GM‐CSF Expression in the Lung During Pneumocystis Pneumonia

Abstract

GRANULOCYTE macrophage-colony stimulating factor (GM-CSF) is an important growth factor that promotes proliferation and maturation of macrophages and monocytes (Shibata et al. 2001). Granulocyte macrophage-colony stimulating factor also mediates cytokine production (Kremlev et al. 1998), stimulates expression of FcgR1 receptors and actin polymerization to increase phagocyte function (Berclaz et al. 2002), inhibits neutrophil apoptosis (Kobayashi et al. 2005), and enhances clearance of surfactant protein by alveolar macrophages in the lung (Ikegami et al. 1996). Granulocyte macrophage-colony stimulating factor present in the alveolar spaces of the lung is produced by alveolar macrophages, T lymphocytes, fibroblasts, and endothelial cells. The expression level of GM-CSF in some cell types is controlled by the ubiquitous calcium binding protein calmodulin through calmodulin-dependent protein kinase II (Liu and Grundstrom 2002). In Pneumocystis pneumonia (PcP), there is a reduction in alveolar macrophage-mediated phagocytosis (Lasbury et al. 2003), a build-up of surfactant protein A (Atochina et al. 2001; Phelps and Rose 1991), and a loss of alveolar macrophages by increased apoptosis (Lasbury et al. 2006). The present study sought to measure the levels of GM-CSF in alveolar macrophages and bronchoalveolar lavage (BAL) fluids from rats with PcP. We also examined the role of calmodulin in controlling GM-CSF expression in alveolar macrophages.