Asthma and clinical outcomes of COVID-19 in a community setting

Jiao, L.; Bujnowski, D.; Liu, P.; Bakota, E.; Liu, L.; Ye, Y.; Dewangan, A.; Duong, C.N.; Kviten, E.; Zaheer, S.; Zangeneh, A.; Roy, R.; Floyd, J.; Monroy, J.; Wiltz-Beckham, D.

doi:10.1016/j.puhe.2023.10.040

Cited by 4 publications

(2 citation statements)

References 36 publications

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“…Children and adults with asthmatic diseases were initially thought to have more severe COVID-19 outcomes, given known deficits in antiviral immunity and that common respiratory viruses can exacerbate asthma. However, many clinical studies failed to show an expected increase in the prevalence of asthmatic patients among COVID-19-infected individuals and instead concluded that the relative risk of severe COVID-19 was relatively small 32,34,[151][152][153] . We show here in a murine experimental OVA/Alum asthma model that underlying allergic-type IIdriven inflammation at the time of SCV2 exposure significantly enhances innate viral replication control in the lungs, arguing that innate aspects of type II immune responses might provide potential antiviral protective rather than detrimental effects early during SCV2 infection.…”

Section: Discussionmentioning

confidence: 99%

“…While certain chronic lung diseases, including tuberculosis (TB) 28,29 and chronic obstructive pulmonary disease (COPD) [30][31][32][33] have been associated with increased severity of COVID-19 in most studies, other chronic pulmonary conditions, such as asthma [32][33][34][35] and cystic fibrosis (CF) [36][37][38] did not consistently correlate with worsened COVID-19 presentation and have even been associated with improved disease outcomes. The immunological factors in the lung that determine such variability in early viral control, and thus the likelihood of developing severe disease, are incompletely understood, and challenging to examine in clinical settings.…”

Section: Introductionmentioning

confidence: 99%

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The inflammatory microenvironment of the lung at the time of infection governs innate control of SARS-CoV-2 replication

Baker,

Bohrer,

Castro

et al. 2024

Preprint

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SARS-CoV-2 infection leads to vastly divergent clinical outcomes ranging from asymptomatic infection to fatal disease. Co-morbidities, sex, age, host genetics and vaccine status are known to affect disease severity. Yet, how the inflammatory milieu of the lung at the time of SARS-CoV-2 exposure impacts the control of viral replication remains poorly understood. We demonstrate here that immune events in the mouse lung closely preceding SARS-CoV-2 infection significantly impact viral control and we identify key innate immune pathways required to limit viral replication. A diverse set of pulmonary inflammatory stimuli, including resolved antecedent respiratory infections with S. aureus or influenza, ongoing pulmonary M. tuberculosis infection, ovalbumin/alum-induced asthma or airway administration of defined TLR ligands and recombinant cytokines, all establish an antiviral state in the lung that restricts SARS-CoV-2 replication upon infection. In addition to antiviral type I interferons, the broadly inducible inflammatory cytokines TNFα and IL-1 precondition the lung for enhanced viral control. Collectively, our work shows that SARS-CoV-2 may benefit from an immunologically quiescent lung microenvironment and suggests that heterogeneity in pulmonary inflammation that precedes or accompanies SARS-CoV-2 exposure may be a significant factor contributing to the population-wide variability in COVID-19 disease outcomes.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The inflammatory microenvironment of the lung at the time of infection governs innate control of SARS-CoV-2 replication

Baker,

Bohrer,

Castro

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

Asthma as a risk factor and allergic rhinitis as a protective factor for COVID-19 severity: a case-control study

Lira Tenório,

dos Santos Menezes Siqueira,

Costa Caldas

et al. 2024

Eur Arch Otorhinolaryngol

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The inflammatory microenvironment of the lung at the time of infection governs innate control of SARS-CoV-2 replication

Baker,

Bohrer,

Castro

et al. 2024

Sci. Immunol.

View full text Add to dashboard Cite

Severity of COVID-19 is affected by multiple factors; however, it is not understood how the inflammatory milieu of the lung at the time of SARS-CoV-2 exposure affects the control of viral replication. Here, we demonstrate that immune events in the mouse lung closely preceding SARS-CoV-2 infection affect viral control and identify innate immune pathways that limit viral replication. Pulmonary inflammatory stimuli including resolved, antecedent respiratory infections with Staphylococcus aureus or influenza, ongoing pulmonary Mycobacterium tuberculosis infection, ovalbumin/alum-induced asthma, or airway administration of TLR ligands and recombinant cytokines all establish an antiviral state in the lung that restricts SARS-CoV-2 replication. In addition to antiviral type I interferons, TNFα and IL-1 potently precondition the lung for enhanced viral control. Our work shows that SARS-CoV-2 may benefit from an immunologically quiescent lung microenvironment and suggests that heterogeneity in pulmonary inflammation preceding SARS-CoV-2 exposure may contribute to variability in disease outcomes.

show abstract

Asthma and clinical outcomes of COVID-19 in a community setting

Cited by 4 publications

References 36 publications

The inflammatory microenvironment of the lung at the time of infection governs innate control of SARS-CoV-2 replication

The inflammatory microenvironment of the lung at the time of infection governs innate control of SARS-CoV-2 replication

Asthma as a risk factor and allergic rhinitis as a protective factor for COVID-19 severity: a case-control study

The inflammatory microenvironment of the lung at the time of infection governs innate control of SARS-CoV-2 replication

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