Abstract

Most microorganisms including Leishmania parasites compete with the innate immune defenses of the infected hosts to acquire iron, an essential nutrient necessary for their growth and replication. In mammals, iron is predominantly bound to protein carriers such as transferrin and ferritin and the strategies adopted by the infected host to restrict its uptake by pathogens are still not elucidated. We compared herein the development of anti-transferrin and anti-ferritin antibodies in hosts that differs by their susceptibility to Leishmania infection. Results showed that Leishmania infantum naturally-infected dogs which have developed canine leishmaniasis (CanL) demonstrated higher titers of IgG antibodies anti-leishmanial antigens and anti-iron binding proteins than those infected without clinical signs. In the experimental mouse model, C57BL/6 mice resisted L. major infection, developed lower titers of Leishmania-specific IgG antibodies than BALB/c susceptible mice but demonstrated also the production of anti-transferrin and anti-ferritin IgG antibodies. Overall, results are in favor that mechanisms, other than the polyclonal activation of B cells associated-hypergammaglobulinemia, a characteristic of susceptible animals, are likely involved and require a replicating parasite for the limitation of iron uptake.

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