This supports a potentiating effect of LTD4 on the expression of eotaxin-3 induced by IL-13 in human primary bronchial epithelial cells and suggests that both IL-13 and LTD4 participate in the accumulation of eotaxin-3 in the lungs, which might be relevant in the physiopathology of asthma. Here, IL13 is linked to asthma.