Subcutaneous, oral, and intranasal immunization of BALB/c mice with 'Leishmania infantum' K39 antigen induces non-protective humoral immune response

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...

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Veröffentlicht in:Tropical medicine and infectious disease 2023-09, Vol.8 (9), p.1-10
Hauptverfasser: Silva, Bruno Bezerra da, Silva Junior, Amauri Barbosa da, Araújo, Lucelina da Silva, Santos, Eduarda Nattaly Ferreira Nobre, Silva, Ana Cláudia Marinho da, Florean, Eridan Orlando Pereira Tramontina, van Tilburg, Maurício Fraga, Guedes, Maria Izabel Florindo
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Sprache:eng
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Zusammenfassung: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.
ISSN:2414-6366
2414-6366
DOI:10.3390/tropicalmed8090444