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 . 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 . 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 . 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 .
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The term vaginitis is one that is applied to any inflammation or infection of the vagina, and there are many different conditions that are categorized together under this ‘broad’ heading, including bacterial vaginosis, trichomoniasis and non-infectious vaginitis.