Analysis of chicken cytokine and chemokine gene expression following Eimeria acervulina and Eimeria tenella infections

The expression levels of mRNA encoding a panel of 28 chicken cytokines and chemokines were quantified in intestinal lymphocytes following Eimeria acervulina and Eimeria tenella primary and secondary infections. Compared with uninfected controls, transcripts of the pro-inflammatory cytokines IFN-α, IL-1β, IL-6, and IL-17 were increased up to 2020-fold following primary infection. By contrast, following secondary infection by either microorganism, pro-inflammatory mRNAs levels were relatively unchanged (≤20-fold). Transcripts encoding the Th1 and Th1 regulatory cytokines IFN-γ, IL-2, IL-10, IL-12, IL-15, IL-16, and IL-18 were uniformly increased 14–2471-fold after E. acervulina primary infection, but either unchanged (IL-15, IL-16, IL-18), increased (IFN-γ, IL-10, IL-12), or decreased (IL-2) following E. tenella primary infection. Following secondary infections, Th1 cytokine mRNA levels were relatively unchanged, with the exception of IL-12 which was increased 1.5 × 105-fold after E. acervulina and decreased 5.1 × 104-fold after E. tenella infection. Transcripts for the Th2 or Th2 regulatory cytokines IL-3 and GM-CSF were increased up to 327-fold following primary or secondary infection with both parasites, while IL-4 and IL-13 mRNAs were decreased 25- to 2 × 105-fold after primary or secondary infection. The dynamics of chicken chemokine expression revealed modest changes (<100-fold) following primary or secondary infection except for lymphotactin. When lymphocyte subpopulations were similarly analyzed, IFN-γ, IL-2, IL-3, IL-15, and MIF were most highly increased in TCR2+ cells following E. acervulina infection, while TCR1+ cells only expressed high levels of IL-16 following E. tenella infection. In contrast, CD4+ cells only expressed highest levels of IL-10 after E. acervulina infection, whereas these cells produced abundant transcripts for IFN-γ, IL-3, IL-15, and MIF after E. tenella infection. We conclude that coccidiosis induces a diverse and robust primary cytokine/chemokine response, but a more subdued secondary response.