity. This article elaborates on the establishment and development of intestinal microbiome, intestinal microbiome characteristics, the mechanisms of intestinal microbiome involvement in the occurrence and development of childhood obesity, and potential intervention strategies, so as to provide more ideas for basic and clinical research on childhood obesity.
ObjectiveTo explore gut microbiome influences on anastomotic healing following gastrointestinal surgery and its mechanism.MethodThe relevant literatures about gut microbiome and its impact on healing of gastrointestinal anastomosis and their mechanisms were reviewed.ResultsSeveral symbiotic intestinal microbiota such as the Enterococcus faecalis, Pseudomonas aeruginosa, Serratia marcescens, etc. could transform into the pathogenic bacteria with high toxic phenotype in an inflammatory environment in the body, and dissolve the extracellular matrix by degrading collagen or activating matrix metalloproteinase 9, resulting in the anastomotic leak.ConclusionIn general, exploring of effect of intestinal microbiome on healing process of anastomotic stoma is just beginning, conditions and mechanisms for transformation of bacteria from symbiotic to pathogenic still need to be explored.
There is increasing evidence that microorganisms play a complex and important role in human health and disease, and that the in vivo microbiome can directly or indirectly affect the host’s immune system, endocrine system, and nervous system. Therefore, a relatively stable equilibrium between the host and the microbiome is crucial in human health. However, in the special pathophysiological state of the perioperative period, preoperative anxiety and sleep deprivation, anesthesia intervention and surgical injury, postoperative medication and complications may all have different effects on the microbial composition of various organs in the body, resulting in pathogenic microorganisms, and the balance between beneficial microorganisms is altered. This may affect patient the outcomes and prognosis in a direct or indirect manner. This paper will provide a systematic review of key studies to understand the impact of perioperative stress on the commensal microbiome, provide a fresh perspective on optimizing perioperative management strategies, and discuss possible potential interventions to restore microbiome-mediated steady state.
Behcet's Disease (BD) is a multisystem vasculitis characterized by disease alternated with recurrent episodes and remissions, involving genital, oral, ocular uvea, cutaneous, and articular manifestations. The nuclear factor (NF)-κB signaling pathway paly an important role in the BD progression. It encompasses diverse gene, protein, and cellular regulatory mechanisms operating across various levels, alongside microbiological and experimental studies involving animals and cells. At the protein research findings, activation of the NF-κB pathway in BD patients is marked by elevated plasma levels of soluble CD40 ligand, which stimulates neutrophils to release reactive oxygen species and extracellular traps, thereby promoting inflammation. At the cellular research findings, macrophages in BD patients polarize towards classically activated macrophages phenotype through the NF-κB pathway, exacerbating the inflammatory response. The activation of NF-κB is associated with increased expression of anti-apoptotic proteins in T cells, leading to prolonged inflammation. Microbiological investigations reveal that the decreased gut microbiota diversity in BD patients compromises intestinal barrier integrity. NF-κB pathway involvement in regulating neutrophil and type 1 helper T cell (Th) 1/Th17 cell function worsens inflammation. Genetically, BD patients exhibit polymorphisms in immune regulatory genes, which contribute to inflammation through the NF-κB pathway. Mutations in NF-κB-associated genes elevate the risk of BD, while mutations in the endogenous inhibitor A20 lead to abnormal NF-κB activity, sustaining inflammation. Animal experiments and in vitro experiments corroborate the efficacy of NF-κB inhibitors in attenuating inflammation. Targeting upstream inflammatory factors within the NF-κB pathway yields positive outcomes in BD patients. In summary, the NF-κB signaling pathway plays a pivotal role in the development of BD. Developing NF-κB inhibitors may open new avenues for treating BD. Further research is necessary to comprehensively elucidate the precise mechanisms by which NF-κB operates in the pathogenesis of BD, as well as its potential clinical applications in therapy.
Microorganism distributes in the organs of human body which connect with external environment, especially those organs in the gastrointestinal tracts, and it also plays a fundamental role in the physiopathology of the host's body. Because the microorganism is very small and has a great variety, it is difficult to reveal the significance of microorganism in the human physiopathology comprehensively and deeply. With the development of molecular biology, genomics, bioinformatics and other disciplines, the microbiome research will be more possible and easier. There are two key contents of microecology. One of these is to identify and quantify the diversity of microorganism, and the other is to reveal activity and the physiopathological function of microorganism in the host. Microbiome research methods, therefore, can be summarized as the traditional detection methods, construction of gene library, the genetic fingerprint analysis and molecular hybridization techniques and so on.
Lung microbiome is defined as the specific microbiota of lung. Lung microbiome can make the lung in a state of chronic inflammation through direct destruction, activation of inflammatory cells and release of inflammatory factors, and then progress to lung cancer. There are significant differences in lung microbiome between lung cancer patients and healthy people. Some specific microbial flora can be used as a diagnostic marker of lung cancer. Specific microbial communities are related to the efficacy of immunotherapy, and microbial composition may be used as a marker of immune-related adverse events. There are both challenges and opportunities for research on the relationship between lung microbiome and lung cancer. This review will focus on the significance and value of lung microbiome in the occurrence, diagnosis and immunotherapy of lung cancer, in order to provide a reference for basic and clinical researchers in related fields.
Objective To investigate the potential causal relationship between specific oral microbiota and peptic ulcer disease (PUD) using a Mendelian randomization (MR) approach. Methods The genome-wide association study (GWAS) data from East Asian populations was utilized to perform a two-sample MR analysis to determine the causal relationship between oral microbiota and PUD. The MR analysis was primarily conducted using the inverse-variance weighted (IVW) method, supplemented by MR-Egger and weighted median methods. Heterogeneity and pleiotropy were assessed, and the leave-one-out method was employed to evaluate the stability of the MR results. Results There was a complex association between specific bacterial genera of the oral microbiota and PUD. Prevotella was found to potentially promote duodenal ulcers while exerting a protective effect against gastric ulcers. Campylobacter and Streptococcus demonstrated differing effects on gastric and duodenal ulcers. Furthermore, Fusobacterium and Haemophilus_A were positively associated with peptic ulcers, suggesting an increased risk of gastroduodenal ulcer development. Conclusion This study explores the causal relationship between oral microbiota and PUD, providing new insights into the prevention and treatment of PUD mediated by oral microbiota.
Objective To explore the relationship between the gut microbiome (GM) and psoriasis using a two-sample two-way Mendelian randomization (MR) approach. Methods The forward analysis uses the gut microbiota as the exposure factor, and its genetic data are derived from the genome-wide association study dataset published by the MiBioGen consortium. Psoriasis was used as the outcome variable, and its genetic data were obtained from the UK Biobank. The reverse MR analysis, on the other hand, took psoriasis as the exposure and the specific gut microbiota taxonomic units identified in the forward analysis as the outcome variable. MR analysis was conducted using maximum likelihood, MR Egger regression, weighted median, inverse variance weighting (IVW), and weighted models to study the causal relationship between the gut microbiota and psoriasis. Then, sensitivity analyses including horizontal pleiotropy test, Cochran’s Q test, and leave-one-out analysis were used to evaluate the reliability of the results. Results A total of 51 single nucleotide polymorphisms from 5 fungi were included in the forward study. The forward IVW analysis results showed that, the class Mollicutes [odds ratio (OR)=1.003, 95% confidence interval (CI) (1.001, 1.006), P=0.004], genus Lachnospiraceae FCS020 group [OR=1.003, 95%CI (1.000, 1.006), P=0.041], and phylum Tenericutes [OR=1.003, 95%CI (1.001, 1.006), P=0.004] were causally associated with an increased risk of psoriasis. The family Victivallaceae [OR=0.998, 95%CI (0.997, 1.000), P=0.005] and order Pasteurellales [OR=0.998, 95%CI (0.996, 1.000), P=0.047] were also linked to a decreased risk of psoriasis. The results of the sensitivity analysis were robust. There was no evidence of a reverse causal relationship from psoriasis to the identified bacterial taxa found in the results of reverse MR analysis results. Conclusions The abundance of three species, class Mollicutes, genus Lachnospiraceae and phylum Tenericutes, may increase the risk of psoriasis. The abundance of two species, family Victivallaceae and order Pasteurellales may reduce the risk of psoriasis. These results provide new directions for the prevention and treatment of psoriasis in the future, but further research is needed to explore how the aforementioned microbiome affects the progression of psoriasis.