Xin Sun1, Lijia Song2, Shuang Feng3, Li Li4, Hongzhi Yu4, Qiaoxing Wang3, Xing Wang4, Zhili Hou5, Xue Li1, Yu Li1, Qiuyang Zhang1, Kuan Li1, Chao Cui6, Junping Wu4, Zhonghua Qin3, Qi Wu7, Huaiyong Chen8. 1. Department of Basic Medicine, Haihe Clinical College of Tianjin Medical University, Tianjin 300070, China. 2. Department of Respiratory Medicine, Tianjin Medical University General Hospital, Tianjin 300052, China. 3. Department of Clinical Laboratory, Tianjin Haihe Hospital, Tianjin 300350, China. 4. Department of Respiratory Medicine, Tianjin Haihe Hospital, Tianjin 300350, China. 5. Department of Tuberculosis, Tianjin Haihe Hospital, Tianjin 300350, China. 6. Department of Thoracic Surgery, Tianjin Haihe Hospital, Tianjin 300350, China. 7. Department of Basic Medicine, Haihe Clinical College of Tianjin Medical University, Tianjin 300070, China; Department of Respiratory Medicine, Tianjin Medical University General Hospital, Tianjin 300052, China; Key Research Laboratory for Infectious Disease Prevention for State Administration of Traditional Chinese Medicine, Tianjin Institute of Respiratory Diseases, Tianjin 300350, China. Electronic address: wq572004@163.com. 8. Department of Basic Medicine, Haihe Clinical College of Tianjin Medical University, Tianjin 300070, China; Key Research Laboratory for Infectious Disease Prevention for State Administration of Traditional Chinese Medicine, Tianjin Institute of Respiratory Diseases, Tianjin 300350, China. Electronic address: huaiyong.chen@foxmail.com.
Abstract
BACKGROUND: Human infections with the H7N9 virus could lead to lung damage and even multiple organ failure, which is closely associated with a high mortality rate. However, the metabolic basis of such systemic alterations remains unknown. METHODS: This study included hospitalized patients (n = 4) with laboratory-confirmed H7N9 infection, healthy controls (n = 9), and two disease control groups comprising patients with pneumonia (n = 9) and patients with pneumonia who received steroid treatment (n = 10). One H7N9-infected patient underwent lung biopsy for histopathological analysis and expression analysis of genes associated with lung homeostasis. H7N9-induced systemic alterations were investigated using metabolomic analysis of sera collected from the four patients by using ultra-performance liquid chromatography-mass spectrometry. Chest digital radiography and laboratory tests were also conducted. FINDINGS: Two of the four patients did not survive the clinical treatments with antiviral medication, steroids, and oxygen therapy. Biopsy revealed disrupted expression of genes associated with lung epithelial integrity. Histopathological analysis demonstrated severe lung inflammation after H7N9 infection. Metabolomic analysis indicated that fatty acid metabolism may be inhibited during H7N9 infection. Serum levels of palmitic acid, erucic acid, and phytal may negatively correlate with the extent of lung inflammation after H7N9 infection. The changes in fatty acid levels may not be due to steroid treatment or pneumonia. INTERPRETATION: Altered structural and secretory properties of the lung epithelium may be associated with the severity of H7N9-infection-induced lung disease. Moreover, fatty acid metabolism level may predict a fatal outcome after H7N9 virus infection.
BACKGROUND:Human infections with the H7N9 virus could lead to lung damage and even multiple organ failure, which is closely associated with a high mortality rate. However, the metabolic basis of such systemic alterations remains unknown. METHODS: This study included hospitalized patients (n = 4) with laboratory-confirmed H7N9 infection, healthy controls (n = 9), and two disease control groups comprising patients with pneumonia (n = 9) and patients with pneumonia who received steroid treatment (n = 10). One H7N9-infectedpatient underwent lung biopsy for histopathological analysis and expression analysis of genes associated with lung homeostasis. H7N9-induced systemic alterations were investigated using metabolomic analysis of sera collected from the four patients by using ultra-performance liquid chromatography-mass spectrometry. Chest digital radiography and laboratory tests were also conducted. FINDINGS: Two of the four patients did not survive the clinical treatments with antiviral medication, steroids, and oxygen therapy. Biopsy revealed disrupted expression of genes associated with lung epithelial integrity. Histopathological analysis demonstrated severe lung inflammation after H7N9 infection. Metabolomic analysis indicated that fatty acid metabolism may be inhibited during H7N9 infection. Serum levels of palmitic acid, erucic acid, and phytal may negatively correlate with the extent of lung inflammation after H7N9 infection. The changes in fatty acid levels may not be due to steroid treatment or pneumonia. INTERPRETATION: Altered structural and secretory properties of the lung epithelium may be associated with the severity of H7N9-infection-induced lung disease. Moreover, fatty acid metabolism level may predict a fatal outcome after H7N9 virus infection.
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