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Chlamydia pneumoniae–specific intrathecal oligoclonal antibody response is predominantly detected in a subset of multiple sclerosis patients with progressive forms

, , , , , & show all
Pages 425-433 | Received 23 Apr 2009, Accepted 28 Sep 2009, Published online: 06 Jan 2010
 

Abstract

The purpose of this study was to verify the actual involvement of Chlamydia pneumoniae in multiple sclerosis (MS) by the evaluation of its specific intrathecal humoral immune response in MS. We measured by enzyme-linked immunosorbent assay (ELISA) technique cerebrospinal fluid (CSF) and serum levels of anti–C. pneumoniae immunoglobulin G (IgG) in 27 relapsing-remitting (RR), 9 secondary progressive (SP), and 5 primary progressive (PP) MS patients, grouped according to clinical and magnetic resonance imaging (MRI) evidence of disease activity. Twenty-one patients with other inflammatory neurological disorders (OIND) and 21 with noninflammatory neurological disorders (NIND) were used as controls. Quantitative intrathecal synthesis of anti–C. pneumoniae IgG was determined by antibody-specific index (ASI), whereas the presence of C. pneumoniae–specific CSF oligoclonal IgG bands was assessed by antigen-specific immunoblotting. ASI values indicative of C. pneumoniae–specific intrathecal IgG synthesis were present in a small proportion of MS (29.3%), OIND (33.3%), and NIND (4.8%) patients and were significantly more frequent (P < .05) in total MS and in OIND than in NIND and in SP (P < .01) and PP MS (P < .05) than in RR MS. C. pneumoniae–specific CSF-restricted OCB were detected only in three SP, one PP, and one RR MS patients. These findings suggest that an intrathecal production of anti–C. pneumoniae IgG is part of humoral polyreactivity driven by MS chronic brain inflammation. However, an intrathecal release of C. pneumoniae–specific oligoclonal IgG can occur in a subset of patients with MS progressive forms in whom a C. pneumoniae–persistent brain infection may play a pathogenetic role.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

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