RESUMO
Schistosoma mansoni infection invariably results in liver fibrosis of the host. This fibrosis may be represented by small focal areas of chronic inflammation and excess extracellular matrix deposited in periovular granulomas, distributed in variable numbers at the periphery of the portal vein system. This is the outcome of 90% of the infected population in endemic areas. Conversely, a minority of infected individuals develop extensive disease with numerous granulomas along the entire extension of the portal spaces. This latter situation is mainly dependent on special hemodynamic changes created by a heavy worm load, with the subsequent production of numerous eggs and represents a severe form of a peculiar chronic hepatopathy. Thus, host-parasite interactions in schistosomiasis help us to understand a number of important features of liver fibrosis: its initiation and regulation, the significance of accompanying vascular changes, the dynamics of fibrosis formation and regression with antiparasitic treatment; host genetic and immunological contributions, and the pathophysiology of portal hypertension.
Assuntos
Fígado/patologia , Esquistossomose/patologia , Animais , Fibrose , Interações Hospedeiro-Parasita , Humanos , Fígado/parasitologia , Schistosoma mansoni/patogenicidade , Schistosoma mansoni/fisiologia , Esquistossomose/parasitologia , VirulênciaRESUMO
Biomphalaria tenagophila is very important for schistosomiasis transmission in Brazil. However its mechanisms of interaction with Schistosoma mansoni are still scantly studied. Since this snail displays strains highly susceptible or completely resistant to the parasite infection, the knowledge of that would be a useful tool to understand the mechanism of snail resistance. Particularly, the Taim strain consistently shows absolute resistance against the trematode, and this resistance is a dominant character. A multidisciplinary research group was created aiming at studying B. tenagophila/S. mansoni interaction. The possibility for applying the knowledge acquired to obtain a biological model for the control of S. mansoni transmission in endemic areas is discussed.
Assuntos
Biomphalaria/parasitologia , Vetores de Doenças , Schistosoma mansoni/fisiologia , Animais , Biomphalaria/fisiologia , Brasil , Interações Hospedeiro-Parasita/fisiologia , Humanos , Esquistossomose mansoni/transmissãoRESUMO
Biomphalaria tenagophila is very important for schistosomiasis transmission in Brazil. However its mechanisms of interaction with Schistosoma mansoni are still scantly studied. Since this snail displays strains highly susceptible or completely resistant to the parasite infection, the knowledge of that would be a useful tool to understand the mechanism of snail resistance. Particularly, the Taim strain consistently shows absolute resistance against the trematode, and this resistance is a dominant character. A multidisciplinary research group was created aiming at studying B. tenagophila/S. mansoni interaction. The possibility for applying the knowledge acquired to obtain a biological model for the control of S. mansoni transmission in endemic areas is discussed.
Assuntos
Humanos , Animais , Biomphalaria , Vetores de Doenças , Interações Hospedeiro-Parasita , Schistosoma mansoni , Brasil , Esquistossomose mansoniRESUMO
We previously demonstrated that mice subjected to a hypoproteinic diet showed milder chronic lesions on infection with Schistosoma mansoni than normally fed mice. Here we compare the immune response of well-nourished and undernourished mice with chronic S. mansoni infection. The proliferative response and cytokine (IFN-gamma and IL-5) production of splenocytes from undernourished mice against the soluble egg antigen (SEA) of S. mansoni or concanavalin A was similar to that of well-nourished mice. The levels of SEA-specific IgG1, IgG2b and IgG3 antibodies were significantly higher in the sera of well-nourished mice in comparison with undernourished mice. Undernourished animals also exhibited diminished periovular granuloma size compared to well-nourished infected controls. Our results support the importance of host nutritional status in the humoral immune response of mice and its effects on the development of periovular granulomas in malnourished animals infected with S. mansoni.
Assuntos
Anticorpos Anti-Helmínticos/sangue , Granuloma/patologia , Distúrbios Nutricionais/imunologia , Schistosoma mansoni/imunologia , Esquistossomose mansoni/patologia , Fenômenos Fisiológicos da Nutrição Animal , Animais , Antígenos de Helmintos/imunologia , Feminino , Granuloma/imunologia , Fígado/imunologia , Fígado/patologia , Ativação Linfocitária , Masculino , Camundongos , Distúrbios Nutricionais/patologia , Esquistossomose mansoni/imunologia , Baço/imunologia , Baço/patologiaRESUMO
Rats infected with the helminth Capillaria hepatica regularly develop septal fibrosis of the liver similar to that induced by repeated ip injections of pig serum. Fibrosis starts when the focal parasitic lesions begin to show signs of resorption, thus suggesting an immunologically mediated pathogenesis of this fibrosis. To explore this possibility, the development of C. hepatica-related hepatic fibrosis was observed in rats exposed to worm antigens from the first neonatal day onward. Wistar rats (150 g) were either injected ip with an extract of C. hepatica eggs (protein concentration: 1 mg/ml) or received immature eggs by gavage from the first neonatal day until adult life and were then infected with 500 embryonated eggs. Changes were monitored on the basis of serum levels of anti-worm antibodies and hepatic histopathology. Rats submitted to immunological oral tolerance markedly suppressed C. hepatica-related serum antibodies and septal fibrosis of the liver when infected with the helminth later on. Tolerance trials with ip injections of worm antigens gave essentially negative results. The partial suppression of septal fibrosis of the liver after the induction of immunological tolerance to C. hepatica antigens in rats indicates an immunological basis for the fibrosis and emphasizes the importance of immunological factors in the pathogenesis of hepatic fibrosis
Assuntos
Animais , Feminino , Masculino , Ratos , Antígenos de Helmintos , Capillaria , Infecções por Enoplida , Cirrose Hepática Experimental , Hepatopatias Parasitárias , Anticorpos Anti-Helmínticos , Cirrose Hepática Experimental , Hepatopatias Parasitárias , Ratos WistarRESUMO
Rats infected with the helminth Capillaria hepatica regularly develop septal fibrosis of the liver similar to that induced by repeated ip injections of pig serum. Fibrosis starts when the focal parasitic lesions begin to show signs of resorption, thus suggesting an immunologically mediated pathogenesis of this fibrosis. To explore this possibility, the development of C. hepatica-related hepatic fibrosis was observed in rats exposed to worm antigens from the first neonatal day onward. Wistar rats (150 g) were either injected ip with an extract of C. hepatica eggs (protein concentration: 1 mg/ml) or received immature eggs by gavage from the first neonatal day until adult life and were then infected with 500 embryonated eggs. Changes were monitored on the basis of serum levels of anti-worm antibodies and hepatic histopathology. Rats submitted to immunological oral tolerance markedly suppressed C. hepatica-related serum antibodies and septal fibrosis of the liver when infected with the helminth later on. Tolerance trials with ip injections of worm antigens gave essentially negative results. The partial suppression of septal fibrosis of the liver after the induction of immunological tolerance to C. hepatica antigens in rats indicates an immunological basis for the fibrosis and emphasizes the importance of immunological factors in the pathogenesis of hepatic fibrosis.
Assuntos
Antígenos de Helmintos/imunologia , Capillaria/imunologia , Infecções por Enoplida/complicações , Cirrose Hepática Experimental/imunologia , Hepatopatias Parasitárias/imunologia , Animais , Anticorpos Anti-Helmínticos/sangue , Feminino , Cirrose Hepática Experimental/parasitologia , Cirrose Hepática Experimental/patologia , Hepatopatias Parasitárias/parasitologia , Hepatopatias Parasitárias/patologia , Masculino , Ratos , Ratos WistarRESUMO
A histopathological and immunophenotypic study was performed on the spleen of patients with hepatosplenic (HS) schistosomiasis mansoni. Morphological data demonstrated that all HS patients presented features related to Schistosoma mansoni-induced splenomegaly, such as red pulp congestion and atrophy/hyperplasia of white pulp. The morphological diversity of the white pulp seems to be associated with the expansion of activated CD4+ T-cell subpopulation. The data obtained suggest that the spleen is an important site for T-cell activation during severe chronic infection with S. mansoni. In addition, we have compared the cell populations/subpopulations presented in the peripheral blood with that observed in the spleen of patients with HS schistosomiasis mansoni. We observed a significant increase in the percentage of activated CD4+HLA-DR+ and CD8+HLA-DR+ T cells in both the spleen and the peripheral blood of HS patients in comparison with noninfected individuals (NOR). These data suggest an exchange of cells between these two compartments. However, we observed normal expression of the CD28 molecule by CD8+ T cells in the spleen, despite a lower percentage of these cells in the peripheral blood. This finding supports the hypothesis that the decrease in CD28 expression, by CD8+ cells, is an event that takes place outside the spleen during human schistosomiasis infection. The most important conclusion is the fact that the analysis of T-cell activation in the peripheral blood reflects the major immunological reactivity that occurs in the spleen during human schistosomiasis and that the morphological aspects of the spleen may reflect the functional activity of T cells. The specificities of T cells and the roles they may play in the pathogenesis during chronic schistosomiasis now need to be determined.
Assuntos
Ativação Linfocitária , Esquistossomose mansoni/imunologia , Baço/imunologia , Subpopulações de Linfócitos T/imunologia , Adolescente , Adulto , Células Sanguíneas/imunologia , Antígenos CD28/análise , Movimento Celular , Feminino , Humanos , Imunofenotipagem , Fígado/patologia , Masculino , Pessoa de Meia-Idade , Esquistossomose mansoni/patologia , Baço/citologia , Baço/patologia , Subpopulações de Linfócitos T/classificaçãoRESUMO
Biomphalaria straminea snails from Argentina fail to shed cercariae even if exposed to high doses of Schistosoma mansoni EC miracidia. Alternative explanations for this failure are that miracidia are unable to penetrate the snail's epithelium or that the miracidia are killed by the snail's defense system. To discriminate between these 2 possibilities, B. straminea snails were individually exposed to increasing doses of miracidia. Susceptible B. glabrata were used as controls. Exposed snails were fixed 12 hr after exposure, and histological sections of the whole specimens were examined. Miracidia were seen to penetrate the epithelium of B. straminea and B. glabrata at similar rates (14.7%), independent of the exposure level. Regardless of the miracidial dose, 94% of the penetrating miracidia appeared encapsulated by the B. straminea defense system, whereas in B. glabrata, only 42% of the miracidia underwent encapsulation. These results show that resistance of B. straminea to S. mansoni EC strain is due to an efficient defense system that destroys miracidia once they have penetrated.
Assuntos
Biomphalaria/parasitologia , Schistosoma mansoni/imunologia , Animais , Argentina , Biomphalaria/imunologia , Suscetibilidade a Doenças , Vetores de Doenças , Interações Hospedeiro-Parasita , Camundongos , Contagem de Ovos de Parasitas , Esquistossomose mansoni/parasitologia , Esquistossomose mansoni/transmissãoRESUMO
Inocula, varying from 15 to 1,000 embryonated Capillaria hepatica eggs, were administered to young adult rats by gastric tube, in an attempt to investigate the influence of worm load in the production of septal fibrosis of the liver. Low doses of 15, 30 or 50 eggs were sufficient to produce septal fibrosis, but it appeared with variable degrees of intensity and always with focal distribution. Septal fibrosis became diffuse, progressive with time, and already well developed 40 days after infection, when 100 eggs or more were administered. However, higher inocula (200, 500 and 1,000 eggs) did not intensify septal fibrosis, although the number of parasitic focal lesions proportionally augmented.
Assuntos
Capillaria , Infecções por Enoplida/complicações , Cirrose Hepática Experimental/parasitologia , Hepatopatias Parasitárias/parasitologia , Animais , Modelos Animais de Doenças , Feminino , Cirrose Hepática Experimental/patologia , Hepatopatias Parasitárias/patologia , Masculino , Ratos , Ratos WistarRESUMO
Biomphalaria glabrata, highly susceptible to Schistosoma mansoni, were seen to shed less and less cercariae along the time of infection. Histological examination kept a close correlation with this changing pattern of cercarial shedding, turning an initial picture of no-reaction (tolerance) gradually into one of hemocyte proliferation with formation of focal encapsulating lesions around disintegrating sporocysts and cercariae, a change that became disseminated toward the 142nd day post miracidial exposure. Findings were suggestive of a gradual installation of acquired immunity in snails infected with S. mansoni.