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Chapter 7 : Mechanisms of Chlamydia-Induced Disease
Category: Microbial Genetics and Molecular Biology; Bacterial Pathogenesis
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This chapter discusses the possible role of gamma interferon (IFN-γ) and heat shock proteins (Hsps) in the pathogenesis of chlamydial disease. It reviews preliminary evidence from trachoma and pelvic inflammatory disease (PID) suggesting that human genotype exerts a substantial influence. It discusses some of the evidence behind current concepts of chlamydial disease mechanisms, and focuses on vitro studies that provide clues as to the potential of chlamydiae to cause enduring, inapparent infection and then examines the clinical evidence from human infection. It describes the role of cytokines in chlamydial infection. Chlamydia-induced expression of cytokines by conjunctival epithelial cells has been observed in biopsies from subjects with trachoma. The chapter then focuses on the role of chlamydial heat shock proteins in the pathogenesis of disease. The most significant advance in the clinical aspects of chlamydial research in the last decade has been the recognition that C. pneumoniae is associated with chronic human disease. The issues surrounding the possible association of C. pneumoniae infection with coronary artery disease (CAD) and the possible mechanisms by which C. pneumoniae might cause heart disease are summarized to illustrate the problems involved in proving that chlamydiae have a significant etiologic role in chronic human disease. The case for a causal role of C. pneumoniae in CAD is greatly strengthened if plausible molecular and cellular mechanisms involving known risk factors can be demonstrated. There is a need for further studies at the cellular and molecular levels on the mechanisms of chlamydia-induced disease.