Innate immune responses induced by Chlamydia pneumoniae infection

Magdalenić, Vjera (2005). Innate immune responses induced by Chlamydia pneumoniae infection. PhD thesis The Open University.



In the current project innate immune responses to C. pneumoniae infection were studied, using a human in vitro model: a combination of lung epithelial cell lines (HEp-2 and A549) and primary blood-derived monocyte-derived macrophages (MdMs). The experiments were designed with a view to identify the host-pathogen interactions early in the infection that may lead to persistence and the development of chronic diseases such as atherosclerosis.

Infected epithelial cells and MdMs released IL-8 and IL-6, while MdMs also released IL-1β, TNF-α and IL-10, but not IL-12. The release of cytokines by infected cells was modulated by IL-17 treatment. Infected MdMs, but not infected epithelial cells displayed an altered surface phenotype: CD14, CD40 and CD54 were up-regulated, whereas MHC class I and II, and CD45 were down-regulated. Medium derived from infected epithelial cells modulated surface profile of MdMs in a different manner: MHC class I and II, and CD91 were up-regulated, while CD14 and CD45 were down-regulated.

IFN-γ plays a key role in controlling chlamydial growth through induction of indoleamine 2,3-dioxygenase (IDO). A549 cells were found not to control chlamydial growth although they inducibly expressed IDO mRNA. The expression of Suppressor of Cytokine Signalling 3 (SOCS3) was investigated and A549 cells constitutively expressed both SOCS3 mRNA and protein, while HEp-2 cells expressed only SOCS3 mRNA. SOCS3 expression was further up-regulated by infection in both cells. IFN-γ treatment of A549 cells did not up-regulate SOCS3 mRNA expression, but did so in HEp-2 cells. The intracellular mechanisms of inhibition of IFN-γ-mediated chlamydial control in these cells remained unclear and require further study.

The findings presented in this thesis are discussed in relation to a hypothesis that early immune responses of infected lung cells play a crucial role in the outcome of the infection and that they contribute to the establishment of persistence.

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