3 research outputs found
Immune and inflammatory responses to Leishmania amazonensis isolated from different clinical forms of human leishmaniasis in CBA mice
Leishmania amazonensis causes different diseases depending on the host and parasitic virulence factors. In this study, CBA mice were infected with L. amazonensis isolates from patients with localized (Ba125), diffuse cutaneous (Ba276) or visceral leishmaniasis (Ba109). Mice infected with Ba125 and Ba276 progressed rapidly and lesions displayed an infiltrate rich in parasitized macrophages and were necrotic and ulcerated. Ba109 induced smaller lesions and a mixed inflammatory infiltrate without necrosis or ulceration. Ba109 induced an insidious disease with lower parasite load in CBA mice, similar to human disease. Levels of IFN-γ, IL-4 and IL-10 did not differ among the groups. Because all groups were unable to control the infection, expression of IL-4 associated with low production of IFN-γ in the early phase of infection may account for susceptibility, but others factors may contribute to the differences observed in inflammatory responses and infection progression. Evaluation of some parasitic virulence factors revealed that Ba276 exhibits higher ecto-ADPase and 5'-nucleotidase activities compared to the Ba109 and Ba125 strains. Both Ba276 and Ba125 had higher arginase activity in comparison to Ba109. Finally, these data suggest that the differences in enzyme activities among parasites can account for differences in host inflammatory responses and infection progression
Immune and inflammatory responses to Leishmania amazonensis isolated from different clinical forms of human leishmaniasis in CBA mice
Leishmania amazonensis causes different diseases depending on the
host and parasitic virulence factors. In this study, CBA mice were
infected with L. amazonensis isolates from patients with localized
(Ba125), diffuse cutaneous (Ba276) or visceral leishmaniasis (Ba109).
Mice infected with Ba125 and Ba276 progressed rapidly and lesions
displayed an infiltrate rich in parasitized macrophages and were
necrotic and ulcerated. Ba109 induced smaller lesions and a mixed
inflammatory infiltrate without necrosis or ulceration. Ba109 induced
an insidious disease with lower parasite load in CBA mice, similar to
human disease. Levels of IFN-γ, IL-4 and IL-10 did not differ
among the groups. Because all groups were unable to control the
infection, expression of IL-4 associated with low production of
IFN-γ in the early phase of infection may account for
susceptibility, but others factors may contribute to the differences
observed in inflammatory responses and infection progression.
Evaluation of some parasitic virulence factors revealed that Ba276
exhibits higher ecto-ADPase and 5'-nucleotidase activities compared to
the Ba109 and Ba125 strains. Both Ba276 and Ba125 had higher arginase
activity in comparison to Ba109. Finally, these data suggest that the
differences in enzyme activities among parasites can account for
differences in host inflammatory responses and infection progression