A systematic analysis of the effect of corn, wheat, and poultry dusts on interleukin-8 production by human respiratory epithelial cells

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Abstract

The objective of this study was to determine the inflammatory response initiated by various organic dusts by measuring in vitro interleukin-8 (I-8) production from transformed respiratory epithelial cells after dust exposure. To accomplish this objective, the following specific tasks were performed: 1) dust samples were collected from grain farms, grain storage facilities, and poultry houses and their endotoxin levels were determined; 2) A549 transformed respiratory epithelial cells were exposed to 0, 10, 100, or 1,000 μg/ml of organic dust or lipopolysaccharide (LPS); and, 3) production was measured using enzyme-linked immunosorbant assays (ELISAs). The results indicate that LPS induced at all concentrations. All dust types (corn, wheat, and poultry) induced at significantly higher levels than control and at significantly different levels between dust types. Overall there was an increasing trend of elevated production as the concentration of dust exposure was increased except at the highest concentration where IL-8 levels decreased and more cell death was observed. Corn dust exposure induced IL-8 that increased with increasing dust concentration and correlated with increasing amounts of LPS in the corn dust samples. However, IL-8 production in response to wheat dust was inversely related to LPS concentration suggesting that other factors besides LPS are present in the dust that are responsible for induction of IL-8 production. This study indicates that IL-8 induction varies between agricultural dust types and does not always correlate with endotoxin levels present in the dust. Therefore, other factors may be present in the dust that also elicit the immune response after exposure. Copyright © Taylor & Francis Group, LLC.

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Redente, E. F., & Massengale, R. D. (2006). A systematic analysis of the effect of corn, wheat, and poultry dusts on interleukin-8 production by human respiratory epithelial cells. Journal of Immunotoxicology, 3(1), 31–37. https://doi.org/10.1080/15476910500496529

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