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Infection and Immunity, February 2003, p. 614-620, Vol. 71, No. 2
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.2.614-620.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Induction of Proinflammatory Cytokines in Human Lung Epithelial Cells during Chlamydia pneumoniae Infection

Jun Yang,1,{dagger} W. Craig Hooper,2 Donald J. Phillips,2 Maria L. Tondella,1 and Deborah F. Talkington1*

Division of Bacterial and Mycotic Diseases,1 Division of AIDS, Sexually Transmitted Diseases, and Tuberculosis Laboratory Research, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 303332

Received 11 June 2002/ Returned for modification 15 August 2002/ Accepted 8 November 2002

Chlamydia pneumoniae is an obligate intracellular human pathogen that causes acute respiratory diseases such as pneumonia and bronchitis. Previous studies have established that C. pneumoniae can induce cytokines in mouse and/or human cells, but little information is available on the cytokine response of respiratory epithelial cells, a first line of infection. In this study, heparin treatment of C. pneumoniae significantly reduced its ability to induce interleukin 8 (IL-8) and tumor necrosis factor alpha (TNF-{alpha}) mRNA in human lung carcinoma cells, indicating that cytadherence is an important early stimulus for induction of proinflammatory mediators. Although the IL-8, gamma interferon, and TNF-{alpha} message was consistently induced by infection of A549 cells not treated with heparin, only an elevation of IL-8 protein was detected in A549 supernatants. A549 IL-ß and IL-6 mRNA and supernatant protein profiles were not significantly changed by infection. Heat or UV inactivation of C. pneumoniae only partially reduced the cytokine response, and inhibition of C. pneumoniae protein or DNA synthesis did not affect its ability to induce cytokine gene expression. To prevent stress-induced cytokine release by the A549 cells, centrifugation was not utilized for infection experiments. These experiments establish the importance of cytadherence in cytokine release by cells of respiratory epithelial origin and suggest that further work in the area of cytokine mediators is warranted to gain valuable pathogenic and therapeutic insights.


* Corresponding author. Mailing address: Mail Stop G03, Division of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, 1600 Clifton Rd., NE, Atlanta, GA 30333. Phone: (404) 639-3918. Fax: (404) 639-4215. E-mail: dft1{at}cdc.gov.

Editor: J. D. Clements

{dagger} Present address: Department of Pathophysiology, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310031, China


Infection and Immunity, February 2003, p. 614-620, Vol. 71, No. 2
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.2.614-620.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.




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