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Organic dust exposure induces stress response and mitochondrial dysfunction in monocytic cells
Sanjana Mahadev Bhat1, Denusha Shrestha1, Nyzil Massey1
1Department of Biomedical Sciences, Iowa State University, 2008 Vet Med Building, Ames, IA, 50011, USA.
Abstract:
Exposure to airborne organic dust (OD), rich in microbial pathogen-associated molecular patterns (PAMPs), is shown to induce lung inflammation. A common manifestation in lung inflammation is altered mitochondrial structure and bioenergetics that regulate mitochondrial ROS (mROS) and feed a vicious cycle of mitochondrial dysfunction. The role of mitochondrial dysfunction in other airway diseases is well known. However, whether OD exposure induces mitochondrial dysfunction remains elusive. Therefore, we tested a hypothesis that organic dust extract (ODE) exposure induces mitochondrial stress using a human monocytic cell line (THP1). We examined whether co-exposure to ethyl pyruvate (EP) or mitoapocynin (MA) could rescue ODE exposure induced mitochondrial changes. Transmission electron micrographs showed significant differences in cellular and organelle morphology upon ODE exposure. ODE exposure with and without EP co-treatment increased the mtDNA leakage into the cytosol. Next, ODE exposure increased PINK1, Parkin, cytoplasmic cytochrome c levels, and reduced mitochondrial mass and cell viability, indicating mitophagy. MA treatment was partially protective by decreasing Parkin expression, mtDNA and cytochrome c release and increasing cell viability.
Insights
Organic dust extract (ODE) exposure causes mitochondrial dysfunction and cell damage in human cells. Ethyl pyruvate and mitoapocynin offer partial protection against these effects, suggesting therapeutic potential.
Area of Science:
- Environmental Health
- Cell Biology
- Immunology
Background:
- Airborne organic dust (OD) exposure is linked to lung inflammation.
- Mitochondrial dysfunction, characterized by altered structure and bioenergetics, is a known factor in lung inflammation.
- The specific impact of OD on mitochondrial function remains unclear.
Purpose of the Study:
- To investigate if organic dust extract (ODE) induces mitochondrial stress in human cells.
- To determine if ethyl pyruvate (EP) or mitoapocynin (MA) can mitigate ODE-induced mitochondrial damage.
Main Methods:
- Utilized a human monocytic cell line (THP-1).
- Exposed cells to ODE, with or without EP or MA co-treatment.
- Analyzed cellular and organelle morphology via transmission electron microscopy.
- Assessed mitochondrial and cellular markers including mtDNA leakage, PINK1, Parkin, cytochrome c, mitochondrial mass, and cell viability.
Main Results:
- ODE exposure altered cellular and organelle morphology.
- ODE increased mitochondrial DNA (mtDNA) leakage into the cytosol.
- ODE exposure upregulated PINK1 and Parkin, reduced mitochondrial mass, and decreased cell viability, suggesting mitophagy.
- Mitoapocynin (MA) partially protected cells by reducing Parkin expression, mtDNA/cytochrome c release, and improving cell viability.
Conclusions:
- Organic dust extract (ODE) exposure induces mitochondrial stress and mitophagy in human monocytic cells.
- Ethyl pyruvate (EP) and mitoapocynin (MA) show potential in mitigating ODE-induced mitochondrial damage.
- Further research into mitochondrial pathways is warranted for understanding and treating dust-related lung inflammation.
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