Fluorescent and electrochemical detection of nuclease activity associated with Streptococcus pneumoniae using specific oligonucleotide probes.

Streptococcus pneumoniae (S. pneumoniae) represents a significant pathogenic threat, often responsible for community-acquired pneumonia with potentially life-threatening consequences if left untreated. This underscores the pressing clinical need for rapid and accurate detection of this harmful bacteria. In this study, we report the screening and discovery of a novel biomarker for S. pneumoniae detection. We used S. pneumoniae nucleases as biomarker and we have identified a specific oligonucleotide that works as substrate. This biomarker relies on a specific nuclease activity found on the bacterial membrane, forming the basis for the development of both fluorescence and electrochemical biosensors. We observed an exceptionally high sensitivity in the performance of the electrochemical biosensor, detecting as low as 102 CFU mL-1, whereas the fluorescence sensor demonstrated comparatively lower efficiency, with a detection limit of 106 CFU mL-1. Moreover, the specificity studies have demonstrated the biosensors' remarkable capacity to identify S. pneumoniae from other pathogenic bacteria. Significantly, both biosensors have demonstrated the ability to identify S. pneumoniae cultured from clinical samples, providing compelling evidence of the potential clinical utility of this innovative detection system.

Role of Dopamine and D2 Dopamine Receptor in the Pathogenesis of Inflammatory Bowel Disease.

BACKGROUND: VEGF-induced vascular permeability and blood vessels remodeling are key features of inflammatory bowel disease (IBD) pathogenesis. Dopamine through D2 receptor (D2R) inhibits VEGF/VPF-mediated vascular permeability and angiogenesis in tumor models. In this study, we tested the hypothesis that pathogenesis of IBD is characterized by the disturbance of dopaminergic system and D2R activity. METHODS: IL-10 knockout (KO) mice and rats with iodoacetamide-induced ulcerative colitis (UC) were treated intragastrically with D2R agonists quinpirole (1 mg/100 g) or cabergoline (1 or 5 µg/100 g). Macroscopic, histologic, and clinical features of IBD, colonic vascular permeability, and angiogenesis were examined. RESULTS: Although colonic D2R protein increased, levels of tyrosine hydroxylase and dopamine transporter DAT decreased in both models of IBD. Treatment with quinpirole decreased the size of colonic lesions in rats with iodoacetamide-induced UC (p < 0.01) and reduced colon wet weight in IL-10 KO mice (p < 0.05). Quinpirole decreased colonic vascular permeability (p < 0.001) via downregulation of c-Src and Akt phosphorylation. Cabergoline (5 µg/100 g) reduced vascular permeability but did not affect angiogenesis and improved signs of iodoacetamide-induced UC in rats (p < 0.05). CONCLUSIONS: Treatment with D2R agonists decreased the severity of UC in two animal models, in part, by attenuation of enhanced vascular permeability and prevention of excessive vascular leakage. Hence, the impairment dopaminergic system seems to be a feature of IBD pathogenesis.