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. 2016;7(3-4):237-254.
doi: 10.1615/ForumImmunDisTher.2017020161.

Chlamydia pneumoniae Infection and Inflammatory Diseases

Rebecca A Porritt  1 , Timothy R Crother  1
Affiliations

Chlamydia pneumoniae Infection and Inflammatory Diseases

Rebecca A Porritt et al. For Immunopathol Dis Therap. 2016.

Abstract

Chlamydia pneumoniae, an obligate intracellular bacterial pathogen, has long been investigated as a potential developmental or exacerbating factor in various pathologies. Its unique lifestyle and ability to disseminate throughout the host while persisting in relative safety from the immune response has placed this obligate intracellular pathogen in the crosshairs as a potentially mitigating factor in chronic inflammatory diseases. Many animal model and human correlative studies have been performed to confirm or deny a role for C. pneumoniae infection in these disorders. In some cases, antibiotic clinical trials were conducted to prove a link between bacterial infections and atherosclerosis. In this review, we detail the latest information regarding the potential role that C. pneumoniae infection may have in chronic inflammatory diseases.

Keywords: Alzheimer’s; Chlamydia pneumoniae; arthritis; asthma; atherosclerosis; cancer.

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Figures

FIG. 1:
FIG. 1:
C. pneumoniae infection and inflammatory disease. In addition to pneumonia, C. pneumoniae infection may contribute to a range of inflammatory diseases including asthma and lung cancer. Dissemination of C. pneumoniae from the lung throughout the body can possibly lead to atherosclerosis, arthritis, and neurological diseases. Some evidence suggests that C. pneumoniae may also be associated with biliary cirrhosis, diabetes, and Bechet’s disease.
FIG. 2:
FIG. 2:
Innate immune response directed against C. pneumoniae. C. pneumoniae EBs are endocytosed, escaping lysosome fusion to create an intracellular niche (inclusion), in which they form RBs and replicate. C. pneumoniae EBs are detected by TLRs on the cell surface, and C. pneumoniae RBs are detected intracellularly by NOD1 and NOD2. Furthermore, cellular stress induced by C. pneumoniae infection such as enhanced ROS production results in activation of the NLRP3 inflammasome. Together, activation of these innate pathways results in the induction of inflammatory cytokines, chemokines, and cell adhesion molecules that act downstream to clear infection. Immune evasion by C. pneumoniae can result in persistent infection.
See this image and copyright information in PMC

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