Sediment, a special realm in aquatic environments, has high microbial diversity. While there are numerous reports about the microbial community in marine sediment, freshwater and intertidal sediment communities have been overlooked. The present study determined millions of Illumina reads for a comparison of bacterial communities in freshwater, intertidal wetland, and marine sediments along Pearl River, China, using a technically consistent approach. Our results show that both taxon richness and evenness were the highest in freshwater sediment, medium in intertidal sediment, and lowest in marine sediment. The high number of sequences allowed the determination of a wide variety of bacterial lineages in all sediments for reliable statistical analyses. Principal component analysis showed that the three types of communities could be well separated from phylum to operational taxonomy unit (OTU) levels, and the OTUs from abundant to rare showed satisfactory resolutions. Statistical analysis (LEfSe) demonstrated that the freshwater sediment was enriched with Acidobacteria , Nitrospira , Verrucomicrobia , Alphaproteobacteria , and Betaproteobacteria . The intertidal sediment had a unique community with diverse primary producers (such as Chloroflexi , Bacillariophyta , Gammaproteobacteria , and Epsilonproteobacteria ) as well as saprophytic microbes (such as Actinomycetales , Bacteroidetes , and Firmicutes ). The marine sediment had a higher abundance of Gammaproteobacteria and Deltaproteobacteria , which were mainly involved in sulfate reduction in anaerobic conditions. These results are helpful for a systematic understanding of bacterial communities in natural sediment environments.

Background: Gut microbiota has been suggested to play a role in almost all major diseases including cardio‐ and cerebrovascular diseases. A possible mechanism is the transformation of dietary choline and l ‐carnitine into trimethylamine by gut bacteria. This metabolite is further oxidized into trimethylamine‐N‐oxide ( TMAO ) in liver and promotes atherogenesis. Nevertheless, little is known about gut microbial diversity and blood TMAO levels in stroke patients. Methods and Results: We performed a case‐control study of patients with large‐artery atherosclerotic ischemic stroke and transient ischemic attack. TMAO was determined with liquid chromatography tandem mass spectrometry. Gut microbiome was profiled using Illumina sequencing of the 16S rRNA V4 tag. Within the asymptomatic control group, participants with and without carotid atherosclerotic plaques showed similar levels of TMAO without a significant difference in gut microbiota; however, the gut microbiome of stroke and transient ischemic attack patients was clearly different from that of the asymptomatic group. Stroke and transient ischemic attack patients had more opportunistic pathogens, such as Enterobacter , Megasphaera , Oscillibacter , and Desulfovibrio , and fewer commensal or beneficial genera including Bacteroides , Prevotella , and Faecalibacterium . This dysbiosis was correlated with the severity of the disease. The TMAO level in the stroke and transient ischemic attack patients was significantly lower, rather than higher, than that of the asymptomatic group. Conclusions: Participants with asymptomatic atherosclerosis did not exhibit an obvious change in gut microbiota and blood TMAO levels; however, stroke and transient ischemic attack patients showed significant dysbiosis of the gut microbiota, and their blood TMAO levels were decreased.

Objective: Pre-eclampsia (PE) is one of the malignant metabolic diseases that complicate pregnancy. Gut dysbiosis has been identified for causing metabolic diseases, but the role of gut microbiome in the pathogenesis of PE remains unknown. Design: We performed a case–control study to compare the faecal microbiome of PE and normotensive pregnant women by 16S ribosomal RNA (rRNA) sequencing. To address the causative relationship between gut dysbiosis and PE, we used faecal microbiota transplantation (FMT) in an antibiotic-treated mouse model. Finally, we determined the microbiome translocation and immune responses in human and mouse placental samples by 16S rRNA sequencing, quantitative PCR and in situ hybridisation. Results: Patients with PE showed reduced bacterial diversity with obvious dysbiosis. Opportunistic pathogens, particularly Fusobacterium and Veillonella , were enriched, whereas beneficial bacteria, including Faecalibacterium and Akkermansia , were markedly depleted in the PE group. The abundances of these discriminative bacteria were correlated with blood pressure (BP), proteinuria, aminotransferase and creatinine levels. On successful colonisation, the gut microbiome from patients with PE triggered a dramatic, increased pregestational BP of recipient mice, which further increased after gestation. In addition, the PE-transplanted group showed increased proteinuria, embryonic resorption and lower fetal and placental weights. Their T regulatory/helper-17 balance in the small intestine and spleen was disturbed with more severe intestinal leakage. In the placenta of both patients with PE and PE-FMT mice, the total bacteria, Fusobacterium , and inflammatory cytokine levels were significantly increased. Conclusions: This study suggests that the gut microbiome of patients with PE is dysbiotic and contributes to disease pathogenesis.

At present, the pathophysiology of autism spectrum disorder (ASD) remains unclear. Increasing evidence suggested that gut microbiota plays a critical role in gastrointestinal symptoms and behavioral impairment in ASD patients. The primary aim of this systematic review is to investigate potential evidence for the characteristic dysbiosis of gut microbiota in ASD patients compared with healthy controls (HCs). The MEDLINE, EMBASE, Web of Science and Scopus were systematically searched before March 2018. Human studies that compared the composition of gut microbiota in ASD patients and HCs using culture-independent techniques were included. Independent data extraction and quality assessment of studies were conducted according to PRISMA statement and Newcastle-Ottawa Scale. Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt) was used to infer biological functional changes of the shifted microbiota with the available data in four studies. Sixteen studies with a total sample size of 381 ASD patients and 283 HCs were included in this systematic review. The quality of the studies was evaluated as medium to high. The overall changing of gut bacterial community in terms of β-diversity was consistently observed in ASD patients compared with HCs. Furthermore, Bifidobacterium, Blautia, Dialister, Prevotella, Veillonella, and Turicibacter were consistently decreased, while Lactobacillus, Bacteroides, Desulfovibrio, and Clostridium were increased in patients with ASD relative to HCs in certain studies. This systematic review demonstrated significant alterations of gut microbiota in ASD patients compared with HCs, strengthen the evidence that dysbiosis of gut microbiota may correlate with behavioral abnormality in ASD patients. However, results of inconsistent changing also existed and further big-sampled well-designed studies are needed. Generally, as a potential mediator of risk factors, the gut microbiota could be a novel target for ASD patients in the future.