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Supplemental oxygen is widely used for dyspnea relief; however, its efficacy is yet to be verified. This study aimed to determine the efficacy of supplemental oxygen for dyspnea relief in patients with advanced progressive illness.

To elucidate the biological significance of selectin for idiopathic pulmonary fibrosis, we titrated the serum soluble E-selectin. From 31 cases of idiopathic pulmonary fibrosis patients without signs or symptoms of infection, the serum was obtained and the concentration was titrated by enzyme-linked immunosorbent assay. The serum soluble E-selectin titer was significantly higher than that of healthy controls. However, significant elevation was not observed in the sera from the patients with other pulmonary diseases, such as pulmonary emphysema, sarcoidosis, or bronchiectasis. In the patients with idiopathic pulmonary fibrosis, the number of white blood cells, C-reactive protein or lactate dehydrogenase activity did not show a significant relationship with the soluble E-selectin titer. About 16 out of the 31 idiopathic fibrosis patients, the serum surfactant apoprotein-A titer, which is a parameter of the disease activity of idiopathic pulmonary fibrosis, was also tested. The surfactant apoprotein-A titer was loosely correlated with the soluble E-selectin titer. These observations suggest that E-selectin may be relevant to the pathogenesis of idiopathic pulmonary fibrosis, and it may be a novel clinical parameter for idiopathic pulmonary fibrosis.

The selectin family adhesion molecules exert a crucial role in accumulation of leukocytes at the site of inflammation. To test the biological effects of soluble selectin on lung inflammation, we introduced an expression plasmid vector of soluble selectin gene via HVJ-liposome into a murine model of LPS-induced lung injury. The myeloperoxidase activity in LPS-injected mice was suppressed by the in vivo injection of soluble P-selectin gene relative to control mice. On the contrary, soluble E- or L-selectin genes did not exert suppressive effects. Our observations suggest that P-selectin plays a crucial role in the initial steps of lung inflammation, and exogenous introduction of soluble P-selectin by in vivo gene transfer method may be a useful strategy for regulating inflammation of the lung.

A number of investigators have reported augmented expression of PDGF in lungs with idiopathic pulmonary fibrosis (IPF) or with other types of pulmonary fibrosis. To accomplish such a regulation of PDGF activity, we constructed an expression plasmid of the extracellular domain of PDGF receptor β chain (XR), which lacks intracellular tyrosine kinase domain and transmembrane portions, and estimated the therapeutic effects of XR gene transfer through the trachea on bleomycin-induced lung fibrosis of C57BL/6 mice using the hemagglutinating virus of Japan(HVJ)-liposome method. The XR gene transfer ameliorated the increases in the wet weight and hydroxyproline content and the histopathologic changes of the lung induced by bleomycin. These findings suggest that PDGF plays a crucial role in the pathogenesis of pulmonary fibrosis, and that XR gene transfer using the HVJ-liposome method may limit the progression of pulmonary fibrosis.

Asthma is a complex phenotype that involves multiple mechanisms, including adaptive and innate immunity as well as physiological and mechanical changes in the airways. A cardinal feature of asthma is airway hyperreactivity (AHR), a multifaceted reaction that can only be assessed in vivo. Mouse models of asthma replicate many of the features of human asthma, including AHR, which can be assessed using standard protocols. Examination of AHR in mice has provided important information about human asthma, primarily because the immunology of allergy is easily studied in mice, especially with the availability of reagents including genetically modified mice. In this unit we discuss the induction and measurement of AHR and the two most common methodologies: noninvasive measurement using a whole‐body plethysmograph (WBP) and invasive measurement of lung resistance and dynamic compliance. Curr. Protoc. Immunol. 79:15.18.1‐15.18.19. © 2007 by John Wiley & Sons, Inc.