Acta Scientific Medical Sciences (ASMS)(ISSN: 2582-0931)

Research Article Volume 8 Issue 8

Exploring Immune Evasion Strategies: CD200 And ATK/TLR2 Upregulation in Response to Chronic T. evansi Vesicular Fraction Stimulation

Nnanna Isaiah Ibeh1*, Onyiyechi Cynthia Okeke1, Micheal Awo Okungbowa2 and Isaiah Nnanna Ibeh3

1Department of Veterinary Anatomy, Faculty of Veterinary Medicine, University of Benin, Nigeria
2Department of Physiology, Igbinedion University, Edo State, Nigeria
3Department of Medical Laboratory Science, School of Basic Medical Sciences, University of Benin, Nigeria

*Corresponding Author: Nnanna Isaiah Ibeh, Department of Veterinary Anatomy, Faculty of Veterinary Medicine, University of Benin, Nigeria.

Received: June 12, 2024; Published: July 15, 2024

Abstract

Background: Trypanosoma evansi, the parasite responsible for surra, a disease affecting livestock and occasionally humans, has evolved strategies to evade the host immune system. A key mechanism involves extracellular vesicles (EVs) that contain proteins and molecules impacting host immune cells. Understanding these interactions is essential for developing effective treatments.

Aim: This study explores how T. evansi-derived EVs affect the expression of immune-related proteins CD200 and AKT/TLR2 in host cells, aiming to understand their role in immune evasion.

Method: We used RAW 264.7 and THP-1 cell lines, stimulating them with T. evansi EVs for 24 to 72 hours. Flow cytometry assessed CD200 expression. Quantitative real-time polymerase chain reaction (qRT-PCR) measured the expression of CD200 and AKT/TLR2, while enzyme-linked immunosorbent assays (ELISA) quantified pro-inflammatory cytokines IL-6 and TNF-α.

Results: Flow cytometry showed a significant upregulation of CD200 after 72 hours of stimulation with T. evansi EVs. ELISA revealed elevated IL-6 and TNF-α levels, suggesting an inflammatory response to the EVs. qRT-PCR indicated increased expression of TLR2 and AKT.

Conclusion: The findings suggest that T. evansi EVs may contribute to immune evasion by upregulating CD200, which can suppress host immune responses. The simultaneous increase in IL-6 and TNF-α implies that immune pathways are activated, indicating a complex host response to T. evansi infection. These insights into the parasite's immune evasion tactics could guide the development of new therapeutic strategies for surra and other parasitic diseases. Further research into CD200's role in immune modulation is warranted.

 Keywords: Trypanosoma evansi; Extracellular Vesicles (EVs); Immune Evasion; CD200 Expression; Pro-inflammatory Cytokines; Host-Pathogen Interactions

References

  1. AL-Hilal EA., et al. “The Modulation of In Vitro Differentiation of Monocyte-derived Macrophage by Trypanosoma evansi Antigens in the Dromedary Camel”. World4 (2023): 587-594.
  2. Carneiro P P., et al. “Blockade of TLR2 and TLR4 attenuates inflammatory response and parasite load in cutaneous leishmaniasis”. Frontiers in Immunology 12 (2021): 706510.
  3. Dantas-Pereira L., et al. “Extracellular vesicles: potential role in remote signaling and inflammation in Trypanosoma cruzi-triggered disease”. Frontiers in Cell and Developmental Biology 9 (2021): 798054.
  4. Gaiser M R., et al. “Merkel cell carcinoma expresses the immunoregulatory ligand CD200 and induces immunosuppressive macrophages and regulatory T cells”. Oncoimmunology5 (2018): e1426517.
  5. Gavinho B., et al. “A new landscape of host–protozoa interactions involving the extracellular vesicles world”. Parasitology12 (2018): 1521-1530.
  6. Hussen J., et al. “A Flow Cytometry Study of the Binding and Stimulation Potential of Inactivated Trypanosoma evansi toward Dromedary Camel Leukocytes”. Pathogens1 (2023): 21.
  7. Jawalagatti V., et al. “Expression kinetics of cytokines and the humoral antibody response concerning short-term protection induced by radiation-attenuated Trypanosoma evansi in bovine calves”. Vaccine10(2023): 1668-1678.
  8. Kern K., et al. “CD200 selectively upregulates prostaglandin E2 and D2 synthesis in LPS-treated bone marrow-derived macrophages”. Prostaglandins and Other Lipid Mediators 133(2017): 53-59.
  9. Li D., et al. “CD200-CD200R1 signalling attenuates imiquimod-induced psoriatic inflammation by inhibiting the activation of skin inflammatory macrophages”. International Immunopharmacology 78 (2020): 106046.
  10. Moncayo Á and Silveira A C. “Current epidemiological trends of Chagas disease in Latin America and future challenges: Epidemiology, surveillance, and health policies”. American Trypanosomiasis Chagas Disease (2017): 59-88.
  11. Silva M JA., et al. “The relationship between 896A/G (rs4986790) polymorphism of TLR4 and infectious diseases: A meta-analysis”. Frontiers in Genetics 13(2022): 1045725.
  12. Singh SK., et al. “Trypanosoma evansi induces detrimental immuno-catabolic alterations and condition like type-2 diabetes in buffaloes”. Parasitology international2 (2018): 140-143.
  13. Verma R., et al. “Molecular and genetic diversity in isolates of Trypanosoma evansi from naturally infected horse and dogs by using RoTat 1.2 VSG gene in Madhya Pradesh, India”. Molecular Biology Reports 9 (2023): 7347-7356.
  14. Wei R., et al. “Trypanosoma evansi evades host innate immunity by releasing extracellular vesicles to activate TLR2-AKT signaling pathway”. Virulence1 (2021): 2017-2036.
  15. Zhang SY., et al. “Human inborn errors of immunity to infection affecting cells other than leukocytes: from the immune system to the whole organism”. Current Opinion in Immunology 59 (2019): 88-100.

Citation

Citation: Nnanna Isaiah Ibeh., et al. “Exploring Immune Evasion Strategies: CD200 And ATK/TLR2 Upregulation in Response to Chronic T. evansi Vesicular Fraction Stimulation”.Acta Scientific Medical Sciences 8.8 (2024): 88-94.

Copyright

Copyright: © 2024 Nnanna Isaiah Ibeh., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.




Metrics

Acceptance rate30%
Acceptance to publication20-30 days
Impact Factor1.403

Indexed In





Contact US