There are three species of Chrysaora (Scyphozoa: Discomedusae) in the Benguela upwelling ecosystem, not two.

Chrysaora (Pèron Lesueur 1810) is the most diverse genus within Discomedusae, and 15 valid species are currently recognised, with many others not formally described. Since Chrysaora fulgida (Reynaud 1830) was first recognised as occurring off the south west (SW) coast off South Africa, the species has been variously synonymised with Chrysaora hysoscella (Linnaeus 1767) and Chrysaora africana (Vanhöffen 1902). Using DNA evidence alongside multivariate tools to analyse quantitative morphometric and meristic data, as well as information from the cnidome, we unambiguously separate C. fulgida from C. hysoscella; we resurrect C. africana as a valid species and recognise a new species, Chrysaora agulhensis sp. nov. Full descriptions of C. fulgida, C. africana and C. agulhensis sp. nov. are provided. The species have different geographical patterns of distribution around the region, with restricted areas of overlap: C. agulhensis sp. nov. is found along the southern coast of South Africa and over the Agulhas Bank, C. fulgida extends from Cape Point in South Africa to southern Angola, and C. africana can be found from southern Namibia northwards to the Gulf of Guinea. The species can be readily separated in the field by a combination of tentacle/lappet number and shape, colour patterns and the form of the oral arms.

A Dual Role for P2X7 Receptor during Porphyromonas gingivalis Infection.

Emerging evidence suggests a role for purinergic signaling in the activation of multiprotein intracellular complexes called inflammasomes, which control the release of potent inflammatory cytokines, such as interleukin (IL) -1ß and -18. Porphyromonas gingivalis is intimately associated with periodontitis and is currently considered one of the pathogens that can subvert the immune system by limiting the activation of the NLRP3 inflammasome. We recently showed that P. gingivalis can dampen eATP-induced IL-1ß secretion by means of its fimbriae in a purinergic P2X7 receptor-dependent manner. Here, we further explore the role of this purinergic receptor during eATP-induced IL-1ß processing and secretion by P. gingivalis-infected macrophages. We found that NLRP3 was necessary for eATP-induced IL-1ß secretion as well as for caspase 1 activation irrespective of P. gingivalis fimbriae. Additionally, although the secretion of IL-1ß from P. gingivalis-infected macrophages was dependent on NLRP3, its adaptor protein ASC, or caspase 1, the cleavage of intracellular pro-IL-1ß to the mature form was found to occur independently of NLRP3, its adaptor protein ASC, or caspase 1. Our in vitro findings revealed that P2X7 receptor has a dual role, being critical not only for eATP-induced IL-1ß secretion but also for intracellular pro-IL-1ß processing. These results were relevant in vivo since P2X7 receptor expression was upregulated in a P. gingivalis oral infection model, and reduced IFN-γ and IL-17 were detected in draining lymph node cells from P2rx7(-/-) mice. Furthermore, we demonstrated that P2X7 receptor and NLRP3 transcription were modulated in human chronic periodontitis. Overall, we conclude that the P2X7 receptor has a role in periodontal immunopathogenesis and suggest that targeting of the P2X7/NLRP3 pathway should be considered in future therapeutic interventions in periodontitis.

Effects of periodontal therapy on white blood cell count and levels of transforming growth factor beta in serum of subjects with severe periodontitis.

This study aimed to investigate the effects of nonsurgical periodontal therapy on white blood cell (WBC) count and levels of transforming growth factor beta (TGF—β) in serum from subjects with severe periodontitis. Serum from 28 subjects with periodontitis (mean age: 34.36±6.24; 32% men) and 27 healthy controls (mean age: 33.18±6.42; 33% men) were collected prior to therapy. Blood samples were obtained from 23 subjects who completed therapy (9—12 months). A well—controlled periodontal treatment protocol was established in three stages: mechanical periodontal therapy (scaling and root planning), reinstrumentation of dental sites, and supportive periodontal therapy. Periodontal and systemic parameters such as the total number of WBCs and TGF—β levels, accessed by enzyme—linked immunosorbent assay (ELISA), were included. After therapy, all clinical periodontal parameters decreased (p<0.0001). There were no statistical differences in WBC count between experimental and control groups before or after therapy. However, after therapy, the mean value of lymphocytes in patients with localized aggressive periodontitis (LAgP) was statistically higher than that of patients with generalized chronic periodontitis (GCP) (p<0.0357). Additionally, TGF—β levels in LAgP and GCP patients were higher compared to controls before therapy (p<0.05 and p<0.01, respectively). In LAgP patients, periodontal therapy was associated with increased number of lymphocytes.