Genome-based reclassification of Paenibacillus dauci as a later heterotypic synonym of Paenibacillus shenyangensis.

Paenibacillus shenyangensis and Paenibacillus dauci are Gram-stain-positive, rod-shaped and endospore-forming bacteria originally isolated from soil and carrot samples, respectively, in China. Preliminary comparative genomic analysis showed that these bacteria could constitute a single species. Therefore, in this study, their taxonomic statuses were clarified through distinct genomic metrics and phylogenetic analyses. Paenibacillus shenyangensis A9T and P. dauci H9T presented values of average nucleotide identity (ANI) and its derivative metrics (gANI and OrthoANI) ranging from 97.88 to 98.08 %, and digital DNA-DNA hybridization equal to 89.08 %. Furthermore, the identities of 16S rRNA, gyrB, rpoB, recA and recN genes were all equal or higher than 98.7 %. Phylogenies of these marker genes and the concatenated core proteome were congruent in the sense that P. shenyangensis A9T and P. dauci H9T are the closest type-strains of the genus Paenibacillus. A review of their profiles revealed that these strains do not present pronounced differences at the phenotypic and chemotaxonomic levels. Considering phylogenetic, genomic, phenotypic and chemotaxonomic data, P. dauci should be reclassified as a later heterotypic synonym of P. shenyangensis.

Guanosine Protects Against Cortical Focal Ischemia. Involvement of Inflammatory Response.

Stroke is the major cause of death and the most frequent cause of disability in the adult population worldwide. Guanosine plays an important neuroprotective role in several cerebral ischemic models and is involved in the modulation of oxidative responses and glutamatergic parameters. Because the excessive reactive oxygen species produced during an ischemic event can trigger an inflammatory response, the purpose of this study was to evaluate the hypothesis that guanosine is neuroprotective against focal cerebral ischemia, inhibits microglia/macrophages activation, and mediates an inflammatory response ameliorating the neural damage. Permanent focal cerebral ischemia was induced in adult rats, and guanosine was administered immediately, 1, 3, and 6 h after surgery. Twenty-four hours after ischemia, the asymmetry scores were evaluated by the cylinder test; neuronal damage was evaluated by Fluoro-Jade C (FJC) staining and propidium iodide (PI) incorporation; microglia and immune cells were evaluated by anti-Iba-1 antibody; and inflammatory parameters such as interleukins (IL): IL-1, IL-6, IL-10; tumor necrosis factors alpha (TNF-α); and interferon-gamma (INF-γ) were evaluated in the brain tissue and cerebrospinal fluid. The ischemic event increased the levels of Iba-1-positive cells and pro-inflammatory cytokines and decreased IL-10 levels (an anti-inflammatory cytokine) in the lesion periphery. The guanosine treatment attenuated the changes in these inflammatory parameters and also reduced the infarct volume, PI incorporation, and number of FJC-positive cells, improving the functional recovery. Thus, guanosine may have been a promising therapeutic agent for the treatment of ischemic brain injury by reduction of inflammatory process triggered in an ischemic event.