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Presenting prevalence, characteristics and outcome of asthmatic patients with T2 diseases in hospitalized subjects with COVID-19 in Madrid, Spain SUPPLEMENT Introduction. The first confirmed case of coronavirus disease 2019 (COVID-19) in Spain was reported in Madrid at the end of February 2020. Soon after, Madrid reported an outbreak, and cases in Spain increased dramatically, as one of the countries had more cases in the world. Material and Methods. Demographic data, smoking status, non-atopic comorbidities, presence of atopy, symptoms, clinical, radiological and laboratory data on-admission and discharge, need of ICU (Intensive Care Unit) admission days of hospitalization and death were analyzed. Severity of COVID-19 on-admission was classified according to the FIO 2 required: A0 (FIO 2 21%), A1 (FIO 2 up to 35%), A2 (35% >FIO 2 ≤60%) and A3 (FIO 2 > 60%). For asthmatic patients, data related to severity [9], treatment, compliance, and control before COVID-19 were collected together with exacerbation during hospitalization. Compliance was based on refill medication data on electronic prescription during the last year, good compliance was considered as  80% of refills. Asthmatic patients were categorized as non-allergic and allergic (by positive prick test to aeroallergens).

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Anaphylaxis is a life-threatening systemic hypersensitivity reaction. During anaphylaxis, mediator release by effector cells causes endothelial barrier breakdown, increasing vascular permeability and leakage of fluids, which may lead to tissue edema. Although endothelial cells (ECs) are key players in this context, scant attention has been paid to the molecular analysis of the vascular system, and further analyses of this cell type are necessary, especially in humans. The protein expression pattern of human microvascular ECs was analyzed in response to sera from anaphylactic patients (EC-anaphylaxis) and sera from non-allergic subjects (EC-control) after 2 hours of contact. Firstly, a differential quantitative proteomic analysis of the protein extracts was performed by mass spectrometry using an isobaric labeling method. Second, the coordinated behavior of the identified proteins was analyzed using systems biology analysis (SBA). The proteome of the EC-anaphylaxis system showed 7,707 proteins, of which 1,069 were found to be significantly altered between the EC-control and EC-anaphylaxis groups (p-value < 0.05). Among them, a subproteome of 47 proteins presented a high rate of change (|ΔZq| ≥ 3). This panel offers an endothelial snapshot of the anaphylactic reaction. Those proteins with the highest individual changes in abundance were hemoglobin subunits and structural support proteins. The interacting network analysis of this altered subproteome revealed that the coagulation and complement systems are the main biological processes altered in the EC-anaphylactic system. The comprehensive SBA resulted in 5,512 functional subcategories (biological processes), 57 of which were significantly altered between EC-control and EC-anaphylaxis. The complement system, once again, was observed as the main process altered in the EC system created with serum from anaphylactic patients. Findings of the current study further our understanding of the underlying pathophysiological mechanisms operating in anaphylactic reactions. New target proteins and relevant signaling pathways operating in the in vitro endothelial-serum system have been identified. Interestingly, our results offer a protein overview of the micro-EC-anaphylaxis environment. The relevance of the coagulation, fibrinolytic, contact and complement systems in human anaphylaxis is described. Additionally, the untargeted high-throughput analysis used here is a novel approach that reveals new pathways in the study of the endothelial niche in anaphylaxis.