The BNT162b2 vaccine, containing lipid nanoparticles-formulated mRNA encoding the full-length spike protein of SARS-CoV-2, has been employed to immunize health care workers in Italy, administered in two doses 21 days apart. In this study, we characterized the antibody response induced by the BNT162b2 vaccine in a group of health care workers, tested at baseline, after the first dose and after the booster. Thirty-nine subjects without previous exposure to SARS-CoV-2 were vaccinated with the BNT162b2 vaccine. IgM, IgG, and IgA anti-receptor binding domain (RBD) were tested by ELISA. Neutralizing antibodies were evaluated testing the inhibition of RBD binding to ACE2. Antibody avidity was measured by urea avidity ELISA. IgM anti-RBD are produced after the first dose of vaccine and persist after the booster. IgG and IgA anti-RBD antibodies are detected in high amounts in all the subjects after the first dose and further increase after the booster. A few subjects, already after the first dose, produce antibodies inhibiting RBD interaction with ACE2. After the booster, high levels of inhibitory antibodies are detected in all the subjects. Affinity maturation takes place with boosting and IgG anti-RBD avidity increases with the number of immunizations. A less pronounced increase is observed with IgA. These data indicate that the BNT162b2 vaccine can induce high levels of protective antibodies of high avidity in vaccinated subjects; both IgG and IgA anti-RBD antibodies are produced. Further studies are needed to evaluate antibody persistence over time.
Mononuclear cell infiltration in glomeruli and renal interstitium is a prominent feature of some types of glomerulonephritis, including lupus nephritis. The mechanism(s) underlying monocyte influx into the kidney is not fully understood. Recently, monocyte chemoattractant protein-1 (MCP-1) has been identified as a chemotactic factor involved in the recruitment of monocytes/macrophages in the glomeruli of rats with mesangioproliferative as well as anti-glomerular basement membrane glomerulonephritis. In the study presented here, renal MCP-1 mRNA expression in New Zealand Black x New Zealand White (NZB/W) F1 mice, a model of genetically determined immune complex disease that mimics systemic lupus in humans, was investigated. Northern blot analysis revealed a single 0.7 kb MCP-1 transcript of very low intensity in kidneys from 2-month-old NZB/W mice that had not yet developed proteinuria nor renal damage. Message levels, which increased markedly with the progression of nephritis and in association with mononuclear cell infiltration, were 10- and 15- fold higher in 8-10-month-old mice than in 2-month-old mice. By in situ hybridization, increased expression of MCP-1 mRNA was demonstrated in glomeruli and, even more striking, in tubular epithelial cells. Western blot analysis demonstrated increased expression of MCP-1 protein in kidneys of 10-month-old NZB/W mice, consistent with MCP-1 mRNA data. When NZB/W mice were treated with cyclophosphamide up to 12 months of age, expression of MCP-1 in the renal tissue remained low, the influx of inflammatory cells did not appear, and glomerular and tubular structures remained well preserved. These data suggest that elevated MCP-1 might act as a signal for inflammatory cells to infiltrate the kidney in lupus nephritis.
ambulance service and the knowledge of new born treatment, as the people working in advanced level ambulance services (p=0.001). Achieved significantly better results, than the staff of a basic level ambulance service (p=0.003). Conclusions: Overall it can be stated that this matter requires special attention and additional trainings need to be provided in the future.
BackgroundAdult onset Still’s disease (AOSD) is a systemic autoinflammatory disorder, sustained by a persistent inflammasome activation with the production of high amounts of IL-1beta and IL-18. Due to the rarity of the disorder, few multicentric cohorts of patients have been so far described.ObjectivesTo analyze clinical manifestations, disease course, treatments and response to therapy in a monocentric cohort of AOSD patients.MethodsWe conducted a retrospective analysis of a cohort of consecutive patients, diagnosed as AOSD in our unit according to Yamaguchi and/or Faultrel criteria. Clinical data and therapeutic approach were analyzed; disease severity was scored by means of Pouchot score. Data were analyzed by multivariate analysis (partial least square model).ResultsWe enrolled 40 patients (21 males, 19 females), mean age 63 yrs (range 21-88), age at disease onset 48 yrs. Fever and arthralgia were present in all the patients, in 77% rash, in 60% sore throat and lymphadenopathy, in 50% hepatosplenomegaly. At disease onset, 5 had intravascular disseminated coagulopathy, 4 acute respiratory distress and 2 myocarditis. In all the patients acute phase reactants were markedly increased and ferritin levels were elevated.Patients were followed for average 6,3 yrs (range 1-16 yrs): 10 patients had a monocyclic pattern, 14 polycyclic, 16 chronic articular. Mean relapses/patient were 3,8; 26% showed >5 relapses and 7% > 25. Chronic articular pattern is the only variable that predicts the number of relapses (p=0,001).Mean Pouchot score at disease onset was 5,5 (>7 in 15 patients); it decreased to 2,2 after 6 months and was 1,2 at the last follow up visit.All the patients were treated with steroids (pulses in 18%), mean steroid dose/patient 9,6 gr. Steroids only were used in 5% of the patients, csDMARDS in 22,5% of the patients (MTX in 60%, Csa in 15%), biologicals in 72,5% (Anakinra in 62%; Tocilizumab in 28%).In 40% of the patients, steroid and one cs or bDMARD allowed to achieve disease control. In 60% one or more therapeutic switches were necessary, because of lack/loss of efficacy or adverse drug reactions.Drug retention rate was 76% at 6 months, 40% at 3 yrs and 4 yrs for Anakinra; 91% at 6 months and 36% at 5 yrs for Tocilizumab. In one patient out of 25 treated with Anakinra and in 3 out of 11 treated with Tocilizumab, the therapy was discontinued for persistent clinical remission.ConclusionThe data we collected confirm the severity and the multisystem involvement of AOSD in a monocentric cohort with a long follow up. Among the different clinical patterns, the chronic articular one is associated with more frequent flares. Severe manifestations of the disease were present at disease onset but did not appear thereafter, suggesting the efficacy of drug therapy and close follow up. Inhibition of IL-1 and IL-6 is a safe and effective therapy. Persistent clinical remission that allows withdrawal of therapy can be obtained albeit in a small number of cases.References[1]Fautrel B. et al Proposal for a new set of classification criteria for adult-onset Still disease. Medicine (Baltimore) 2002;81:194-200[2]Yamaguchi M. et al Preliminary criteria for classification of adult Still’s disease. J Rheumatol 19(3):424-430[3]Ruscitti P. et al. Adult Onset Still Disease: evaluation of prognostic tools and validation of the systemic score by analysis of 100 cases from three centers. 2016 BMC Med 14:194Acknowledgements:NIL.Disclosure of InterestsNone Declared.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.