Expression of IL-10 and GM-CSF in Blood Monocytes and Alveolar Macrophages

Abstract

Peripheral blood monocytes (PBMs) and alveolar macrophages (AMs) are widely recognized as cells that play a central role in the regulation of immune and inflammatory activities, as well as in tissue remodeling. The fulfillment of these activities is mediated by complex and multifactorial processes involving products derived from macrophages and monocytes (1). Monocytes are an important source of cytokines that are released in asthma and are likely precursor cells to AMs. Macrophages usually elaborate powerful suppressive signals to limit the proliferative potential of T-cells, thus maintaining local immunologic homeostasis (2). In asthma, macrophages and monocytes may be stimulated by specific allergens to augment T-cell proliferation (3), which may result from a different profile of cytokines released from these cells. For example, increased release of granulocyte-macrophage colony-stimulating factor (GM-CSF) may inhibit the immunosuppressive effect of macrophages (4). Indeed, macrophages and monocytes from asthmatic subjects release increased amounts of proinflammatory cytokines, such as interleukin-1β (IL-1), tumor necrosis factor-α, Interferon-γ (IFN-γ), IL-6, and GM-CSF (5–8). Inhaled steroids used for the treatment of asthma reduce the number of infiltrating eosinophils, T-cells, macrophages, and mast cells in the airway submucosa (9). Suppression of proinflammatory cytokine release, such as GM-CSF, IL-4, IL-5, and regulated upon activation, normal T-cell expressed and secreted (RANTES), from many inflammatory and resident airway cells, is a likely mechanism of steroid action (10–12). Proinflammatory cytokine expression