The following is a summary of “IL-1 receptor antagonist attenuates proinflammatory responses to rhinovirus in airway epithelium,” published in the JUNE 2023 issue of Allergy & Immunology by Schworer, et al.
Asthma exacerbations triggered by rhinoviruses (RVs) are common, and current therapies do not specifically target these viral-induced exacerbations. Neutrophilic inflammation, resistant to glucocorticoids, is a characteristic response to RV infection. Treatment with IL-1 receptor antagonist (IL-1RA) has been shown to reduce neutrophilic inflammation in individuals exposed to inhaled endotoxin, suggesting its potential as a therapeutic option for RV-induced asthma exacerbations. For a study, researchers sought to investigate whether treating airway epithelium with IL-1RA could reduce RV-induced production of proinflammatory cytokines, which are crucial for neutrophil recruitment.
Human bronchial epithelial cells obtained from deceased donors without pulmonary disease were cultured at the air-liquid interface and exposed to IL-13 to simulate an asthmatic inflammatory environment. Subsequently, the cells were infected with human RV-16 and treated with or without IL-1RA.
RV infection stimulated the release of IL-1α and proinflammatory cytokines, including IL-6, IL-8, and CXCL10, which attract neutrophils to the site of infection. Treatment with IL-1RA significantly reduced the secretion of these proinflammatory cytokines without affecting the release of IFN-β or the RV viral load. Furthermore, IL-1RA treatment decreased the expression of MUC5B, a mucin gene associated with excessive mucus production, following RV infection, without impacting MUC5AC expression.
The findings indicated that IL-1RA treatment effectively reduces the production of proinflammatory cytokines involved in neutrophil recruitment while preserving the antiviral response. The results supported a further investigation into IL-1RA as a potential targeted therapy for inhibiting the release of neutrophil-attractant cytokines in airway inflammatory responses induced by RV infection.
Source: jacionline.org/article/S0091-6749(23)00089-1/fulltext