The following is a summary of “Retinoic acid promotes fibrinolysis and may regulate polyp formation,” published in the November 2022 issue of Allergy and clinical immunology by Sakashita, et al.
Severe nasal polyposis is a common symptom of aspirin-exacerbated respiratory disease (AERD) patients. According to studies, chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by a significant drop in epithelial tissue plasminogen activator (tPA) and excessive fibrin deposition. Retinoids, such as vitamin A and its active metabolite retinoic acid (RA), are well-known inducers of tPA in endothelial cells and are essential for sustaining epithelial function. For a study, researchers sought to ascertain if endogenous retinoids contributed to the pathogenesis of NP and the severity of the disease in individuals with CRSwNP and AERD.
Patients with AERD or CRSwNP’s NP tissue was taken, and retinoids and fibrinolysis indicators were evaluated using ELISA. In addition, RA and IL-13 were used to activate normal human bronchial epithelial cells for 24 hours.
In comparison to patients with CRSwNP or healthy controls, patients with AERD had reduced amounts of retinoid in their nasal polyps, according to the research (P< .01). AERD polyps (P< .01) had the lowest levels of the fibrin-breakdown product d-dimer, which was associated with decreased tPA expression (P< .01). All-trans RA increased tPA levels in healthy human bronchial epithelial cells by 15 times in vitro and reversed the reduction of tPA expression caused by IL-13 in cultured cells (P< .01).
AERD patients’ tissue had lower amounts of RA, which was strong in vitro inducer of epithelial tPA. The discovery raised the possibility that lower levels of tPA and fibrinolysis were related to AERD. Furthermore, because RA may restore IL-13-induced tPA suppression in vitro and activate tPA in epithelial cells, it suggested that RA may be useful in treating individuals with CRSwNP and/or AERD.
Reference: jacionline.org/article/S0091-6749(22)00836-3/fulltext
