The Expression of IL-6, TNF-α, and MCP-1 in Respiratory Viral Infection in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Author:

Zheng Jingtong1,Shi Yue1,Xiong Lingxin12ORCID,Zhang Weijie3,Li Ying4,Gibson Peter G.5,Simpson Jodie L.6ORCID,Zhang Chao1,Lu Junying17,Sai Jingying18,Wang Guoqiang1,Wang Fang1ORCID

Affiliation:

1. Departments of Pathogenic Biology, College of Basic Medical Sciences, Jilin university, Changchun, China

2. School of Pharmaceutical Sciences, Jilin University, Jilin, China

3. Department of Respiratory Disease, Jilin Provincial People’s Hospital, Changchun, China

4. Department of Disease Control and Prevention, Beijing Shunyi District Center, Beijing, China

5. Department of Respiratory and Sleep Medicine, John Hunter Hospital, Newcastle, NSW, Australia

6. Department of Respiratory and Sleep Medicine, University of Newcastle, New Lambton, NSW, Australia

7. Department of Intensive Care Unit, First Hospital of Jilin University, Changchun 130021, China

8. Department of Clinical Laboratory, The Second Hospital of Jilin University, Changchun 130021, China

Abstract

Viral infection is a common trigger for acute exacerbations of chronic obstructive pulmonary disease (AECOPD). The aim of this study is to investigate the expression of cytokines in AECOPD. Patients with AECOPD requiring hospitalization were recruited. Meanwhile healthy volunteers of similar age that accepted routine check-ups and showed no clinical symptoms of inflammatory diseases were also recruited. Induced sputum and serum were collected. Induced sputum of participants was processed and tested for thirteen viruses and bacteria. Forty cytokines were assayed in serum using the Quantibody Human Inflammation Array 3 (Ray Biotech, Inc.). The most common virus detected in virus positive AECOPD (VP) was influenza A (16%). No virus was found in controls. Circulating levels of IL-6, TNF-α, and MCP-1 were elevated in VP and coinfection subjects (p<0.05), while the levels of 37 other cytokines showed no difference, compared with virus negative groups and controls (p>0.05). Additionally, VP patients were less likely to have received influenza vaccination. VP patients had a systemic inflammation response involving IL-6, TNF-α, and MCP-1 which may be due to virus-induced activation of macrophages. There are important opportunities for further investigating AECOPD mechanisms and for the development of better strategies in the management and prevention of virus-related AECOPD.

Funder

China Postdoctoral Science Foundation

Publisher

Hindawi Limited

Subject

Immunology,General Medicine,Immunology and Allergy

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