Literature DB >> 10223347

Liver pathology and immune response in experimental Fasciola hepatica infections of goats.

A Martínez-Moreno1, V Jiménez-Luque, T Moreno, E S Redondo, J M de las Mulas, J Pérez.   

Abstract

The relationship between the immune response and the pathogenesis of the disease was studied in different primary and secondary experimental Fasciola hepatica infections of goats. The establishment of the infection, measured as percentage of recovered flukes at the necropsy, was similar in primarily and secondarily infected animals (between 19.7% and 24.3%), but the hepatic damage was much more severe in secondarily infected goats, as revealed by the levels of serum hepatic enzymes GGT and LDH. Primary infection evolves to chronic fasciolosis that did not induce the development of resistance, since goats were highly susceptible to secondary infection, showing severe acute and chronic hepatic lesions that led to the death of some animals in each group. The immune response to the infection was proved by the production of specific IgG antibodies to ESP of F. hepatica and the involvement of CD3+ T lymphocytes and lambda IgG+ plasma cells in the hepatic infiltrate. Secondary infection did not induce any difference in either IgG response or in the cellular composition of the infiltrate of hepatic lesions, although this was much more extended. However, neither antibodies nor cell-mediated response were protective: there was no correlation between IgG levels and fluke burden and there was no evidence of cell-mediated killing of the parasite. This suggests the existence of some immune evasion mechanisms in goat infection with F. hepatica. The parasite may depress the local inflammatory and immune response, as suggested by the scarcity of CD3+ T cells in the infiltrate surrounding acute migratory tunnels. Moreover, in secondary infected goats can be suspected an immunological damage of the liver, since a very severe infiltrate of immune cells replaced wide areas of hepatic parenchyma and an immune-mediated damage of hepatocytes could occur.

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Year:  1999        PMID: 10223347     DOI: 10.1016/s0304-4017(98)00262-3

Source DB:  PubMed          Journal:  Vet Parasitol        ISSN: 0304-4017            Impact factor:   2.738


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