Literature DB >> 31112544

NLRP3 inflammasome activity is upregulated in an in-vitro model of COPD exacerbation.

Noy Nachmias1,2,3, Sheila Langier3, Rafael Y Brzezinski2,4, Matan Siterman3, Moshe Stark3, Sara Etkin3, Avital Avriel1, Yehuda Schwarz3, Shani Shenhar-Tsarfaty2, Amir Bar-Shai3.   

Abstract

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is an inflammatory disease characterized by a progressive and irreversible deterioration of lung function. Exacerbations of COPD have prolonged negative effects on pulmonary function and a major impact on health status and outcomes. NLRP3 inflammasome is a cardinal component of the inflammatory response, with marked evidence in stable and exacerbations of COPD. The aim of our study was to evaluate the NLRP3 inflammasome activity during COPD exacerbation by using an in vitro model.
METHODS: A549 cells were stimulated with different concentrations (10%, 4%, 2%) of cigarette smoke extract (CSE) with or without LPS (0.1μg/ml) for 24 hours. Cell viability was assessed by using XTT test. Levels of inflammatory cytokines (IL-8, MCP-1, and IL-1β) were measured by ELISA and the activity level of NLRP-3 was evaluated by flow cytometry.
RESULTS: Cells exposed to CSE present an increase in inflammatory cytokines (IL-8 and MCP-1) production in a dose-dependent manner. Incubation with LPS to these cells results in higher levels of IL-8 and MCP-1 compared to stimulation of CSE alone. NLRP3 inflammasome activity and IL-1β levels were significantly increased in cells exposed to both CSE and LPS compared to CSE alone.
CONCLUSIONS: NLRP3 inflammasome is upregulated in an in-vitro model of COPD and COPD exacerbation. Our findings provide novel biomarkers for COPD exacerbation and may present new targets for future research.

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Year:  2019        PMID: 31112544      PMCID: PMC6529002          DOI: 10.1371/journal.pone.0214622

Source DB:  PubMed          Journal:  PLoS One        ISSN: 1932-6203            Impact factor:   3.240


  21 in total

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