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Chronic Rhinosinusitis and the Coagulation System.

Dong Young Kim¹, Seong H Cho², Tetsuji Takabayashi³

¹Division of Allergy and Immunology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.; Department of Otorhinolaryngology-Head and Neck Surgery, Seoul National University College of Medicine, Seoul, Korea.

Allergy, Asthma & Immunology Research

|July 1, 2015

Summary

This summary is machine-generated.

The coagulation system, specifically fibrin deposition, plays a key role in chronic rhinosinusitis with nasal polyps (CRSwNP). Understanding these mechanisms offers new therapeutic targets for CRSwNP treatment.

Keywords:

Rhinosinusitis coagulation factor XIIIa fibrinolysis nasal polyps tissue plasminogen activator

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Area of Science:

Immunology
Hematology
Otorhinolaryngology

Background:

Chronic rhinosinusitis (CRS) is a prevalent condition impacting adult quality of life, with uncertain etiologic factors.
The coagulation cascade's role in inflammatory diseases like asthma is recognized, but its involvement in CRS pathogenesis is a recent area of investigation.

Purpose of the Study:

To investigate the role of the coagulation system, particularly fibrin deposition, in the pathophysiology of chronic rhinosinusitis with nasal polyps (CRSwNP).
To explore potential therapeutic targets for CRSwNP based on elucidated fibrin deposition mechanisms.

Main Methods:

Analysis of fibrin deposition and coagulation factors in nasal polyp (NP) tissues from CRSwNP patients.
Validation of findings using a newly established murine model of NP.
Assessment of thrombin activation, tissue plasminogen activator (t-PA) levels, and coagulation factor XIII-A (FXIII-A) expression.

Main Results:

Excessive fibrin deposition was observed in NP tissues from CRSwNP patients.
Evidence of thrombin activation, reduced t-PA, and increased FXIII-A was found, contributing to fibrin deposition and crosslinking.
These pathological findings were successfully replicated in the murine NP model.

Conclusions:

The coagulation system, particularly excessive fibrin deposition driven by thrombin activation and altered t-PA/FXIII-A levels, is implicated in the pathophysiology of CRSwNP.
Understanding these fibrin-related mechanisms is crucial for comprehending tissue remodeling in NP and developing novel treatment strategies for CRSwNP.