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.

Keywords: COVID-19; IgE; asthma; biologics; omalizumab.

Figure 1

Characteristics of the Th2-high endotype asthma vs. Th2-low endotype asthma that may confer different effects against COVID-19. ACE2, angiotensin-converting enzyme 2 receptor; COVID-19, coronavirus disease 2019; IL, interleukin; NETs, neutrophil extracellular traps; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; Th2, T-helper type 2.

Figure 2

Role of IgE and effects of IgE blockade with omalizumab in antiviral response. Cross-linking of IgE bound to FcɛRI on pDCs, which are mainly located in lung interstitium, diminishes IFN-α antiviral response. Anti-IgE therapy omalizumab binds to free IgE, prevents binding of IgE to FcɛRI, and reduces the expression of FcɛRI, thereby increases IFN-α antiviral response. FcɛRI, high-affinity IgE receptor; IFN-α, interferon-α; IgE, immunoglobulin E; and pDC, plasmacytoid dendritic cell.