AI Article Synopsis

  • - 'Surra' is a disease in livestock caused by the protozoan Trypanosoma evansi. This study focuses on how both innate and adaptive immunity, especially T-helper cells, play critical roles in fighting this infection through antibody responses.
  • - Bovine calves were immunized with γ-radiation-attenuated T. evansi and later exposed to the virulent form. Results showed significant increases in pro-inflammatory cytokines (Th1 and Th17) and IgG2 antibody levels, which correlated with effective protection against the disease.
  • - In contrast, a control group with low Th1 cytokine levels experienced the infection more severely, indicating that these cytokines are essential for short-term immunity against T.

Article Abstract

'Surra', an economically important disease of livestock, is caused by the parasitic blood protozoon Trypanosoma evansi. Both innate and adaptive immunity contribute to the protection against this infection. T-helper cells play a crucial role in the antibody-mediated clearance of T. evansi. We present here the data on the kinetics of expression of important Th1, Th2 and Th17 cytokines, vis-a-vis the dynamics of humoral response in bovine calves following immunization with γ-radiation-attenuated live T. evansi and later challenged with homologous virulent T. evansi. Significant upregulation of the pro-inflammatory Th1 and Th17 cytokines was correlated with the IgG2-mediated protection in the immunized bovine calves post-challenge. The calves were immunized with 5 × 10 500 Gy γ-radiation-attenuated live T. evansi (horse isolate) thrice at 15 days intervals through the subcutaneous route and subsequently, challenged with 1 × 10 virulent T. evansi on day 50. Significantly high serum IgG (1:1600) and IgM (1:800) titres were recorded on week 2 PC, whereas the peak serum IgG2 titre (1:800) was recorded on week 6 PC. Significant upregulation of IFN-γ, TNF, IL-1β, and IL-2 was recorded between days 1 to 3 PC, while the same for IL-17 was recorded on day 14 PC. The immunized calves were free from parasitemia post-challenge and were clinically healthy till the end of the experiment. Significant upregulation of IL-10 and IL-4 transcripts and a corresponding increase of serum IgG1 titre in the placebo group helped patency of the parasite in an anti-inflammatory environment and clinical exacerbation of the disease. The expression of the important Th1 cytokines was crucial for antibody-mediated short-term protection against a lethal challenge of T. evansi in cattle.

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http://dx.doi.org/10.1016/j.vaccine.2023.01.046DOI Listing

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