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Samsum ant venom modulates the immune response and redox status at the acute toxic dose in vivo

Hossam Ebaid1, Bahaa Abdel-Salam2, Ibrahim Alhazza1, Jameel Al-Tamimi1, Iftekhar Hassan1, Ahmed Rady1, Ashraf Mashaly1, Ahmed Mahmoud1, Reda Sammour1 [ + show more ]

J Venom Anim Toxins incl Trop Dis, 2019, 25:e20190020
Received: 16 May 2019 | Accepted: 5 November 2019 | Published online: 2 December 2019


Background: Ant venoms express surface molecules that participate in antigen presentation involving pro- and anti-inflammatory cytokines. This work aims to investigate the expression of MHC-II, CD80 and CD86 on the polymorphonuclear cells (PMNs) in rats injected with samsum ant venom (SAV). Methods: Rats were divided into three groups – control, SAV-treated (intraperitoneal route, 600 μg/kg), and SAV-treated (subcutaneous route, 600 μg/kg). After five doses, animals were euthanized and samples collected for analysis. Results: The subcutaneous SAV-trated rats presented decreased levels of glutathione with increased cholesterol and triglyceride levels. Intraperitoneal SAV-treated animals displayed significantly reduced concentrations of both IFN-γ and IL-17 in comparison with the control group. However, intraperitoneal and subcutaneous SAV-treated rats were able to upregulate the expressions of MHC-II, CD80 and CD86 on PMNs in comparison with the control respectively. The histological examination showed severe lymphocyte depletion in the splenic white pulp of the intraperitoneal SAV-injected rats. Conclusion: Stimulation of PMNs by SAV leads to upregulation of MHC-II, CD 80, and CD 86, which plays critical roles in antigen presentation and consequently proliferation of T-cells. Subcutaneous route was more efficient than intraperitoneal by elevating MHC-II, CD80 and CD86 expression, disturbing oxidative stability and increasing lipogram concentration.


Keywords: Samsum ant venom, Polymorphonuclear cells (PMNs), Costimulatory molecules (CD80 and CD86), Major histocompatibility complex (MHC), MHC-II, Interferon gamma (INF-γ), Interleukin-17 (IL-17).

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