Hyperoxia accelerates Fas-mediated signaling and apoptosis in the lungs of Legionella pneumophila pneumonia

Hyperoxia accelerates Fas-mediated signaling and apoptosis in the lungs of Legionella pneumophila pneumonia

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Abstract Background Oxygen supplementation is commonly given to the patients with severe pneumonia including Legionella thy art is murder oslo disease.Recent data suggested that apoptosis may play an important role, not only in the pathogenesis of Legionella pneumonia, but also in oxygen-induced tissue damage.In the present study, the lethal sensitivity to Legionella pneumonia were compared in the setting of hyperoxia between wild-type and Fas-deficient mice.

Findings C57BL/6 mice and B6.MRL-Faslpr mice characterized with Fas-deficiency were used in this study.After intratracheal administration of L.

pneumophila, mice were kept in hyperoxic conditions (85-90% O2 conc.) in an airtight chamber for 3 days.Bone-marrow derived macrophages infected with L.

pneumophila were also kept in hyperoxic conditions.Caspase activity and cytokine production were determined by using commercially available kits.Smaller increases of several apoptosis markers, such as caspase-3 and -8, were demonstrated in Fas-deficient mice, even though the bacterial burdens in Fas-deficient and wild type mice were similar.

Bone-marrow china glaze beaches and toes derived macrophages from Fas-deficient mice were shown to be more resistant to Legionella-induced cytotoxicity than those from wild-type mice under hyperoxia.Conclusions These results demonstrated that Fas-mediated signaling and apoptosis may be a crucial factor in the pathogenesis of Legionella pneumonia in the setting of hyperoxia.