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J Infect Dis. Cytokine and Chemokine Levels in Patients Infected with the Novel Avian Influenza A (H7N9) Virus in China
[Source: Journal of Infectious Diseases, full page: (LINK). Abstract, edited.]
Cytokine and Chemokine Levels in Patients Infected with the Novel Avian Influenza A (H7N9) Virus in China
Ying Chi 1,a, Yefei Zhu 2,a, Tian Wen 1,a, Lunbiao Cui 1, Yiyue Ge 1, Yongjun Jiao 1, Tao Wu 1, Aihua Ge 2, Hong Ji 2, Ke Xu 2, Changjun Bao 2, Zheng Zhu 1, Xian Qi 2, Bin Wu 2, Zhiyang Shi 1, Fenyang Tang 2, Zheng Xing 3 and Minghao Zhou 2
Author Affiliations: <SUP>1</SUP>Key Laboratory of Enteric Pathogenic Microbiology, Ministry of Health, Institute of Pathogenic Microbiology, Jiangsu Provincial Center for Disease Control and Prevention , Nanjing, China <SUP>2</SUP>Department of Acute Infectious Disease Prevention and Control, Jiangsu Provincial Center for Disease Control and Prevention , Nanjing, China <SUP>3</SUP>Nanjing University Medical School, Nanjing, China
Correspondence: Minghao Zhou, Department of Acute Infectious Disease Control and Prevention, Jiangsu Provincial Center for Disease Control and Prevention, Nanjing, 210009, China (zmh@jscdc.cn).
a Y. C., Y. Z., T. W. contributed equally to the study.
Abstract
H7N9 avian influenza is an emerging viral disease in China caused by avian influenza A H7N9 virus. We investigated host cytokine and chemokine profiles in serum samples of H7N9 patients by multiplex-microbead immunoassays. Statistical analysis showed that IP-10, IL-6, IL-17 and IL-2 were increased in H7N9 infected patients. Furthermore, IL-6 and the chemokine IP-10 were significantly higher in severe H7N9 patients compared to non-severe H7N9 cases. We suggest that proinflammatory cytokine responses, characterized by a combined Th1/Th17 cytokine induction, are partially responsible for the disease progression of patients with H7N9 infection.
Received May 3, 2013. Revision received July 12, 2013. Accepted July 25, 2013.
? The Author 2013. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved.
For Permissions, please e-mail: journals.permissions@oup.com.
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Cytokine and Chemokine Levels in Patients Infected with the Novel Avian Influenza A (H7N9) Virus in China
Ying Chi 1,a, Yefei Zhu 2,a, Tian Wen 1,a, Lunbiao Cui 1, Yiyue Ge 1, Yongjun Jiao 1, Tao Wu 1, Aihua Ge 2, Hong Ji 2, Ke Xu 2, Changjun Bao 2, Zheng Zhu 1, Xian Qi 2, Bin Wu 2, Zhiyang Shi 1, Fenyang Tang 2, Zheng Xing 3 and Minghao Zhou 2
Author Affiliations: <SUP>1</SUP>Key Laboratory of Enteric Pathogenic Microbiology, Ministry of Health, Institute of Pathogenic Microbiology, Jiangsu Provincial Center for Disease Control and Prevention , Nanjing, China <SUP>2</SUP>Department of Acute Infectious Disease Prevention and Control, Jiangsu Provincial Center for Disease Control and Prevention , Nanjing, China <SUP>3</SUP>Nanjing University Medical School, Nanjing, China
Correspondence: Minghao Zhou, Department of Acute Infectious Disease Control and Prevention, Jiangsu Provincial Center for Disease Control and Prevention, Nanjing, 210009, China (zmh@jscdc.cn).
a Y. C., Y. Z., T. W. contributed equally to the study.
Abstract
H7N9 avian influenza is an emerging viral disease in China caused by avian influenza A H7N9 virus. We investigated host cytokine and chemokine profiles in serum samples of H7N9 patients by multiplex-microbead immunoassays. Statistical analysis showed that IP-10, IL-6, IL-17 and IL-2 were increased in H7N9 infected patients. Furthermore, IL-6 and the chemokine IP-10 were significantly higher in severe H7N9 patients compared to non-severe H7N9 cases. We suggest that proinflammatory cytokine responses, characterized by a combined Th1/Th17 cytokine induction, are partially responsible for the disease progression of patients with H7N9 infection.
Received May 3, 2013. Revision received July 12, 2013. Accepted July 25, 2013.
? The Author 2013. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved.
For Permissions, please e-mail: journals.permissions@oup.com.
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