At sites of inflammation, multiple inflammatory cells including eosinophils, neutrophils, and macrophages are capable of generating reactive oxygen species (ROS), which can contribute to development of various diseases. In case of allergic inflammation, for example, the lung cells obtained by bronchoalveolar lavage (BAL) following antigen challenge generates superoxide anion at nanomolar concentrations. Eosinophils obtained from BAL following a segmental allergen challenge generate more superoxide anion than eosinophils obtained from the peripheral circulation. Such ROS may contribute not only to tissue injury but also to inflammatory reactions. For example, hydrogen peroxide can stimulate both neutrophil and eosinophil adhesion as an autocrine or paracrine mediator via the upregulation of beta2 integrin. Furthermore, ROS may alter morphological or functional properties of endothelial cells, including permeability and adhesion molecule expression. Thus, ROS can promote adhesive interaction between inflammatory and endothelial cells, which could culminate in manifestations of inflammatory diseases such as bronchial asthma.