Alveolar Macrophages

Gene therapy targeted to the alveolar regions of the lung or to the systemic circulation via the alveoli may be limited by the actions of alveolar macrophages (AM^). AM^ phagocytose and digest bacteria and other invaders, leading to cytokine secretion and inflammation [165,166]. The inhibitory effects of AM^ on transfection efficiencies with viral and liposomal gene vectors have been demonstrated [167,168]. Transfection efficiencies in gene therapy trials for cystic fibrosis have been dramatically reduced in comparison to in vitro studies [167]. The inflammatory response has been implicated as a potential reason for the reduced expression levels, with a 10-fold increase in the AM^ population and a 1000-fold increase in the polymorphonuclear neutrophil population [167]. However, macrophages may also serve as potential targets of gene therapy. Cytokine gene therapy in the lung with interferon-g (IFN-g) increased AM^ phagocytic and destructive capacity against bacteria, parasites, and fungi [166]. Murine studies have demonstrated that IFN-g plays a key role in normal host defense from a number of pulmonary pathogens, including Pseudomonas, Histoplasma, Candida, Mycoplasma, Hemophilus, Legionella, Chlamydia, and Pneumocytis [166].

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