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A Chlamydia pneumoniae-Specific Peptide Induces Experimental Autoimmune Encephalomyelitis in Rats¹

Derek C. Lenz^*, Lin Lu^*, Stephanie B. Conant^*, Norbert A. Wolf^*, Hervé C. Gérard^*, Judith A. Whittum-Hudson^*,,, Alan P. Hudson^* and Robert H. Swanborg^2,*

Departments of ^* Immunology and Microbiology, Internal Medicine, and Ophthalmology, Wayne State University School of Medicine, Detroit, MI 48201

It has been reported recently that the bacterial respiratory pathogen Chlamydia pneumoniae is present in the cerebrospinal fluid of a subset of multiple sclerosis (MS) patients. However, it is not known whether this organism is a causative agent of MS, or merely an opportunistic pathogen that takes advantage of a disease process initiated by some other means. We report identification of a 20-mer peptide from a protein specific to C. pneumoniae which shares a 7-aa motif with a critical epitope of myelin basic protein, a major CNS Ag targeted by the autoimmune response in MS. This bacterial peptide induces a Th1 response accompanied by severe clinical and histological experimental autoimmune encephalomyelitis in Lewis rats, a condition closely reflective of many aspects of MS. Studies with peptide analogues suggest that different populations of encephalitogenic T cells are activated by the C. pneumoniae and myelin basic protein Ags. Mild experimental autoimmune encephalomyelitis was also observed when rats were immunized with sonicated C. pneumoniae in CFA.

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