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.
Neonatal brain hypoxic ischemic injury is a devastating event causing permanent brain damage. The current study set out to explore the role of Kruppel-like factor 2 (KLF2) and its downstream molecular mechanism on hypoxic-ischemic brain damage (HIBD) in neonatal rats. First, we adopted a modified Rice method to develop a HIBD model in postnatal day seven Sprague Dawley (SD) rat pups. Next, neuronal damage, morphological changes, and neuronal apoptosis were documented in the vulnerable hippocampal CA1 region and evaluated using Nissl staining, H&E staining, and TUNEL assay, respectively. Meanwhile, a hypoxic-ischemic model using the oxygen-glucose deprivation (OGD) method was established in cortical neurons isolated from day one SD rat pups, followed by MTT and flow cytometry detections of the cell survival rate and apoptotic ability. Experimental findings revealed that KLF2 was poorly-expressed in the brain tissues of HIBD rats and in the OGD-induced neurons. We found that KLF2 overexpression inhibited neuron apoptosis in vitro and in vivo, which was also observed to inhibit brain injury in the HIBD rats and alleviate neuronal damage of OGD-treated neurons. Besides, as dual luciferase reporter gene assay and chromatin immunoprecipitation established that KLF2 bound to the interferon regulatory factor 4 (IRF4) promoter, which promoted the binding of IRF4 in the promoter of histone deacetylase 7 (HDAC7) to augment its expression, thereby inhibiting neuronal apoptosis and brain damage. In conclusion, our findings indicated that KLF2 could increase the expression of IRF4 to up-regulate the expression of HDAC7, which protects against HIBD in neonatal rats.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.