No abstract

angiotensin-converting enzyme 2 expression levels correlate with allergic sensitization, higher levels of total immunoglobulin E, and type 2 inflammatory cytokines. [3][4][5] Interleukin 13, a major type 2 inflammatory cytokine, is found to significantly reduce angiotensinconverting enzyme 2 expression in airway epithelial cells. 5 Our findings of the association of AR and eczema with decreased need of hospitalization for COVID-19 provide robust clinical data to support these mechanistic findings.The role of asthma and its association with COVID-19 severity is more complicated. 6,7 Asthma was not reported in previously published cohorts of COVID-19 from China 1,2 ; although data from the Centers for Disease Control indicate that asthma is present in as high as 27% of hospitalized COVID-19 patients in the United States in the 20 to 49 year age range. 6 This could be explained by the lower rates of asthma in China (2%-4%) than those in the United States (8%-11%). 8,9 In the current report, allergic asthma was not associated with any COVID-19 outcome variable despite AR being protective against hospitalization. Furthermore, nonallergic asthma was associated with a prolonged intubation time which confirms an earlier study. 10 It is possible that asthma, as a chronic pulmonary disease susceptible to viral-induced exacerbations, places those with more severe COVID-19 illness at risk for more prolonged lung involvement. However, a coexisting atopic background may mitigate the severe inflammatory response syndrome of COVID-19 in those with allergic asthma, leading to the absence of the prolonged intubation time reported in individuals with nonallergic asthma.The knowledge that atopy is associated with less severe COVID-19 outcomes can be instructive in clinical risk stratification. Further studies are needed to understand the underlying mechanism of these apparent protective physiological factors that may prove advantageous in future prevention and treatment strategies.