Alteration of the oral and gut microbiota in patients with Kawasaki disease.

Background: Kawasaki disease (KD) is a multi-systemic vasculitis that primarily affects children and has an unknown cause. Although an increasing number of studies linking the gut microbiota with KD, the unchallengeable etiology of KD is not available. Methods: Here, we obtained fecal and oral samples from KD patients and healthy controls, and then we use high-throughput sequencing to examine the diversity and composition of microbiota. Results: Results showed that both in the gut and oral microbiota, the diversity of KD patients was significantly lower than that of the healthy controls. In the gut microbiota, a higher abundance of Enterococcus (40.12% vs less than 0.1%), Bifidobacterium (20.71% vs 3.06%), Escherichia-Shigella (17.56% vs 0.61%), Streptococcus (5.97% vs 0.11%) and Blautia (4.69% vs 0.1%) was observed in the KD patients, and enrichment of Enterococcus in the patients was observed. In terms of oral microbiota, the prevalence of Streptococcus (21.99% vs 0.1%), Rothia (3.02% vs 0.1%), and Escherichia-Shigella (0.68% vs 0.0%) were significantly higher in the KD patients, with the enrichment of Streptococcus and Escherichia-Shigella. Additionally, significant differences in microbial community function between KD patients and healthy controls in the fecal samples were also observed, which will affect the colonization and reproduction of gut microbiota. Conclusions: These results suggested that the dysbiosis of gut and oral microbiota are both related to KD pathogenesis, of which, the prevalence of Enterococcus in the gut and higher abundance of Streptococcus and Escherichia-Shigella in the oral cavity will be a potential biomarker of the KD. Overall, this study not only confirms that the disturbance of gut microbiota is a causative trigger of KD but also provides new insight into the oral microbiota involved in KD pathogenesis.

Pterostilbene induces Nrf2/HO-1 and potentially regulates NF-κB and JNK-Akt/mTOR signaling in ischemic brain injury in neonatal rats.

Hypoxic-ischemic (HI) brain injury has a high occurrence rate of 1-4 per 1000 live births and is the leading cause of neurological disabilities. Despite the improvement in neonatal care, the effectiveness of current therapeutic strategies is limited, and thus, additional therapies with better results are of much needed. Pterostilbene is a stilbenoid possessing numerous preventive and therapeutic properties. The current study aimed to assess whether pterostilbene exerted protective effects in neonatal rats against experimentally induced ischemic brain injury. Pterostilbene was administered via oral gavage from postnatal day 3 to day 8. Rat pups that were seven-day-old were exposed to hypoxic-ischemic insult via ligation of the common carotid artery and hypoxic environment exposure. Pterostilbene treatment reduced neuronal loss and infarct volume. Pterostilbene administration regulated the NF-κB pathway, and the levels of inflammatory mediators (Nitric oxide, TNF-α, IL-1ß, and IL-6) were reduced. HI-induced oxidative stress was significantly reduced by pterostilbene, as presented by decreased production of malondialdehyde and reactive oxygen species. Levels of glutathione were enhanced by pterostilbene. Pterostilbene regulated Nrf2/HO-1 and JNK expression and activated the PI3K/Akt-mTOR signals. These findings suggest that pterostilbene is a candidate compound for the treatment of neonatal HI.