Migration of Schistosoma mansoni sambon (Trematoda, Schistosomatidae) from skin to lungs in immunized NZ rabbits (Lagomorpha, Leporidae) by autoradiographic analysis

Pinto, Roberto Magalhães; Noronha, Dely; Almeida, Marília Sirianni dos Santos; Katz, Naftale; Tendler, Míriam

doi:10.1590/s0101-81751994000400006

Cited by 3 publications

(5 citation statements)

References 18 publications

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“…worms, which affects mainly children of tropical and subtropical regions ( 33 ). Severe symptoms include liver damage, pulmonary hypertension and even pericarditis ( 4 , 5 , 34 ). During infection of mammalian hosts, schistosomula migrate through the pulmonary-systemic vasculature before they reach the hepatic portal system ( 3 ).…”

Section: Discussionmentioning

confidence: 99%

“…The parasites penetrate the skin within the first hours and migrate through systemic vasculature circuit, peaking in the lungs between 5 and 7 days of infection ( 3 ). Larvae that pass through the lung vasculature are delivered to the hepatoportal circulation, where they mature into adult worms and later migrate to mesenteric venules, mate, and begin egg deposition ( 4 , 5 ).…”

Section: Introductionmentioning

confidence: 99%

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CD18 Regulates Monocyte Hematopoiesis and Promotes Resistance to Experimental Schistosomiasis

et al. 2018

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Infection with Schistosoma mansoni causes a chronic parasitic disease that progress to severe liver and gastrointestinal damage, and eventually death. During its development into mammalian hosts, immature schistosomula transit through the lung vasculature before they reach the liver to mature into adult worms. A low grade inflammatory reaction is induced during this process. However, molecules that are required for efficient leukocyte accumulation in the lungs of S. mansoni-infected subjects are unknown. In addition, specific leukocyte subsets that mediate pulmonary response during S. mansoni migration through the lung remain to be elucidated. β2 integrins are fundamental regulators of leukocyte trans-endothelial migration and function. Therefore, we investigated their role during experimental schistosomiasis. Mice that express low levels of CD18 (the common β2 integrin subunit) and wild type C57BL/6 mice were subcutaneously infected with S. mansoni cercariae. Cellular profiles of lungs and livers were evaluated in different time points after infection by flow cytometry. Low levels of CD18 affected the accumulation of patrolling Ly6Clow, intermediate Ly6Cinter monocytes, monocyte-derived macrophages and monocyte-derived dendritic cells in the lungs 7 days after infection. This correlated with increased TNF-α levels. Strikingly, low CD18 expression resulted in monocytopenia both in the peripheral blood and bone marrow during acute infection. After 48 days, S. mansoni worm burdens were higher in the hepatic portal system of CD18low mice, which also displayed reduced hepatic accumulation of patrolling Ly6Clow and intermediate Ly6Cinter, but not inflammatory Ly6Chigh monocytes. Higher parasite burden resulted in increased granulomatous lesions in the liver, increased egg deposition and enhanced mortality. Overall, our data point for a fundamental role of CD18 for monocyte hematopoiesis during infection, which promotes an efficient host response against experimental schistosomiasis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

CD18 Regulates Monocyte Hematopoiesis and Promotes Resistance to Experimental Schistosomiasis

et al. 2018

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“…The early recovery of larval parasite loads of S. mansoni either from the skin or from the lungs has been frequently reported worldwide in an attempt to shorten experiments in which this protection is being tested. However, together with antigenically induced responses, much has been discussed about the temporal distribution of schistosomula and parasite attrition sites where death of schistosomula occurs, with a natural decrease of adult worms in the definitive mammalian host (Pinto et al, 1987(Pinto et al, , 1990(Pinto et al, , 1994Coulson & Mountford, 1989;Dean & Mangold, 1992).…”

Section: Discussionmentioning

confidence: 99%

“…The patterns of infection and migration of S. mansoni by different routes in mice and other permissive hosts often refer to either naive or vaccinated animals, since this parameter must be taken into account to properly evaluate different biological assays in experimental schistosomiasis. In Brazil, reports considering this aspect are those of Holanda et al (1974), Tendler et al (1985), Pinto et al (1987Pinto et al ( , 1990Pinto et al ( , 1994, in which different routes of infection with S. mansoni and migration patterns are discussed.…”

Section: Introductionmentioning

confidence: 99%

Reappraisal of experimental infections with cercariae and schistosomula of a brazilian strain of Schistosoma mansoni in mice

Vilar¹,

Pinto

2005

Braz. J. Biol.

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The present investigation involves a reevaluation of previous results obtained after experimental infection of Swiss Webster mice with cercariae and schistosomula of the Schistosoma mansoni LE strain maintained under laboratory conditions. Three experimental groups of mice were considered: the animals of the first group were percutaneously (ring method) infected with cercariae, those of the second were subcutaneously inoculated with cercariae and the mice of the third were inoculated by the same route with schistosomula transformed in vitro. The data obtained so far indicated that the most effective method of infection is the subcutaneous injection with schistosomula, with a mean adult worm burden recovery of 54.1% when compared to the abdominal percutaneous and subcutaneous routes of infection with cercariae, in which the values were 36.7% and 32.4%, respectively. This suggests that, in experimental infections of SW mice with a LE S. mansoni strain, the skin is to be considered an effective attrition site in the percutaneous route, whereas in the case of inoculation with cercariae, a small amount of larvae fails to be transformed into viable schistosomula, possibly due to skin phase avoidance. A brief discussion about attrition sites and elimination of larval S. mansoni worms in mice is presented.

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“…hipertensão pulmonar e até pericardite (PINTO et al, 1994;CROSBY et al, 2010;DE JESUS et al, 2002). Durante a infecção no hospedeiro mamífero, os esquitossômulos migram através da vasculatura até atingirem os pulmões (WILSON, 2009), antes de chegarem no sistema porta hepático e migrarem para as vênulas mesentéricas, onde acasalam-se, e a fêmea deposita os ovos (MCMANUS et al, 2018).…”

Section: Discussionunclassified

CD18 coordena o desenvolvimento de monócitos e a diferenciação em macrófagos alternativamente ativados conferindo resistência à infecção por Schistosoma mansoni

Souza¹

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Migration of Schistosoma mansoni sambon (Trematoda, Schistosomatidae) from skin to lungs in immunized NZ rabbits (Lagomorpha, Leporidae) by autoradiographic analysis

Cited by 3 publications

References 18 publications

CD18 Regulates Monocyte Hematopoiesis and Promotes Resistance to Experimental Schistosomiasis

CD18 Regulates Monocyte Hematopoiesis and Promotes Resistance to Experimental Schistosomiasis

Reappraisal of experimental infections with cercariae and schistosomula of a brazilian strain of Schistosoma mansoni in mice

CD18 coordena o desenvolvimento de monócitos e a diferenciação em macrófagos alternativamente ativados conferindo resistência à infecção por Schistosoma mansoni

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