Effects of inhaled eotaxin on airway function and inflammatory cell influx in sensitised and non-sensitised guinea pigs.

Eotaxin is a chemokine that has high potency and selectivity as a chemoattractant agent for eosinophils, signalling exclusively through the CCR3 receptor. Eotaxin is upregulated in the lungs within 3 h of antigen challenge, levels peak at 6 h in lung tissue and bronchoalveolar (BAL) fluid, and fall within 12 h of exposure. This study aimed to look at the effect(s) of eotaxin inhalation on airway function in guinea pigs, to determine if the expected inflammatory cell (eosinophil) infiltration could induce airway hyperreactivity (AHR) and a bronchoconstrictor response equivalent to the late asthmatic response (LAR) seen after antigen challenge.

Elastolytic activity and alveolar epithelial type-1 cell damage after chronic LPS inhalation: effects of dexamethasone and rolipram.

This study investigated whether a correlation between leukocyte-derived elastolytic activity, alveolar epithelial type-1 cell damage, and leukocyte infiltration of the airways existed in guinea-pigs chronically exposed to inhaled lipopolysaccharide (LPS). The airway pathology of this model, notably the neutrophilia, resembles chronic obstructive pulmonary disease (COPD). The effect of the corticosteroid, dexamethasone, or the phosphodiesterase-4 (PDE4)-inhibitor, rolipram, on these features was studied.