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MPO-Mediated oxidative stress regulates lung tissue damage in T-COPD through activation of the NLRP3 inflammasome

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dc.contributor.authorKaican Zong
dc.contributor.authorE Jiang
dc.contributor.authorChunyan Luo
dc.contributor.authorHengyi Chen
dc.contributor.authorWen Li
dc.contributor.departmentBiología Celular e Histología
dc.contributor.editorUniversidad de Murcia, Departamento de Biologia Celular e Histiologia
dc.date.accessioned2026-05-20T08:52:04Z
dc.date.available2026-05-20T08:52:04Z
dc.date.issued2026
dc.description.abstracturpose. This study aimed to investigate the role of MPO in regulating the NLRP3 signaling pathway and its impact on lung injury in a Mycobacterium tuberculosis-induced chronic obstructive pulmonary disease (T-COPD) model. Methods. T-COPD was induced in mice by stimulating with M. tuberculosis, and lung tissues were collected for histological analysis. ELISA, qPCR, and western blot assays were performed to assess the expression of pro-inflammatory cytokines and markers of lung injury, including Myeloperoxidase (MPO) and NOD-like receptor protein 3 (NLRP3). MPO-IN-5, an MPO inhibitor, was used to treat T-COPD mice, and its effects on inflammation and lung damage were evaluated. In vitro, murine lung epithelial MLE-12 cells were treated with LPS, CSE, and M. tuberculosis with or without MPO treatment, followed by assessments of cell viability, apoptosis, ROS levels, and NLRP3 pathway activity. Results. Histological analysis of the M. tuberculosis/ COPD group revealed significant pulmonary edema, inflammatory cell infiltration, and granuloma formation in the liver and spleen, compared with the COPD group. Pro-inflammatory cytokines TNF-α, IL-18, and IL-6 were elevated in the blood of the M. tuberculosis/COPD group. In the lungs, MPO expression and NLRP3 pathway activation were significantly increased. Treatment with MPO-IN-5 reduced the levels of LDH, CRP, and PCT, and reversed the morphological and inflammatory changes in lung tissue. Furthermore, MPO-IN-5 treatment also significantly decreased ROS production and the expression of inflammatory cytokines. In vitro, MPO treatment exacerbated NLRP3 activation in murine lung epithelial MLE-12 cells, while MPO inhibition (with MPO-IN-5) or NLRP3 knockdown mitigated these effects, enhancing cell proliferation and reducing apoptosis. Conclusion. Our results suggest that MPO plays a critical role in regulating the NLRP3 signaling pathway, contributing to lung injury in the T-COPD model. Inhibition of MPO with MPO-IN-5 effectively alleviates inflammation, reduces oxidative stress, and suppresses NLRP3 pathway activation, highlighting its potential as a therapeutic target for T-COPD.
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dc.format.extent12
dc.identifier.doihttps://doi.org/10.14670/HH-25-006
dc.identifier.eissn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/233421
dc.languageeng
dc.relationSin financiación externa a la Universidad
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectNLRP3 signaling pathway
dc.subjectT-COPD
dc.subjectMycobacterium tuberculosis Lung injury
dc.subjectMPO-IN-5 inhibitor
dc.subjectOxidative stress
dc.subjectInflammatory cytokines
dc.subjectMPO
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleMPO-Mediated oxidative stress regulates lung tissue damage in T-COPD through activation of the NLRP3 inflammasome
dc.typeinfo:eu-repo/semantics/article
dspace.entity.typePublication
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Histology and histopathology, Vol.41, Nº6, (2026)