High nutrient induces virulence in the AHPND-causing Vibrio parahaemolyticus, interpretation from the ecological assembly of shrimp gut microbiota.

Shrimp diseases frequently occur during the later farming stages, when the rearing water is eutrophic. This observation provides clue that the virulence of pathogens could be induced by elevated nutrient, whereas the underlying ecological mechanism remains limited. To address this pressing knowledge, we explored how gut microbiota responded to the infection of oligotrophic (OVp) or eutrophic (EVp) pre-cultured Vibrio parahaemolyticus, a causing pathogen of shrimp acute hepatopancreatic necrosis disease (AHPND). Resulted revealed that OVp and EVp infections caused dysbiosis in the gut microbiota and compromised shrimp immunity, while the later infection led to earlier and higher mortality. Significant associations were detected between the gut microbiota and each of the measured immune activities. Neutral community model showed that the assembly of gut microbiota was more strongly governed by deterministic processes in EVp infection, followed by EVp infected and control shrimp. Additionally, there were significantly lower temporal turnover rate and average variation degree in the gut microbiota in EVp infected shrimp compared with control individuals. Notably, we identified 22 infection-discriminatory taxa after ruling out the ontogenic effect. Using profiles of the 22 indicators as independent variables, the diagnosis model accurately distinguished (an overall 85.9% accuracy) the infected status (control, OVp or EVp infected shrimp), with 81.3% accuracy at the initial infection stage. The convergent and deterministic gut microbiota in EVp infected shrimp could partially explain why it is challenge to cure APHND from an ecological viewpoint. In addition, we provided a sensitive approach for diagnosing the onset of infection, when disease symptom is unobservable.

Elevated Sad1 and UNC84 Domain Containing 2 (SUN2) level inhibits cell growth and aerobic glycolysis in oral cancer through reducing the expressions of glucose transporter 1 (GLUT1) and lactate dehydrogenase A (LDHA).

BACKGROUND/PURPOSE: Oral cancer is a malignant tumor accompanied by high morbidity, mortality, and poor prognosis. Therefore, it is urgent to explore the percise regulation mechanisms underlying oral cancer. Sad1 and UNC84 Domain Containing 2 (SUN2) was considered as a tumor suppressor in some cancers. The purpose of the study was to define the role of SUN2 in oral cancer progression. MATERIALS AND METHODS: Tumor tissues and paired paracancerous healthy tissues from 56 oral cancer patients were collected. Cell viability was measured using MTT assay. The colony formation assay was applied to determine cell proliferation ability. The mRNA and protein levels were assessed by qRT-PCR and Western blot, respectively. RESULTS: SUN2 expression was decreased in oral cancer tissues and cell models. SUN2 overexpression suppressed the growth of oral cancer cells, while the down-regulation of SUN2 promoted cell growth. SUN2 overexpression restrained the glucose uptake, lactate production, and ATP level of oral cancer cells, whereas down-regulation of SUN2 promoted glycolysis. Besides, elevated SUN2 inhibited the glucose transporter 1 (GLUT1) and lactate dehydrogenase A (LDHA) levels. However, SUN2 knockdown increased the levels of GLUT1 and LDHA. CONCLUSION: SUN2 was decreased in oral cancer in vivo and in vitro. SUN2 overexpression suppressed cell growth and glycolysis via reducing the levels of GLUT1 and LDHA in oral cancer.