感染期間可能會發生肋膜積液, 但肋膜積液能否用於區別敗血症與其他病因仍然不確 定。一些研究中發現小囊泡體在敗血症的發展中扮演一定的角色。由於小囊泡體相關的蛋 白質不會被分泌, 這些蛋白質理論上只能在體液的囊泡中被偵測到。在本研究中, 我們的目 的是研究小囊泡體在肋膜積液的狀態, 這是一種由細胞釋放的納米粒子並可攜帶各種胞內蛋 白, 同時也能攜帶訊息傳遞相關蛋白質。我們收集2016年1月1日至2016年12月31日在台北慈 濟醫院治療的疑似感染患者的肋膜積液樣本。患者分為感染併發敗血症、感染、沒有感染 三組，並依1：2：2比例的病例對照觀察研究，性別和年齡相匹配，共納入65例肋膜積液患 者。同時也依照疾病成因分為不同次群組。ExoQuick 試劑套組用以沉澱純化肋膜積液之外 泌體，包括括65例胸腔積液病人, 其中13人敗血症, 26 人感染, 26 無感染。我們的研究結果 顯示，非感染、感染和敗血症患者小囊泡體蛋白量沒有差異（p> 0.05），顯示蛋白載入小囊 泡體不受敗血症的影響。然而，惡性腫瘤和肺炎組肋膜積液中小囊泡體的蛋白量顯著高於 心臟衰竭組，這表明在兩種狀態下蛋白質加載到小囊泡體中都是增加的。我們的研究結果 表明惡性腫瘤和肺臟發炎可能會增加胸腔積液中的小囊泡體蛋白量，但感染和敗血症不能 增加小囊泡體蛋白量。 檢測外泌體蛋白可能有助於區分肋膜積液的病因以進行區別診斷。

Pleural effusion can occur during infection, but whether pleural effusion can be used to differentiate sepsis from other diseases is still uncertain. Exosome has potential to play roles in development of sepsis. Since exosome-carried proteins are not secretory, theoretically, these proteins can only be found in vesicles of body fluids. In this study, we aimed to investigate the states of exosome in pleural effusion samples. Exosome are cell-released nanoparticles which carry various intracellular proteins, and also carry signaling proteins. We collected pleural effusion samples from patients with or without sepsis at Taipei Tzu Chi Hospital from January 1, 2016 to December 31, 2016. Patients were case-controlled, and divided into three groups, including sepsis, infection, and non-infection groups at a ratio of 1:2:2, matched for sex and age, and also divided into subgroups with different etiologies. Exosomes from exudates were obtained by precipitation using an ExoQuick kit, and Bradford assay was used to quantify exosome proteins. A total of 65 patients with pleural effusion were included, of whom 13 had infection with sepsis, 26 had infection without sepsis, and 26 had no infection. Our results showed that there is no difference of exosome protein level between non-infection, infection and sepsis patients (p > 0.05), indicating that loading of protein into exosome is not affected by sepsis. However, protein levels of exosome in pleural effusion in the malignancy and pneumonia groups were significantly higher than those in heart-failure group, suggesting that loading of proteins into exosomes were increased in both states. Our findings suggest that malignancy and inflammation may increase exosome protein levels in pleural effusion, but infection and sepsis cannot increase the levels. Testing exosome proteins might be useful and helpful for making differential diagnosis of pleural effusion.