本研究為研究社區型肺炎(community-acquired pneumonia ; CAP)患者在經抗生素治療前與治療後,血漿中ICAM-1 (Intercellular adhesion molecule-1)濃度的變化,以及其與其他肺炎指標的相關性。本實驗利用酵素連結免疫吸附法(enzyme-linked immunosorbent assay ; ELISA)觀察來偵測78個CAP患者與69個健康對照組,共147組血漿中ICAM-1的濃度。結果發現C-reactive protein (CRP)、白血球、嗜中性白血球、ICAM-1的濃度在經過抗生素治療後均較治療前為下降;而經統計發現CAP患者血漿中ICAM-1濃度與肺炎嚴重指數具有相關性(r = 0.431, p < 0.001)。而ICAM-1的濃度在死亡風險高的CAP患者明顯高於死亡風險中低的患者;研究也發現ICAM-1的濃度與CAP患者住院天數有正相關。機制探討部份我們使用小鼠巨噬細胞RAW264.7,經由西方點墨法與即時定量聚合酶連鎖反應證明,LPS (Lipopolysaccharide)誘發之ICAM-1表現,是經由JNK (c-Jun N-terminal kinase)訊息傳遞路徑。因此,本實驗結果證明CAP患者血漿中ICAM-1的濃度可當作生物指標用來評估CAP患者嚴重程度,並且希望未來可以應用於臨床治療上的依據。
The aim of this study was to investigate the differential plasma levels of ICAM-1 before and after antibiotic treatment in hospitalized patients with community-acquired pneumonia (CAP). Plasma ICAM-1 levels were measured in 78 adult patients with CAP and 69 healthy controls using commercial enzyme-linked immunosorbent assay (ELISA). A decrease in the levels of C-reactive protein (CRP) and neutrophils and decreases in the number of white blood cells (WBCs), and ICAM-1 were observed after antibiotic treatment. The plasma level of ICAM-1 was correlated with the severity of CAP based on the Pneumonia Severity Index score (PSI) (r = 0.431, p < 0.001). However, there was no significant correlation between ICAM-1 and CRP levels in patients with CAP. The ICAM-1 levels in patients with CAP with high mortality risk were significantly higher than those in patients with CAP with medium or low mortality risk. Moreover, the ICAM-1 level showed a significant correlation with the length of hospital stay (r = 0.488, p < 0.001). Mechanistic investigations found that bacterial LPS induced upregulation of ICAM-1 expression through the c-Jun N-terminal kinase pathway in RAW264.7 macrophages. In conclusion, plasma ICAM-1 might play a further role in the clinical assessment of the severity of CAP, which could potentially guide the development of future treatment strategies.