Exploring CHIT1 and YKL-40 in tuberculous pleural effusion: insights and implications

Author:

Przysucha Natalia1,Paplińska-Goryca Magdalena1,Górska Katarzyna1,Misiukiewicz-Stępień Paulina1,Mlącki Michał2,Cyran Agata1,Krenke Rafal1

Affiliation:

1. Medical University of Warsaw

2. Molecure SA

Abstract

Abstract

Background and objective: Chitinases and chitinase-like proteins are thought to be involved in the pathophysiology of lung diseases. The study was designed to evaluate the significance of chitotriosidase (CHIT1) and YKL-40 in tuberculous pleural effusion (TPE), to identify the cellular sources of these proteins in pleural fluid, and to assess the diagnostic performance of chitinases as potential biomarkers of TPE. Methods: This retrospective, single-centre study included 66 patients with pleural effusion of different origins: malignant pleural effusion (MPE), TPE, parapneumonic pleural effusion (PPE), and pleural transudate (TE). YKL-40 and CHIT1 protein levels were measured in pleural effusions, while YKL-40 and CHIT1 expression was evaluated by the immunohistochemical staining in tuberculoid granulomas. Results: The highest levels of CHIT1 and YKL-40 were found for TPE 70.51 ng/ml (49.65-136.98 ng/ml) and 569.84 ng/ml (530.32-706.01 ng/ml), respectively. The amount of YKL-40 in TPE was significantly higher than in PPE [387.98 ng/ml (262.94-539.09 ng/ml),(p<0.01)] and TE [(254.95 ng/ml (188.93-334.1 ng/ml), (p<0.001)]. A strong positive correlations between YKL-40 level in TPE and the percentage of macrophages (r=0.73, p=0.003) and adenosine deaminase activity (r=0.82, p<0.001) were demonstrated. Pleural YKL-40 (higher than 500 ng/ml) could be helpful in differentiating between tuberculosis vs. non-tuberculosis effusions (sensitivity 78.85%, specificity 85.7%, and AUC of 0.85). We revealed a clearly detectable expression of YKL-40 in the tuberculoid granulomas, whereas the presence of CHIT1 in this material was negligible. Conclusion: Our study showed that YKL-40 but not CHIT-1 may contribute to the pleural inflammatory response associated with tuberculosis.

Publisher

Springer Science and Business Media LLC

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