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Inhibition of Both Cyclooxygenase-1 and -2 Promotes Epicutaneous Th2 and Th17 Sensitization and Allergic Airway Inflammation on Subsequent Airway Exposure to Protease Allergen in Mice. | LitMetric

AI Article Synopsis

  • Epicutaneous (e.c.) allergen exposure plays a crucial role in developing allergic diseases, and proteases in allergens, like those from house dust mites, contribute to this process while being regulated by prostanoids from cyclooxygenase (COX) pathways.
  • In an experiment with mice, treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) during e.c. sensitization to a protease allergen, papain, showed increased immune responses, including higher IgE levels and cytokine production linked to allergic reactions.
  • The study concludes that COX-derived prostanoids have a suppressive effect on the immune response, particularly on Th2 and Th17 cells, suggesting that inhibiting COX pathways

Article Abstract

Introduction: Epicutaneous (e.c.) allergen exposure is an important route of sensitization toward allergic diseases in the atopic march. Allergen sources such as house dust mites contain proteases that involve in the pathogenesis of allergy. Prostanoids produced via pathways downstream of cyclooxygenases (COXs) regulate immune responses. Here, we demonstrate effects of COX inhibition with nonsteroidal anti-inflammatory drugs (NSAIDs) on e.c. sensitization to protease allergen and subsequent airway inflammation in mice.

Methods: Mice were treated with NSAIDs during e.c. sensitization to a model protease allergen, papain, and/or subsequent intranasal challenge with low-dose papain. Serum antibodies, cytokine production in antigen-restimulated skin or bronchial draining lymph node (DLN) cells, and airway inflammation were analyzed.

Results: In e.c. sensitization, treatment with a nonspecific COX inhibitor, indomethacin, promoted serum total and papain-specific IgE response and Th2 and Th17 cytokine production in skin DLN cells. After intranasal challenge, treatment with indomethacin promoted allergic airway inflammation and Th2 and Th17 cytokine production in bronchial DLN cells, which depended modestly or largely on COX inhibition during e.c. sensitization or intranasal challenge, respectively. Co-treatment with COX-1-selective and COX-2-selective inhibitors promoted the skin and bronchial DLN cell Th cytokine responses and airway inflammation more efficiently than treatment with either selective inhibitor.

Conclusion: The results suggest that the overall effects of COX downstream prostanoids are suppressive for development and expansion of not only Th2 but also, unexpectedly, Th17 upon exposure to protease allergens via skin or airways and allergic airway inflammation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8491500PMC
http://dx.doi.org/10.1159/000514975DOI Listing

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