TH1/TH2 repolarization in induction of immune tolerance to non-steroidal anti-inflammatory drugs during the management of sickle cell disease vaso-occlusive crisis.

Respiratory manifestations related to the intake of non-steroidal anti-inflammatory drugs (NSAIDs) during the treatment of the painful vaso-occlusive crisis of sickle cell disease are either a type I hypersensitivity mechanism of the Gell and Coombs classification, or a pharmacological mechanism of NSAIDs. The use of NSAIDs is essential in the Abidjan school because of the absence of therapeutic alternatives in the management of the inflammatory crisis of this disease. The induction of tolerance to NSAIDs initiated by the authors has had clear clinical success. The basic biological reasons for this tolerance were evaluated in this study. A group of 11 sickle cell patients aged 12 to 39 years in whom post-NSAID respiratory manifestations disappeared for at least 6 months following a short tolerance induction protocol with ibuprofen, was assayed by ELISA for TNFα, INF (Th1 cytokines), IL-4 (Th2 cytokine), IL-10, TGF-ß (immunosuppressive cytokines) and total IgE, before induction or pre-induction (D-1) and at day one (D1), D2- 3, one month (M1), and M6 after induction. A repolarization of the Th1/Th2 balance was noted during the post induction period. The high concentration of IL-4 observed at D-1 gradually decreased in favor of the cytokines TNFα, INF. The decrease in cytokine IL-4 with the level of total IgE was accompanied by the increase of IL-10 and TGF-ß demonstrating the regulatory role of these cytokines in the control of allergic diseases. In conclusion, the induction of immuno-tolerance to NSAIDs through a short protocol is well supported by immune regulation. The medium-term effects are real, unlike the results of allergen desensitization or specific immunotherapy. However, this protocol could be used in certain circumstances such as in the case of intolerance to trimethoprim-sulfamethoxazole, used as the treatment of choice for the prevention of opportunistic diseases in people living with human immunodeficiency virus.

Analysis of total antibody levels in university hospitals health workers vaccinated against COVID-19 in Abidjan (Côte d'Ivoire).

Discovered in China in December 2019, coronavirus disease-19 (COVID-19) has confronted the world with an unprecedented crisis. Healthcare workers, the first line of defense against this pandemic, have been severely affected. Clinical trial results of the emergency vaccines showed that they all produced IgG antibodies against severe acute respiratory syndrome corona virus-2 (SARS-CoV-2) with high rates of seroconversion. While immunization against natural challenge (COVID-19 infection) and artificial challenge (vaccination) in health care workers is relatively well described in the West, the issue is not well understood in Sub-Saharan Africa, particularly in Côte d'Ivoire, where populations are genetically distinct from Caucasians. Our aim was to investigate the magnitude of post-vaccination IgG responses to SARS-CoV-2 in healthcare workers in our African epigenetic context. A cross-sectional, multicenter, analytical study was conducted from March to May 2022 among health workers employed at the University Hospital of Abidjan and vaccinated against COVID-19. The study included 77 health workers. IgG immunoassays were performed with an enzyme-linked fluorescent assays. Data were analyzed using SPSS version 22.0 software, with a p-value ˂ 0.05 considered as a significant difference. All enrolled subjects developed anti-SRAS-Cov-2 IgG, of which 88.3% had a strong response (titer ≥ 250 Binding Antibody Units/ml). IgG titers varied significantly by gender (p=0.04). Vaccine type and number of doses did not affect IgG titers. However, a history of COVID-19 infection was associated with a 5-fold greater likelihood of developing a strong IgG response after vaccination. In conclusion, humoral IgG responses developed after vaccination against SARS-CoV-2 were robust and would be influenced by a variety of factors..