Abstract: Objective  To explore the deposition of fibrin and the expression of genes related to fibrin formation and degradation in nasal mucosa of patients with chronic rhinosinusitis with nasal polyps (CRSwNP) and patients with CRSwNP comorbid asthma (CRSwNP+AS). Methods  Immunofluorescence staining was used to evaluate the deposition of fibrin in the nasal mucosa. Real-time fluorescence quantitative polymerse chain reaction (RT-qPCR) was used to detect the expression of genes related to fibrin formation and degradation ［factor ⅩⅢ A chain 1 (F13A1)， plasminogen (PLG)， plasminogen activator tissue type (PLAT)， plasminogen activator urokinase (PLAU) and plasminogen activator inhibitor 1 (PAI-1)］ in nasal mucosa of CRSwNP, CRSwNP+AS and control subjects. The patients received glucocorticoid treatment. Results  Compared with the control group, immunofluorescence staining showed obvious deposition of crosslinked fibrin in the nasal mucosa of patients with CRSwNP, and CRSwNP+AS group had more significant fibrin deposition. Gene expression analysis showed that the expression of F13A1, a gene that promotes fibrin formation, and PAI-1, a gene that inhibits fibrin degradation, were both significantly increased in the CRSwNP and CRSwNP+AS groups. In addition, the expression of F13A1 was significantly higher in CRSwNP+AS group than that in CRSwNP group. The expression of PLAT, which promotes fibrin degradation, was significantly lower in the CRSwNP+AS group than that in the CRSwNP and control groups. PLAU is upregulated in both types of CRSwNP. Glucocorticoid treatment significantly downregulates F13A1 and upregulates the expression of PLAT in patients with CRSwNP+AS. Conclusion  Patients with CRSwNP have excessive fibrin deposition in the nasal mucosa, which may be caused by the dysregulation of genes related to fibrin formation and degradation. Dysregulated F13A1 and PLAT were more significant in CRSwNP+AS. 

Key words: chronic rhinosinusitis with nasal polyps, asthma, fibrin, factor ⅩⅢ A, plasminogen activator