Abstract
Chlamydial infection causes a number of clinically relevant diseases and induces significant morbidity in humans. Immune and inflammatory responses contribute to both the clearance of Chlamydia infection and pathology in host tissues. Chlamydia infection stimulates host cells to produce a large number of cytokines that trigger and regulate host immune responses against Chlamydia. However, inappropriate responses can occur with excessive production of cytokines, resulting in overreactive inflammatory responses and alterations in host or Chlamydia metabolism. As a result, Chlamydia persists and causes wound healing delays, leading to more severe tissue damage and triggering long-lasting fibrotic sequelae. Here, we summarize the roles of cytokines in Chlamydia infection and pathogenesis, thus advancing our understanding chlamydial infection biology and the pathogenic mechanisms involved.
Highlights
Chlamydia are gram-negative prokaryotic organisms with obligate intracellular parasitism [1]
We summarized the effects and interactions of important cytokines involved in Chlamydia infection (Figure 2), and offered some valuable insights into the potential mechanisms and proposed countermeasures
A range of factors contribute to cytokine production during Chlamydia infection (Supplementary Table 1)
Summary
Chlamydia are gram-negative prokaryotic organisms with obligate intracellular parasitism [1]. It is critical for the host to mount an immune response, including production of cytokines such as interleukin (IL)-1, IL6, IL-8, and tumor necrosis factor alpha (TNF-a) that activate or recruit immune cells to trigger or amplify inflammation against Chlamydia [7, 8] These cytokines can be used by immune system to inhibit Chlamydia growth and control infection, which is helpful for preventing or slowing down the progression of chlamydial lesions [9, 10], and used for microbial survival but not for clearance, and result in irreversible lesions and severe tissue damage (Table 1). Severe combined immunodeficiency (SCID) mice treated with neutralized antiIFN-g antibody, or RAG-1-/-/IFN-gR-/- mice exhibit increased susceptibility to C. trachomatis compared with RAG-1-/- mice, suggesting that IFN-g exerts beneficial effects on host innate immunity for controlling Chlamydia infection [38]
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