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Infection & disease

Interleukin 17A is an immune marker for chlamydial disease severity and pathogenesis in the koala (Phascolarctos cinereus)

Mathew, M, Waugh, C, Beagley, KW, Timms, P & Polkinghorne, A 2014, Development and Comparative Immunology, vol. 46, pp. 423-429.

Chlamydial disease is a significant threat to the survival of koala populations, with management and control of this pathogen restricted by a narrow insight into the koala’s immune response. To develop a greater understanding of koala immunology, this study outlined the cytokine responses of immune cells sampled from koalas possessing chlamydial disease with varying stages of severity. Four different cytokines were targeted for inspection. Findings revealed significantly higher gene expression of Interleukin (IL) 17A (Th17 cytokine) in those koalas currently affected by chlamydial disease than those unaffected.

  Blood samples were taken from 41 wild koalas and immune cells were harvested, with gene expression levels of cytokines identified through koala-specific assays. Koalas were tested for chlamydial disease, including past history of infection. Twelve were identified as currently having chlamydial disease, yet all koalas tested positive for the presence of the C. pecorum pathogen. To measure cytokine response and immune recognition in koalas with evidence of chlamydial disease, harvested immune cells were stimulated with C. pecorum. Fold-increase in expression of IL17A, Tumor Necrosis Factor (TNF), Interferon gamma (IFN) and IL10 was subsequently assessed. For most of the koalas, a greater than 50-fold increase in expression was identified in at least one cytokine. However, in view of the other cytokines, IL10 expression was considerably weaker, with a mean fold change of less than ten. When stimulated with C. pecorum, 55% koalas showing no signs of chlamydial disease exhibited very low expression of IL17A and no expression was detected in 7%. Additionally, it was noted that for these asymptomatic koalas, TNF expression was significantly greater than that of IL10 and IFN. In diseased koalas, higher gene expression was recorded for IL17A, with fold-increase significantly greater than in IL10 and TNF.

  Compared to asymptomatic koalas, activation of pro-inflammatory cytokines in diseased koalas was significantly higher. In particular, considerable increases in IL17A gene expression were identified, suggesting that Th17 cytokines increased in abundance throughout the bloodstream. Other research has revealed the role of IL17A in immunopathology, encouraging Th1 immunity development, recruitment of immune cells and tissue growth/repair. While these abilities have not been assessed directly, greater IL17A expression in diseased koalas may be consistent with a heightened amplification of the inflammatory response once infectious cells have been detected. Considerable variations in cytokine response were detected in both asymptomatic and diseased koalas, however this can be attributed to individuals being at distinct phases of infection.

  In targeting a range of cytokines and evaluating their role in immune responses, this study has provided a foundation for the assessment of chlamydial severity in those koalas affected by the disease. Future research focusing on chlamydial infection should elaborate on the individual roles of these cytokines and how they influence development of the disease.


Summarised by Julian Radford-Smith


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