In tissue of CRSwNP patients with an immune response to SAE, the production of pLTs, LTB4 and LXA4 is further upregulated [90], while SAEB significantly downregulated PGE2, COX2, and prostanoid receptor EP2 mRNA expression in fibroblasts, pointing to a direct role of SAE in regulating eicosanoids as a possible mechanism of SAE inflammatory reaction [88]. This evidence concerns the gene PTGER2 and chronic rhinosinusitis with nasal polyps.