Environmental Contaminants and Respiratory Innate Immunity: In Vitro Effects of Polycyclic Aromatic Hydrocarbons and Crude Oil on Tracheal Antimicrobial Peptide Gene Expression.
Respiratory disease is an important cause of morbidity and mortality in cetaceans, which are also threatened by environmental pollutants such as polycyclic aromatic hydrocarbons (PAHs; immunotoxic constituents of crude oil). Cetaceans exposed to oil spills may inhale volatile PAHs which could potentially affect respiratory immunity. PAHs activate the aryl hydrocarbon receptor which can affect immunity through interaction with NF-κB. β-defensins are potent antimicrobial peptides that play an important role in defending the lower airway from pathogens. β-defensin expression is known to be dependent on NF-κB, and so we hypothesized that PAHs may suppress pulmonary β-defensins and to pneumonia pathogenesis. This hypothesis was modeled by measuring the effects of benzo(a)pyrene (BAP), phenanthrene, naphthalene, and crude oil on tracheal antimicrobial peptide (TAP) gene expression in primary cell cultures of bovine tracheal epithelial cells. It was found that exposure to either crude oil or PAHs was associated with suppression of TAP gene expression in cultures. However, the consistency of this result varied in significance between both PAHs and calves. BAP consistently caused a statistically significant (P = 0.002) suppression of TAP gene expression in a dose dependent manner in the majority of calves. These are the first data to show that exposure to PAHs suppresses β-defensin gene expression.