| Summary: | 碩士 === 國防醫學院 === 微生物及免疫學研究所 === 105 === Staphylococcus aureus is the commensal bacterium residing in human upper respiratory tract. However, S. aureus is also frequently isolated from community acquired pneumonia or induces secondary bacterial pneumonia after influenza virus infection. Severe pneumonia leading to lung injury could progressive into acute respiratory distress syndrome (ARDS), representing as edema, wide spread damage of the alveolar capillary, and uncontrolled neutrophils infiltration. It was reported that patients developing ARDS and/or disseminated intravascular coagulation was associated with staphylococcal phosphoinositide phospholipase C (PI-PLC), suggesting PI-PLC is a possible virulence factor contributing to ARDS. In this study, the role of PI-PLC in S. aureus induced ARDS was further addressed using primary and secondary bacterial infection murine model. The histopathological examination revealed that wild type S. aureus caused more severe cell influx and protein edema in airspace than plc- mutant in both primary and secondary staphylococcal pneumonia model after 6 hr of infection. PI-PLC-expressing S. aureus induced lung edema revealed by elevated wet/dry ratio and albumin level in BALF in primary pneumonia model; moreover, the presence of plc gene activated upregulated IL-1β production in BALF. Furthermore, staphylococcal PI-PLC could enhance adherence and invasion of S. aureus to human alveolar epithelial cells, A549, suggesting the role of PI-PLC in the colonization during infection. In conclusion, the data showed that the presence of plc gene in S. aureus accelerated the progression of severe pneumonia to ARDS, possibly through rapidly adherence and invasion into lung epithelial cells.
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