Swine barn dust stimulates CCL9 expression in mouse monocytes through PKC-delta activation.

Exposure to organic barn dusts has been shown to cause numerous lung problems to chronically exposed animal barn workers. Bacterial components in these dusts trigger innate immunity in the lungs that we are still trying to fully characterize. CCL9/MIP-1γ is constitutively expressed in high quantities in the mouse circulation, but at much lower levels in the lungs where it is inducible under certain circumstances.

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

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 CO at 8 h exposure limit levels (5000 ppm) could alter innate immune responses to HDE.

Effect of elevated carbon dioxide on bronchial epithelial innate immune receptor response to organic dust from swine confinement barns.

Hypercapnia is known to have immunoregulatory effects within the lung. Cell culture systems demonstrate this in both macrophages and alveolar cell lines, suggesting that the alveoli are affected by changes in CO2 levels. We hypothesized that hypercapnia would also modulate human bronchial epithelial cell immune responses.