The advanced analysis of immune parameters describing differentiation profile, activation and exhaustion of lymphocytes, monocytes and granulocytes of patients with moderate and severe/critical COVID-19 pneumonia was performed.
RATIONALE: Little is known about function and dynamic changes in the myeloid compartment in COVID-19 patients. This study analyzes the myeloid cells subsets counts in COVID-19 patients. METHODS: 57 patients with PCR and chest CT confirmed diagnosis of COVID-19 pneumonia were included in the study. Patients were divided into 2 groups: severe/critical (S/C) patients (n518) which were treated in ICU and required IMV; and moderate (M) patients (n539) which received oxygen support through nasal mask. Blood samples from 19 healthy donors (HD) controls were also used. Granulocytic and monocytic myeloidderived suppressor cells (G/M-MDSC), monocytes (Mon), myeloid and plasmacytoid dendritic cells (mDC and pDC) were assayed using Attune NxT flow cytometer. Nonparametric statistics were used.
Data from the Coronavirus-19 disease (COVID-19) pandemic suggests asthma is not a risk factor for severe disease in adults; it is unclear if this applies to pediatric patients. This study was undertaken to determine if pediatric patients with asthma or atopic disease had altered risk for severe disease when hospitalized with COVID-19. METHODS: A retrospective chart review was performed of SARS-CoV-2 positive patients admitted to Nationwide Children's Hospital from March 1 to July 31. Charts were evaluated for history of asthma or atopic disease (including asthma) and surrogate markers of COVID-19 severity, including ICU admission, supplemental oxygen requirement, and intubation. RESULTS: 49 patients were identified as positive for SARS-CoV-2, 22 of whom were admitted for COVID-19 related symptoms. Of the admitted patients, six patients (12%) had asthma and 18 (37%) atopic disease (including those with asthma). ICU admission rate for asthma versus nonasthma was 17% versus 12% (p50.78) and for atopic versus non-atopic was 17% versus 6.4% (p50.32), while supplemental oxygen rates were 17% versus 16% asthma versus non-asthma (p50.98) and 22% versus 13% atopic versus non-atopic (p50.43). Only two patients required intubation and both had atopic dermatitis. Two patients had Multisystem Inflammatory Syndrome in Children -one with allergic rhinitis and atopic dermatitis, the other without any atopic disease. CONCLUSIONS: Markers of COVID-19 disease severity do not differ based on asthma or atopic status in pediatric patients. In children, like adults, the presence of asthma or atopy does not appear to alter the risk of severe COVID-19.248 COVID-19 pandemia: Atopy and prospective analysis of the clinical evolution of patients infected with the SARS-CoV-2 virus
The prevalence of asthma and allergic airway diseases has increased since the 1960s. The use of dishwasher and household detergents showed a similar trend, leading us to hypothesize that increased exposure to detergents might contribute to development of allergic diseases. The goal of this project was to test this hypothesis by using in vitro and in vivo models. METHODS: We exposed normal human bronchial epithelial (NHBE) cells that overexpress the IL-33 gene to sodium dodecyl benzene sulfonate (SDBS) as a model for detergent. Various pharmacologic agents were used to dissect the mechanisms for IL-33 release. SDBS was also administered intranasally (i.n.) to na€ ıve BALB/c mice. RESULTS: Exposure to SDBS induced IL-33 release from NHBE cells. The dose-response curve was bell-shaped, and the maximum effect was observed at a 3-fold lower concentration (i.e. 50 mg/ml) than the critical micelle concentration for SDBS. At this concentration, more than 90% of NHBE cells were alive, released ATP extracellularly and showed increase in intracellular calcium concentration. IL-33 release was abolished by treating the cells with purinergic receptor antagonists or oxygen radical scavengers or by chelating extracellular calcium. Moreover, the levels of type 2 cytokines in lung homogenates were increased in mice exposed to SDBS in vivo. CONCLUSIONS: Exposure of airway epithelial cells to a low concentration of detergents induces active release of IL-33 likely through the pathway(s) involved in cellular stress responses. Detergents may dysregulate the homeostasis of epithelium and promote development of type 2 immune responses to environmental allergens.
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