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Published on: February 20, 2015
Methylisothiazolinone induces apoptotic cell death via matrix metalloproteinase activation in human bronchial
1Graduate School of East-West Medical Science, Kyung Hee University, Yongin 17104, Republic of Korea.
Abstract:
Methylisothiazolinone (MIT) has been used in wide spectrum of fields due to its ability to inhibit microbial proliferation with low toxicity. Meanwhile, in Korea, the concern about the hazardous effects of MIT was amplified by the occurrence of patients that have humidifier disinfectant-associated pulmonary disease. However, the toxic mechanism for the pathological lesion is still unclear. In our previous study, we identified that cell viability decreased more rapidly in bronchial epithelial cells (BEAS-2B cells) compared to keratinocytes and liver epithelial cells under the same exposure condition. In this study we demonstrated that MIT (2, 4 and 8 μg/mL) induced dose-dependent cytotoxicity 24 h after exposure to BEAS-2B cells. Additionally, MIT impaired structure and function of intracellular organelles via oxidative stress, ultimately leading to apoptotic cell death. We also found notable activation of matrix metalloproteinases (MMPs) and clear aggregation of nucleolus proteins in MIT-treated cells. Furthermore, MIT increased secretion of proinflammatory cytokines (Interleukin (IL)-1β, IL-6, and interferon-γ) and a chemokine (IL-8), and microarray and the KEGG pathway analysis proposed possible carcinogenesis following exposure to MIT. Taken together, we conclude that MIT induces apoptotic cell death and inflammatory response by activating MMPs in BEAS-2B cells. We also suggest that further study is necessary to clarify the possible carcinogenesis of MIT.
Insights
Methylisothiazolinone (MIT) causes cell death and inflammation in lung cells by damaging organelles and activating MMPs. Further research is needed to understand its potential role in cancer development.
Area of Science:
- Toxicology
- Cell Biology
- Pulmonary Medicine
Background:
- Methylisothiazolinone (MIT) is a widely used biocide with concerns regarding its toxicity, particularly after humidifier disinfectant-associated pulmonary disease cases in Korea.
- The precise toxic mechanisms of MIT, especially in lung epithelial cells, remain unclear.
Purpose of the Study:
- To investigate the cytotoxic effects and underlying mechanisms of Methylisothiazolinone (MIT) exposure in human bronchial epithelial cells (BEAS-2B).
- To explore the role of oxidative stress, organelle damage, and inflammatory responses in MIT-induced toxicity.
Main Methods:
- BEAS-2B cells were exposed to varying concentrations of MIT (2, 4, 8 μg/mL) for 24 hours.
- Assessed cytotoxicity, organelle function, oxidative stress markers, matrix metalloproteinases (MMPs), nucleolus protein aggregation, and proinflammatory cytokine secretion.
- Utilized microarray and KEGG pathway analysis to explore potential carcinogenesis.
Main Results:
- MIT induced dose-dependent cytotoxicity in BEAS-2B cells.
- MIT exposure led to impaired intracellular organelle structure and function via oxidative stress, resulting in apoptotic cell death.
- Activation of MMPs, nucleolus protein aggregation, and increased secretion of IL-1β, IL-6, IFN-γ, and IL-8 were observed. KEGG analysis suggested potential carcinogenesis.
Conclusions:
- Methylisothiazolinone (MIT) induces apoptotic cell death and inflammatory responses in bronchial epithelial cells, partly through MMP activation.
- Oxidative stress and organelle damage are key mechanisms in MIT toxicity.
- Further investigation is warranted to elucidate the potential carcinogenic effects of MIT.
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