The Journal of Experimental Medicine
Rockland Immunochemicals for Research
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Published online 9 December 2002 doi:10.1084/jem.20020393
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© Rockefeller University Press, 0022-1007/2002/12/1639/ $5.00
The Journal of Experimental Medicine, Volume 196, Number 12, December 16, 2002 1639-1644

Brief Definitive Report

Chlamydia pneumoniae Infection of the Central Nervous System Worsens Experimental Allergic Encephalitis

Caigan Du, Song-Yi Yao, Åsa Ljunggren-Rose and Subramaniam Sriram

Department of Neurology, Multiple Sclerosis Research Center, Vanderbilt University Medical Center, Nashville, TN 37212

Address correspondence to Dr. S. Sriram, Multiple Sclerosis Research Laboratory, 1222 Vanderbilt Stallworth Rehabilitation Hospital, 2201 Capers Ave., Nashville, TN 37212. Phone: 615-963-4042; Fax: 615-321-5247; E-mail: srirams{at}ctrvax.vanderbilt.edu

Experimental allergic encephalitis (EAE) is considered by many to be a model for human multiple sclerosis. Intraperitoneal inoculation of mice with Chlamydia pneumoniae, after immunization with neural antigens, increased the severity of EAE. Accentuation of EAE required live infectious C. pneumoniae, and the severity of the disease was attenuated with antiinfective therapy. After immunization with neural antigens, systemic infection with C. pneumoniae led to the dissemination of the organism into the central nervous system (CNS) in mice with accentuated EAE. Inoculation with Chlamydia trachomatis did not worsen EAE and infectious organisms were not seen in the CNS. These observations suggest that dissemination of C. pneumoniae results in localized infection in CNS tissues in animals with EAE. We propose that infection of the CNS by C. pneumoniae can amplify the autoreactive pool of lymphocytes and regulate the expression of an autoimmune disease.

Key Words: Chlamydia • autoimmunity • multiple sclerosis • demyelination • bystander activation


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