Dive into the latest research exploring how the upregulation of cyclooxygenase-2 influences chronic rhinosinusitis with nasal polyps, shedding light on potential therapeutic targets.
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The cyclooxygenase-2 upregulation mediates production of PGE2 autacoid to positively regulate interleukin-6 secretion in chronic rhinosinusitis with nasal polyps and polyp-derived fibroblasts.
Shieh et al., Sci Rep 2024
<!– DOI: 10.1038/s41598-024-58143-2 //–>
https://doi.org/10.1038/s41598-024-58143-2
This study delves into the role of cyclooxygenase-2 (COX-2) in chronic rhinosinusitis with nasal polyps (CRSwNP), a condition traditionally classified by clinical phenotypes but now increasingly understood through endotypes. The research found that COX-2 protein and mRNA levels were significantly higher in nasal polyp (NP) tissues of Taiwanese CRSwNP patients compared to controls and CRS without nasal polyps (CRSsNP) patients. The overexpression was primarily in the epithelium and subepithelial stroma. The study also discovered that COX-2 upregulation, triggered by CRS-related stimuli in NP-derived fibroblasts, led to increased secretion of prostaglandin E2 (PGE2), thromboxane A2 (TXA2), and interleukin-6 (IL-6). Further, it was shown that PI3K/Akt pathway activation is essential for this process, particularly for IL-6 production, which is speculated to be modulated by PGE2 but not TXA2. The findings suggest COX-2 as a potential biomarker for CRSwNP and underscore the potential therapeutic value of COX-2 inhibitors in treating this condition. This contributes to the understanding of CRSwNP pathophysiology by highlighting the molecular mechanisms involved in nasal polyposis and inflammation.