Abstract
To date, there has been no reliable test to identify unfavorable course of Chronic Rhinosinusitis with Nasal Polyps (CRSwNP), especially in aspirin intolerant patients. The research aimed to analyze the expression of transcript variants of PTGS1 and PTGS2 genes in the pathobiology of the disease. The study was performed on 409 adult patients: 206 CRSwNP patients including 44 (21.36%) aspirin intolerant patients and 203 healthy volunteers in the control group. Transcript variants of the PTGS1 and PTGS2 genes named as follows: COX1.1 for NM_000962, COX1.2 for NM_080591, COX1.3 for NM_001271165.1, COX1.4 for NM_001271368.1, COX1.5 for NM_001271166.1, COX2.1 for NM_000963.3, COX2.2 for AY_151286 and COX2.3 for BQ_722004 were confirmed using direct sequencing and quantified using targeted qPCR. The coexistence of all examined transcript variants in the study and the control group and significant differences between both were found. In aspirin sensitive patients, the levels of COX1.2, COX1.3, COX1.4 and COX1.5 isoforms were higher compared to aspirin-tolerant patients. The severity of symptoms was bigger in patients with higher expressions of variants: COX1.1 (R with dCt = −0.134; p = 0.0490), COX1.3 (R = −0.1429; p = 0.0400) and COX1.5 (Rs = −0.1499; p = 0.032). The expression of COX1.1 (Rs = −0.098; p = 0.049) and COX1.5 (Rs = −0.141; p = 0.043) isoforms increased with polyposis advancement in endoscopy. With the CT extent of sinuses opacification, COX1.1 isoform also significantly increased (Rs = −0.163; p = 0.020). The isoforms COX1.3, COX1.4, COX1.5 and COX2.1 may promote milder CRSwNP course. On the contrary, the variants COX1.1, COX1.2 and COX2.2 may be involved in a more aggressive disease.
Highlights
The exact mechanism of Chronic rhinosinusitis with nasal polyps (CRSwNP) is still unknown; one of the hypotheses suggests that impaired epithelial cells function and eosinophilic mucosal inflammation are pivotal in nasal polyps development [6]
The study was performed on 409 adult patients: 206 patients suffering from CRSwNP and 203 healthy volunteers in the control group, all treated in Department of Otolaryngology, Head and Neck Oncology, Medical University of Lodz, Poland
It should be noticed that the expression of the studied transcriptional variants of the PTGS1 and PTGS2 genes is different in patients with CRSwNP compared to the control group
Summary
Chronic rhinosinusitis with nasal polyps (CRSwNP) is a relapsing disease with growing incidence rate [1,2]. Despite using proper conservative treatment, advanced surgical techniques and complementary long-term pharmacotherapy, CRSwNP is characterized by irregular and hard to predict recurrences [5]. The exact mechanism of CRSwNP is still unknown; one of the hypotheses suggests that impaired epithelial cells function and eosinophilic mucosal inflammation are pivotal in nasal polyps development [6]. This process is followed by damaging factors, including bacterial biofilm, viruses, allergens, toxic substances or hypoxia resulting from existing airflow barriers (e.g., deviated nasal septum, concha bullosa) [7].
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