The data revealed a tendency to higher tissue parasitism in the skin compared to mucous lesion sites and a reduction with disease progression. Parasite load was lower in poor compared to good responders to antimonials, and was also reduced in recurrent lesions compared to primary ones. However, parasite load became higher with sequential relapses, pointing to an immune system inability to control the infection. Therefore the parasite burden does not seem to be a good predictor of disease progression.
BACKGROUND
Dendritic cells (DCs) specific intercellular adhesion molecule (ICAM)-3-grabbing non integrin receptor (DC-SIGN) binds to subgenera
Leishmania
promastigotes mediating its interaction with DC and neutrophils, potentially influencing the infection outcome.
OBJECTIVES
In this work, we investigated whether DC-SIGN receptor is expressed in cells from cutaneous leishmaniasis (CL) lesions as well as the
in vitro
binding pattern of
Leishmania
(
Viannia
)
braziliensis
(Lb) and
L.
(
L.
)
amazonensis
(La) promastigotes.
METHODS
DC-SIGN receptor was labeled by immunohistochemistry in cryopreserved CL tissue fragments.
In vitro
binding assay with CFSE-labeled Lb or La promastigotes and RAJI-transfecting cells expressing DC-SIGN (DC-SIGN
POS
) or mock-transfected (DC-SIGN
NEG
) were monitored by flow cytometry at 2 h, 24 h and 48 h in co-culture.
RESULTS
In CL lesion infiltrate, DC-SIGN
POS
cells were present in the dermis and near the epidermis. Both Lb and La bind to DC-SIGN
POS
cells, while binding to DC-SIGN
NEG
was low. La showed precocious and higher affinity to DC-SIGN
hi
population than to DC-SIGN
low
, while Lb binding was similar in these populations.
CONCLUSION
Our results demonstrate that DC-SIGN receptor is present in
L. braziliensis
CL lesions and interact with Lb promastigotes. Moreover, the differences in the binding pattern to Lb and La suggest DC-SIGN can influence in a difference way the intake of the parasites at the first hours after
Leishmania
infection. These results raise the hypothesis that DC-SIGN receptor could participate in the immunopathogenesis of American tegumentary leishmaniasis accounting for the differences in the outcome of the
Leishmania
spp. infection.
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