Diesel exhaust particles modify natural killer cell function and cytokine release
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Müller, Loretta, et al. Diesel Exhaust Particles Modify Natural Killer Cell Function and Cytokine Release. BioMed Central Ltd, 2013. https://doi.org/10.17615/ys37-tj89APA
Müller, L., Chehrazi, C., Henderson, M., Noah, T., & Jaspers, I. (2013). Diesel exhaust particles modify natural killer cell function and cytokine release. BioMed Central Ltd. https://doi.org/10.17615/ys37-tj89Chicago
Müller, Loretta, Claire Chehrazi, Michael W Henderson, Terry Noah, and Ilona Jaspers. 2013. Diesel Exhaust Particles Modify Natural Killer Cell Function and Cytokine Release. BioMed Central Ltd. https://doi.org/10.17615/ys37-tj89- Creator
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Müller, Loretta
- Affiliation: School of Medicine, Department of Medicine
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Chehrazi, Claire
- Affiliation: School of Medicine, Department of Medicine
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Henderson, Michael W.
- Affiliation: Biological and Biomedical Sciences Program
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Noah, Terry
- Affiliation: School of Medicine, Department of Medicine
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Jaspers, Ilona
- Affiliation: School of Medicine, Department of Medicine
- Abstract
- Abstract Background Natural killer (NK) cells are an important lymphocyte population in the nasal mucosa and play important roles in linking the innate and the adaptive immune response. Their two main functions are direct cell-mediated cytotoxicity and the release of cytokines. They are important during viral infections and cancer. Due to their location in the nasal mucosa, NK cells are likely exposed to inhaled pollutants, such as diesel exhaust. Whether and how exposure to diesel exhaust particles (DEP) affects NK cell function in the context of viral infections has not been investigated. Methods NK cells were isolated from peripheral blood obtained from normal healthy volunteers and subsequently stimulated with the viral mimetic polyinosinic:polycytidylic acid (pI:C), DEP, or pI:C+DEP for 18 hours. NK cells were subsequently analyzed for changes in surface marker expression, cytokine production, gene expression changes, and cytotoxic function using flow cytometry, ELISA, qRT-PCR, and cell-mediated cytotoxicity assay, respectively. Results Stimulation of NK cells with pI:C and pI:C+DEP, but not DEP alone, increased the release of IL-1β, IL-2, IL-4, IL-8, IL-10, IL-12p70, IFN-γ and TNF-α. As compared to pI:C alone or pI:C+DEP, the release of IL-1β, IL-8 and TNF-α was significantly lower after DEP stimulation alone. Stimulation with pI:C alone increased the gene and protein expression of granzyme B and perforin, which was completely blunted by adding DEP. Addition of DEP further reduced CD16 expression in pI:C stimulated cells. Similarly, cell-mediated cytotoxicity was significantly reduced by the addition of DEP. Conclusions In the context of viral infection, DEP potentially reduces NK cells' ability to kill virus-infected host cells, in spite of normal cytokine levels, and this may increase susceptibility to viral infections . This reduction in the potential ability of NK cells to kill virus-infected host cells may increase the susceptibility to viral infections after DEP exposure.
- Date of publication
- April 24, 2013
- DOI
- Identifier
- Resource type
- Article
- Rights statement
- In Copyright
- Rights holder
- Loretta Müller et al.; licensee BioMed Central Ltd.
- License
- Journal title
- Particle and Fibre Toxicology
- Journal volume
- 10
- Journal issue
- 1
- Page start
- 16
- Language
- English
- Is the article or chapter peer-reviewed?
- Yes
- ISSN
- 1743-8977
- Bibliographic citation
- Particle and Fibre Toxicology. 2013 Apr 24;10(1):16
- Publisher
- BioMed Central Ltd
- Access right
- Open Access
- Date uploaded
- November 6, 2015
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