Nonhuman primate models to study chemokine mechanisms for eosinophil trafficking

Exposure to air pollutants during early life may contribute to the pathogenesis of allergic airways disease. Using an infant rhesus monkey model, we have reported that chronic inhalation of house dust mite (HDM) can result in airway eosinophilia in association with increased eotaxin‐3 expression. In this study, we have determined the effects of episodic ozone exposure on HDM‐induced airway eosinophilia and esoinophilic chemokine expression in 3 month old infant monkeys. In response to HDM and/or ozone, airway eosinophils were significantly increased in lavage samples. In contrast, the volume of airway tissue eosinophils increased only in animals treated with house dust mite alone. Eotaxin‐3 expression correlated with eosinophil volume in airway tissue, but not lavage. A significant increase in eotaxin‐2 protein and gene expression was observed with combined HDM+ozone exposure that did not correlate with the presence of eosinophils. These findings provide further support for the role of eotaxin‐3 as a prevalent chemokine mediator of eosinophil trafficking in the lung, and suggest that oxidative stress alters the eosinophilic chemokine profile of airways during postnatal development.