ABSTRACT
Leishmania (Leishmania) amazonensis is a protozoan of the American Continent that causes localized cutaneous leishmaniasis and, rarely, the diffuse cutaneous form of disease in humans. It has become clear in recent years that the course of Leishmania major infection in the mouse model differs when low numbers of purified metacyclic forms are used as inocula in comparison with the traditionally hitherto studied infection models that used large numbers of stationary-phase (SP) promastigotes. The low-number metacyclic inocula are thought to reproduce more closely the natural infection transmitted by the vector. In the present study the course of L. amazonensis infection, its local and distant dissemination patterns, and parasite load were compared in susceptible BALB/c and relatively resistant C57BL/6 mice infected in the footpad with inocula of 107 SP-promastigotes or with 104 purified metacyclic forms. Longer lag-phases were observed for infection with purified metacyclics but the characteristic patterns of disease susceptibility and cytokine production for either mouse strain were similar to those observed for SP-promastigote inocula. An inoculation dose of the order of 104 metacyclics was required to obtain consistent infections; 10- or 100-fold lower doses resulted in variable infection rates. Characteristically, L. amazonensis infection spread to distant organs and persisted there also in the relatively resistant C57BL/6 mice examined after 6 months of infection.
Subject(s)
Leishmania/physiology , Leishmaniasis/parasitology , Life Cycle Stages , Animals , Antibodies, Protozoan/metabolism , Complement System Proteins/metabolism , Cytokines/metabolism , Female , Humans , Leishmania/cytology , Leishmania/growth & development , Lymph Nodes/immunology , Lymph Nodes/parasitology , Mice , Mice, Inbred BALB C , Mice, Inbred C57BL , Survival Analysis , Time FactorsABSTRACT
The proximal and distal stumps of severed mouse sciatic nerves were inserted into opposite ends of polyethylene tubes. The tubes were implanted either empty ofr filled with collagen alone or in combination with interleukin-1 (IL1). Six weeks later, neurons in the L3-L5 dorsal root ganglia were back-filled with HRP. The number of HRP reactive sensory neurons detected in the IL1-treated animals was significantly greater than that seen in the other experimental groups. Thus, exogenous IL1 may partially mimic the effects obtained with in vivo administration of nerve growth factor in protecting sensory neurons from lesion-induced death
