Asthma and COVID-19 Associations: Focus on IgE-Related Immune Pathology

Abstract

Management of patients with asthma during the coronavirus disease 2019 (COVID-19) pandemic is a concern, especially since asthma predisposes patients to respiratory problems. Interestingly, asthma characterized by type 2 inflammation, also known as T-helper type 2-high endotype, displays a cellular and molecular profile that may confer protective effects against COVID-19. The results of experimental and clinical studies have established the actions of immunoglobulin E (IgE) in inducing airway hyperreactivity and weakening an interferon-mediated antiviral response following respiratory viral infection. Robust evidence supports the beneficial effect of the anti-IgE biologic treatment omalizumab on reducing respiratory virus-induced asthma exacerbations and reducing the frequency, duration, and severity of respiratory viral illness in patients with asthma. Indeed, accumulating reports of patients with severe asthma treated with omalizumab during the pandemic have reassuringly shown that continuing omalizumab treatment during COVID-19 is safe, and in fact may help prevent the severe course of COVID-19. Accordingly, guidance issued by the Global Initiative for Asthma recommends that all patients with asthma continue taking their prescribed asthma medications, including biologic therapy, during the COVID-19 pandemic. The impact of biologic treatments on patients with asthma and COVID-19 will be better understood as more evidence emerges.

Omalizumab may protect allergic patients against COVID-19: A systematic review

“…Only 12 patients interrupted the treatment (because they were afraid of pandemic and refused to return to the hospital): the risk of infection and severe disease was higher in these second group (relative risk of 2.71; 95% CI, 1.21-6.06). 1,47 Between 13 Turkish patients with severe asthma (treated with omalizumab or mepolizumab) that contracted SARS-CoV-2, five (38.5%) had mild COVID-19, eight (61.5%) had moderate disease, none required mechanical ventilation or intensive care, all patients fully recovered. 1,47 In the Garcıa-Menaya cohort, only 1 patient of 113 with COVID-19 had taken omalizumab before hospital admission.…”

“…During the early stages of the disease, type I interferon (including IFN-a) and adaptive immunity preclude the disease progression. [1][2][3][4][5][6][7] When this immune response is impaired, high virus loads lead to pathological inflammation, massive organ dysfunction, and acute respiratory distress syndrome (ARDS). 9 This hyperinflammatory immune response, evoked by immune cells and various cytokines, 6 causes an exaggerated immune response (called "cytokine storm") with multi-organ damage, leading to high mortality.…”

“…9 This hyperinflammatory immune response, evoked by immune cells and various cytokines, 6 causes an exaggerated immune response (called "cytokine storm") with multi-organ damage, leading to high mortality. 1,10 Type I interferon is a family of potent antiviral cytokines that restricts viral replication and improves antiviral immunity. 3 Each cell can produce IFN (type I), but only plasmacytoid cells can produce it rapidly in high quantities.…”

COVID-19 Prevention and Treatment

“…Five of the papers of the Special Issue focus on the general and specific conditions of COVID-19 pathology [ 29 , 30 , 31 , 32 , 33 ]: one paper explored the potential role of inflammation as a prognostic hallmark of clinical outcome in infected patients. The main objective of a second study was to describe the role of host genetic variability in modulating COVID-19 clinical outcomes.…”

Coronavirus disease 2019 and severe asthma

“…This is attributable to a reduction of innate and acquired immunity which can predispose to infections. The RECOVERY study, a multicenter randomized controlled trial, showed that dexamethasone reduced 28-day mortality compared to those who did not receive it [54,55]. The Open-SAFELY study highlighted how the use of OCS within the two weeks prior hospitalization for COVID-19 was associated to higher risk of death in asthmatic people [50].…”