Abstract
Complement-depleted and -non-depleted BALB/c mice were inoculated with Leishmania (Leishmania) amazonensis promastigotes into the hind footpad to study the role of the complement system in cutaneous leishmaniasis. Total serum complement activity was measured by hemolytic assay and C3 fragment deposit at the inoculation site was determined by direct immunofluorescence in the early period of infection, i.e., at 3, 24, 48 h and 7 days post-infection. The inflammatory reaction and the parasite burden were evaluated in the skin lesion at 7 and 30 days post-infection. Total serum complement activity decreased in the early phase of infection, from 3 to 24 h, in non-depleted mice compared to non-infected and non-depleted mice. C3 fragment deposit at the site of parasite inoculation was present throughout the period of infection in non-depleted mice. In contrast, no C3 fragment deposit was observed at the inoculation site in complement-depleted mice. Complement-depleted mice showed a significant decrease in the inflammatory response and a significant increase in the number of parasites (70.0 +/- 5.3 vs 5.3 +/- 1.5) at 7 days of infection (P<0.05). A higher number of parasites were also present at 30 days of infection at the inoculation site of complement-depleted mice (78.5 +/- 24.9 vs 6.3 +/- 5.7). These experiments indicate that complement has an important role at the beginning of experimental cutaneous leishmaniasis caused by L. (L.) amazonensis by controlling the number of parasites in the lesion.
Highlights
Leishmaniasis develops when Leishmania survives the nonspecific defense mechanism or innate immunity, such as phagocytosis by inflammatory cells and the activity of the complement system
The mechanisms of promastigote opsonization in normal human serum are controversial; some data indicate that promastigotes activate complement via the classical pathway [1,2], but most reports show that Leishmania activation of complement is antibody independent by activation of lectin or alternative complement pathway [3,4]
The evolution of the infection in BALB/c mice infected with L. (L.) amazonensis showed a consumption of complement hemolytic activity in the sera at the beginning of the infection, between 3 and 24 h, with recovery from 48 h onwards
Summary
Leishmaniasis develops when Leishmania survives the nonspecific defense mechanism or innate immunity, such as phagocytosis by inflammatory cells and the activity of the complement system. The mechanisms of promastigote opsonization in normal human serum are controversial; some data indicate that promastigotes activate complement via the classical pathway [1,2], but most reports show that Leishmania activation of complement is antibody independent by activation of lectin or alternative complement pathway [3,4]. Promastigotes of cutaneous strains of Leishmania are susceptible to lysis by normal serum, regardless of the presence of a specific antibody, suggesting that complement activation in vitro occurs through the alternative pathway [5]. The susceptibility of the parasite to complement lysis depends on the growth phase of the culture. Most of the promastigotes in the logarithmic phase of culture growth are lysed by the action of normal human serum, while promastigotes in the stationary phase, depending on the parasite species, may not be lysed [6]. Amastigotes of cutaneous strains are more susceptible to complement lysis than visceral strains, suggesting the important role of complement factors in limiting the infection in the skin [10]
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Schedule a callMore From: Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
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