The Immunology of Schistosomiasis

Smithers, S. R.; Terry, R. J.

doi:10.1016/s0065-308x(08)60434-0

Cited by 133 publications

(11 citation statements)

References 218 publications

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“…Three related mechanisms will facilitate eosinophil adherence: (a) binding to IgG-coated schistosomula through Fc interaction; (b) adherence mediated by antibodies which can activate complement through the classical pathway (in these conditions, C3 bound to the Fc piece of the antibody would react with C3 receptors on the eosinophih it is well known that antibodies which activate complement and are specific for the schistosomular surface are present in infected hosts [20]); and (c) a direct interaction between C3 receptors on the eosinophil and C3 on the parasite surface activated by the alternative pathway.…”

Section: Discussionmentioning

confidence: 99%

Complement-mediated killing of schistosomula of Schistosoma mansoni by rat eosinophils in vitro.

Ramalho-Pinto¹,

McLaren²,

Smithers³

1978

The Journal of Experimental Medicine

169

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Recently there has been growing evidence for the role of the eosinophil in the effector mechanism of immunity to reinfection with schistosomes. Mice immune to Schistosoma mansoni are no longer able to resist reinfection after treatment with anti-mouse eosinophil serum (1). In vitro studies using human serum and eosinophils (2) or rat serum and cells (3), have demonstrated antibody-mediated damage to schistosomula by eosinophils. These cells adhere to IgG-coated schistosomula by Fc receptors (3), and peroxidase, from the matrix of the eosinophil granule, is secreted onto the surface of the worm (4).Eosinophils have been shown to possess C3 receptors in addition to Fc (5, 6), and schistosomula are known to activate complement by the alternative pathway, binding C3 to their surface (7). It seemed appropriate, therefore, to investigate the adherence of rat eosinophils to schistosomula through the C3 receptor, and to monitor the effects of this interaction. Materials and MethodsParasite Cycle and Preparation of Schistosomula. A Puerto Rican strain of S. mansoni was maintained in laboratory bred Biomphalaria glabrata and outbred Parkes mice, as described elsewhere (8).Schistosomula were prepared in vitro from cercariae .by a mechanical method (9). Briefly, cercariae freshly shed from snails were concentrated by addition of peniciUin-stroptemycin, followed by chilling and spinning at 1,000 rpm for 15-30 s. 1 ml of deionized water was added to the pellet and the suspension was whirled in a Vortex mixer (Scientific Industries, Inc., Bohemia, N. Y.) for 1 rain. This effected the rupture of tails from bodies, which were afterwards separated by sedimentation in Hanks' balanced salt solution. The cercarial bodies were then incubated at 37°C in RPMI-1640 (Flow Labs. Ltd., Ayrshire, Scotland) and 20 mM N-2-hydroxyethyl-piperazine-N'-2-ethane sulfonic acid (Hepes) ~ for 3 h. The schistosomula were used on the day of preparation. Formalin-fixed schistosomula were prepared as previously described (10).5-Day schistosomula were recovered from the lungs of CBA mice after exposure to 1,000 * Supported by Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (Brazil), and the WeUcome Trust. Present address:

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Section: Discussionmentioning

confidence: 99%

Complement-mediated killing of schistosomula of Schistosoma mansoni by rat eosinophils in vitro.

Ramalho-Pinto¹,

McLaren²,

Smithers³

1978

The Journal of Experimental Medicine

169

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“…Furthermore, nature has proven to us that immunity against parasites can be achieved. 'Concomitant immunity is a state of resistance to reinfection in hosts which are already infected (82). Whether the result of a shared antigen between resident and infective forms or of a stage-specific antigen (9), apparently, resident parasites have succeeded where we have so far failed.…”

Section: Discussionmentioning

confidence: 99%

Complement Evasion by Parasites: Search for “Achilles' Heel”

Fishelson

1991

Clinical and Experimental Immunology

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PREFACEParasitic diseases continue to be a major cause of hunfian morbidity and mortality. Each year, more than one billion people are affected by one or more of the common human parasites and more than one million infected patients die. Generally, mammalian parasites are divided into protozoan parasites which include the Trypanosoma, Leishmania, Entamoeba, Giardia. Plasmodium, Babesia and Toxoplasma and to helminthic parasites which can be subdivided into trematodes (e.g. Sctiistosoma and Fasciola), cestodes (e.g. Taenia and Ectiinococcu^ and nematodes (e.g. Trichinella and Onchocerca). The parasites contain multiple antigenic determinants which are recognized by the host's immune system as non-self and may potentially trigger an immune response that will destroy the parasite. This has been proven by serological and skin tests. Nevertheless, parasites are equipped with multiple, sophisticated immune evasion mechanisms which permit them to be infective and pathogenic (1-8). Intensive efforts in the past decade to produce a human parasite vaccine have not been successful yet and perhaps, as recently suggested (9) this issue will have to be reconsidered and efforts reoriented. This summary will focus primarily on the interaction of parasites with the complement system. Recent progress made in the elucidation of the complement evasion mechanisms of certain parasites will be discussed in light of the urgent need to develop new strategies for immunising against parasites. COMPLEMENT AT LARGEThe complement system is one of the weapons the body utilize to fight intruders like bacteria, viruses and parasites. To achieve maximal protection, the complement system enlists several effector mechanisms. On one hand, it directly attacks the surface of pathogenic agents via the membranolytic attack complex, O5b-9 (MAO), and on the other hand it can induce and potentiate opsonization, chemotaxis and many other inflammatory processes which culminate in lysis and clearance of the intruder. More than 30 different proteins participate in this concentrated effort of the complement system to eliminate potential pathogens. Twenty of them are soluble plasma proteins and the others are membrane proteins acting as receptors or regulatory molecules. Several detailed reviews and books have been recently published which describe the complement proteins and genes and their molecular organization and functions (e.g. 10-16).The complement cascade is activated via the classical or altemative pathway, mostly but not exclusively, by antibodies or complex carbohydrates, respectively. Each pathway employs a distinct set of proteins to produce proteases which cleave the 03 and 05 complement components. These are called the 03 and 05 convertases. Despite the fact that the convertases of the classical and alternative pathways are composed of distinct proteins, they cleave identical sites in 03 and 05. Oleavage of the 03 molecule by the 03 convertases (and by trypsin) sensitizes a metastable intra-molecular thioester bond and facilitates covalent bindin...

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“…Os moluscos dos GI, após o 10 o dia de observação, eram colocados individualmente em frascos contendo 10 ml de água declorada e expostos à ação de luz e calor 13 , durante duas horas. Em seguida, as cercárias eram contadas em lupas estereoscópicas.…”

Section: Obtenção De Cercáriasunclassified

“…Estudos realizados no sentido de esclarecer aspectos da relação parasita-hospedeiro mostram que, durante a evolução da esquistossomose, ocorrem modificações estruturais, tanto por parte do parasita como do hospedeiro 4 ; que o mosaico antigênico de superfície corporal do verme adquire características próprias relacionadas com a espécie hospedeira 13 e que estas características induzem uma resposta parasito--imunológica específica capaz de levar ao estabelecimento de linhagens do verme 2,3,6 Bastos e col. 8 2,3 . A suspensão final foi colocada em placas de Petri e exposta à luz e à temperatura de 28°C, provenientes de lâmpadas elétricas 14 .…”

Section: Introductionunclassified

Ocorrência de linhagens humana e silvestre de Schistosoma mansoni, na pré-amazônia: I - estudo em moluscos

et al. 1982

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RESUMO:Foram isoladas na região da Baixada Maranhense (Brasil), linhagens humana (H) e silvestre(S) de Schistosoma mansoni a partir de miracídios eclodidos de ovos encontrados em fezes de doentes humanos autóc-tones da Região e de fígados de roedores silvestres naturalmente infectados. Biomphalaria glabrata, descentes de caramujos coletados no campo, foram expostos, isoladamente, aos miracídios H e S, mantidos isolados em moluscário e observados durante 100 dias. Moluscos normais foram mantidos nas mesmas condições de ambiente em que foram submetidos os infectados e tomados como controle da experiência. Foram anotados os indices de infecção dos moluscos, as datas da eliminação de cercárias, quantidade de larvas eliminadas e mortalidade dos moluscos. Os dados sugeriram melhor adaptação do esquistossomo da linhagem H à B. glabrata. A linhagem S, por sua vez, foi três vezes mais virulenta do que a linhagem H. Estes dados foram comparados com os encontrados na literatura especializada e verificado diversidades nos comportamentos parasitológicos das linhagens em estudo, quando comparados com os encontrados nas linhagens H e S oriundas do Vale do Rio Paraíba do Sul, no Estado de São Paulo (Brasil).

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The Immunology of Schistosomiasis

Cited by 133 publications

References 218 publications

Complement-mediated killing of schistosomula of Schistosoma mansoni by rat eosinophils in vitro.

Complement-mediated killing of schistosomula of Schistosoma mansoni by rat eosinophils in vitro.

Complement Evasion by Parasites: Search for “Achilles' Heel”

Ocorrência de linhagens humana e silvestre de Schistosoma mansoni, na pré-amazônia: I - estudo em moluscos

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