Subcutaneous, Oral, and Intranasal Immunization of BALB/c Mice with Leishmania infantum K39 Antigen Induces Non-Protective Humoral Immune Response.
Bruno Bezerra da SilvaAmauri Barbosa da Silva JuniorLucelina da Silva AraújoEduarda Nattaly Ferreira Nobre SantosAna Cláudia Marinho da SilvaEridan Orlando Pereira Tramontina FloreanMauricio Fraga van TilburgMaria Izabel Florindo GuedesPublished in: Tropical medicine and infectious disease (2023)
Visceral leishmaniasis is a high-burden disease caused by parasites of the Leishmania genus. The K39 kinesin is a highly antigenic protein of Leishmania infantum , but little is known about the immune response elicited by this antigen. We evaluated the humoral immune response of female BALB/c mice ( n = 6) immunized with the rK39-HFBI construct, formed by the fusion of the K39 antigen to a hydrophobin partner. The rK39-HFBI construct was administered through subcutaneous, oral, and intranasal routes using saponin as an adjuvant. We analyzed the kinetics of IgG, IgG1, and IgG2a production. The groups were then challenged by an intravenous infection with L. infantum promastigote cells. The rK39-HFBI antigen-induced high levels of total IgG ( p < 0.05) in all groups, but only the subcutaneous route was associated with increased production of IgG1 and IgG2a 42 days after immunization ( p < 0.05), suggesting a potential secondary immune response following the booster dose. There was no reduction in the splenic parasite load; thus, the rK39-HFBI failed to protect the mice against infection under the tested conditions. The results presented here demonstrate that the high antigenicity of the K39 antigen does not contribute to a protective immune response against visceral leishmaniasis.
Keyphrases
- immune response
- dendritic cells
- toll like receptor
- high fat diet induced
- induced apoptosis
- metabolic syndrome
- cell death
- wild type
- adipose tissue
- oxidative stress
- low dose
- risk assessment
- high dose
- insulin resistance
- cell cycle arrest
- endothelial cells
- small molecule
- drug induced
- signaling pathway
- diabetic rats
- binding protein
- toxoplasma gondii
- inflammatory response
- cell proliferation
- antiretroviral therapy
- endoplasmic reticulum stress
- human health