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01.12.2017 | Research | Ausgabe 1/2017 Open Access

Journal of Occupational Medicine and Toxicology 1/2017

Effect of low-level CO2 on innate inflammatory protein response to organic dust from swine confinement barns

Zeitschrift:
Journal of Occupational Medicine and Toxicology > Ausgabe 1/2017
Autoren:
David Schneberger, Jane M. DeVasure, Kristina L. Bailey, Debra J. Romberger, Todd A. Wyatt

Abstract

Background

Organic hog barn dust (HDE) exposure induces lung inflammation and long-term decreases in lung function in agricultural workers. While concentrations of common gasses in confined animal facilities are well characterized, few studies have been done addressing if exposure to elevated barn gasses impacts the lung immune response to organic dusts. Given the well documented effects of hypercapnia at much higher levels we hypothesized that CO2 at 8 h exposure limit levels (5000 ppm) could alter innate immune responses to HDE.

Methods

Using a mouse model, C57BL/6 mice were nasally instilled with defined barn dust extracts and then housed in an exposure box maintained at one of several CO2 levels for six hours. Bronchiolar lavage (BAL) was tested for several cytokines while lung tissue was saved for mRNA purification and immunohistochemistry.

Results

Exposure to elevated CO2 significantly increased the expression of pro-inflammatory markers, IL-6 and KC, in BAL fluid as compared to dust exposure alone. Expression of other pro-inflammatory markers, such as ICAM-1 and matrix metalloproteinase-9 (MMP-9), were also tested and showed similar increased expression upon HDE + CO2 exposure. A chemokine array analysis of BAL fluid revealed that MIP-1γ (CCL9) shows a similar increased response to HDE + CO2. Further testing showed CCL9 was significantly elevated by barn dust and further enhanced by CO2 co-exposure in a dose-dependent manner that was noticeable at the protein and mRNA levels. In all cases, except for ICAM-1, increases in tested markers in the presence of elevated CO2 were only significant in the presence of HDE as well.

Conclusions

We show that even at mandated safe exposure limits, CO2 is capable of enhancing multiple markers of inflammation in response to HDE.
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