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September 26, 20250 citationsOpen Access

Asthma, Infections and Immunodeficiency

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AGAlberto GarcíaUniversidad VeracruzanaEAEbymar ArismendiInstituto de Salud Carlos IIIMPMariona PascalHospital Clínic de Barcelona

Key Points

  • Asthma exacerbations can be triggered by early viral infections, increasing susceptibility to lung infections.
  • Defects in both innate and adaptive immunity contribute to higher infection risks in asthma patients.
  • Immunoglobulin therapy has shown to control symptoms, while biologic therapies reduce asthma exacerbations.
  • Current guidelines do not support routine checks for immunodeficiencies despite high infection risk.

Abstract

The relationship between asthma, infections, and immunodeficiencies is complex and affects disease progression. Immune deficiencies can occur independently or because of the inflammatory processes associated with asthma. Early viral infections like respiratory sinticial virus and rhinovirus trigger asthma attacks, while bacteria such as Haemophilus influenzae, Streptococcus pneumoniae, Mycoplasma pneumoniae, and Chlamydia pneumoniae worsen airway inflammation. People with asthma often have defects in innate (mucociliary clearance, interferons, defensins, NK cell, and eosinophils) and adaptive immunity such as immunoglobulin (Ig) deficiencies, making them more vulnerable to lung infections. Combined and selective deficiencies of IgA, IgG, IgM, and IgE are linked to higher asthma rates and reduced effectiveness of treatments, but immunoglobulin therapy can help control symptoms. Biologic therapies also decrease asthma exacerbations during periods of high viral activity by boosting immune responses and airway defenses. However, the link between asthma and higher infection risk is not well studied or understood, so guidelines do not recommend routinely checking for immunodeficiencies in cases of poor treatment response. More research is needed to clarify these connections and improve management strategies.

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Cite This Study

García et al. (2025) studied this question.

synapsesocial.com/papers/68d6cd68b1249cec298b392ehttps://doi.org/10.20944/preprints202509.1855.v1
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