Expe
rimental models of infe
ction with
Leishmania spp. have p
rovided knowledge of seve
ral immunologi
cal events involved in the
resistan
ce me
chanism used by the host to
rest
rain pa
rasite g
rowth. It is well a
ccepted that
con
comitant immunity exists, and the
re is some eviden
ce that it would play a majo
r role in long-lasting a
cqui
red
resistan
ce to infe
ction. In this pape
r, the
resistan
ce to
Leishmania amazonensis infe
ction in C57BL/6 mi
ce infe
cted with
Leishmania major was investigated. C57BL/6 mi
ce, whi
ch spontaneously heal lesions
caused by infe
ction with
L. major, we
re infe
cted with
L. amazonensis at diffe
rent times befo
re and afte
r L. major. We demonst
rated that C57BL/6 mi
ce p
reviously infe
cted with
L. major rest
rain pathogeni
c responses indu
ced by
L. amazonensis infe
ction and de
crease pa
rasite bu
rdens by one o
rde
r of magnitude. Co-infe
cted mi
ce showed p
rodu
ction of IFN-γ in lesions simila
r to mi
ce infe
cted solely with
L. major, but highe
r TNF-
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r="0"> and nit
ri
c oxide synthase (iNOS) mRNA exp
ression was obse
rved. Su
rp
risingly, the
rest
rained pathogeni
c response was not
related to IL-10 p
rodu
ction, as eviden
ced by lowe
r levels of both mRNA, p
rotein exp
ression in lesions f
rom
co-infe
cted mi
ce and in
co-infe
ctions in IL-10
−/− mi
ce. Examination of the inflammato
ry infilt
rate at the site of infe
ction showed a
redu
ced numbe
r of mono
cytes and lympho
cytes in
L. amazonensis lesions. Additionally, diffe
rential p
rodu
ction of the CCL3/MIP-1
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r alpha" bo
rde
r="0"> and CCL5/RANTES was obse
rved. We suggest that the
cont
rol of lesion p
rog
ression
caused by
L. amazonensis in C57BL/6 mi
ce p
re-infe
cted with
L. major is
related to the indu
ction of a down-
regulato
ry envi
ronment at the site of infe
ction with
L. amazonensis.