Pin-Yu Chang1, Shih-Ming Tsao2, Jer-Hwa Chang3, Ming-Hsien Chien4, Wen-Yueh Hung5, Yi-Wen Huang6, Shun-Fa Yang7. 1. Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Senior Citizen Services, National Tainan Junior College of Nursing, Tainan, Taiwan. 2. School of Medicine, Chung Shan Medical University, Taichung, Taiwan; Division of Chest, Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung, Taiwan. 3. Division of Pulmonary Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan; School of Respiratory Therapy, College of Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan. 4. Graduate Institute of Clinical Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan; Department of Medical Education and Research, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan. 5. Division of Pulmonary Medicine, Department of Internal Medicine, Taipei Medical University Hospital, Taipei, Taiwan. 6. Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan; Pulmonary and Critical Care Unit, Changhua Hospital, Department of Health, Changhua, Taiwan. Electronic address: hiwen@chhw.mohw.gov.tw. 7. Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan; Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan. Electronic address: ysf@csmu.edu.tw.
Abstract
BACKGROUND: Community-acquired pneumonia (CAP) is characterized as an acute inflammation of the lung associated with the activation of macrophages and neutrophils. Intercellular adhesion molecule-1 (ICAM-1) is an essential adhesion molecule involved in immune cell recruitment in lung inflammation. We investigated whether ICAM-1 is a useful biomarker for assessing the disease severity of hospitalized adult patients with CAP. METHODS: Plasma soluble ICAM-1 (sICAM-1) levels were measured in 78 patients with CAP and 69 healthy controls by using a commercial enzyme-linked immunosorbent assay. The pneumonia severity index scores were used to determine CAP severity in patients upon initial hospitalization. RESULTS: The sICAM-1 and C-reactive protein (CRP) levels decreased significantly in patients with CAP after antibiotic treatment. The plasma concentration of sICAM-1 alone, but not CRP, was correlated with CAP severity according to the pneumonia severity index scores (r=0.431, p<0.001). The sICAM-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 sICAM-1 level showed a significant correlation with the length of hospital stay (r=0.488, p<0.001). Mechanistic investigations found that bacterial lipopolysaccharide induced upregulation of ICAM-1 expression through the c-Jun N-terminal kinase pathway in RAW264.7 macrophages. CONCLUSIONS: Plasma sICAM-1 levels may play a role in the diagnosis and clinical assessment of CAP severity. Copyright Â
BACKGROUND: Community-acquired pneumonia (CAP) is characterized as an acute inflammation of the lung associated with the activation of macrophages and neutrophils. Intercellular adhesion molecule-1 (ICAM-1) is an essential adhesion molecule involved in immune cell recruitment in lung inflammation. We investigated whether ICAM-1 is a useful biomarker for assessing the disease severity of hospitalized adult patients with CAP. METHODS: Plasma soluble ICAM-1 (sICAM-1) levels were measured in 78 patients with CAP and 69 healthy controls by using a commercial enzyme-linked immunosorbent assay. The pneumonia severity index scores were used to determine CAP severity in patients upon initial hospitalization. RESULTS: The sICAM-1 and C-reactive protein (CRP) levels decreased significantly in patients with CAP after antibiotic treatment. The plasma concentration of sICAM-1 alone, but not CRP, was correlated with CAP severity according to the pneumonia severity index scores (r=0.431, p<0.001). The sICAM-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 sICAM-1 level showed a significant correlation with the length of hospital stay (r=0.488, p<0.001). Mechanistic investigations found that bacterial lipopolysaccharide induced upregulation of ICAM-1 expression through the c-Jun N-terminal kinase pathway in RAW264.7 macrophages. CONCLUSIONS: Plasma sICAM-1 levels may play a role in the diagnosis and clinical assessment of CAP severity. Copyright Â