The cellular and humoral immune response to Schistosoma mansoni infections in inbred rats

Phillips, S M; Reid, William A.; Bruce, J. I.; Hedlund, Kenneth; Colvin, Robert C.; Campbell, Robert J.; Diggs, Carter L.; Sadun, E. H.

doi:10.1016/0008-8749(75)90295-6

Cited by 78 publications

(48 citation statements)

References 36 publications

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“…For example, Fischer rats are quite tolerant of a low dose (<50 cercariae) challenge (Phillips et al, 1975) while almost completely eliminating a high dose (>500 cercariae) challenge approximately 4 weeks p.i. (Knopf et al, 1977; Phillips et al, 1977; Cioli et al, 1978).…”

Section: Introductionmentioning

confidence: 99%

Schistosoma mansoni host-exposed surface antigens characterized by sera and recombinant antibodies from schistosomiasis-resistant rats

Sepúlveda

Tremblay

DeGnore

et al. 2010

International Journal for Parasitology

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Antibodies from Schistosoma mansoni-infected rats, unlike mice, show a higher titer for schistosome apical tegumental antigens compared with non-apical membrane antigens. These antibodies bind to the surface of living lung stage worms and to formaldehyde-fixed adult worms. We produced a singlechain antibody Fv domain (scFv) phage library displaying the antibody repertoire of rats highly immune to schistosome infection and we selected for scFvs that recognize the host-exposed surface of worms. Five unique rat scFvs (Teg1, Teg4, Teg5, Teg20 and Teg37) were obtained which recognize schistosome surface epitopes. Each of the scFvs recognizes the surface of living schistosomula and lung stage schistosomules and/or the surface of formaldehyde-fixed adult worms. None of these scFvs reproducibly stained living adult worms. This suggests that a change occurs during the transition from lung schistosomules to 4 week adults such that at least some surface antigens, although remaining on the surface in living adult worms, can no longer be immunologically stained. Teg1 and Teg4 scFvs both recognize specific bands on Western blots. No bands were observed for the other three scFvs, suggesting that these scFvs may recognize non-protein or conformationally-dependent epitopes. Teg1 was unambiguously identified as recognizing the S. mansoni tetraspanin antigen, SmTSP-2, within the large extracellular domain. Teg4 recognizes a 35 kD band tentatively identified as Sm29 by proteomic analysis. These scFvs can now be used to characterize schistosome epitopes at the host-parasite interface, to target worms in vivo, and to study the mechanisms by which these worms naturally evade immune damage to the tegument within permissive hosts.

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Section: Introductionmentioning

confidence: 99%

Schistosoma mansoni host-exposed surface antigens characterized by sera and recombinant antibodies from schistosomiasis-resistant rats

Sepúlveda

Tremblay

DeGnore

et al. 2010

International Journal for Parasitology

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“…Laboratory rats eliminate a primary schistosome infection from day 28 onwards when the maturing worms are resident in the hepatic portal distributaries (Cioli, Knopf & Senft 1977). It has been suggested that worm death is the result of a nutritional deficiency (Cioli et al 1977, Cioli, Blum & Ruppel, 1978 but the much delayed elimination of worms in athymic (Phillips et al 1983) and thymectomized rats (Cioli & Dennert 1975, Phillips et al 1975 argues for an immunological basis. Helminth infections induce remarkable, specific and non-specific IgE antibody responses in humans and animals (Sadun & Gore 1970, Rousseaux-Prevost, Bazin & Capron 1977, Rousseaux-Prevost et al 1978, Dunne et al 1992a.…”

Section: Introductionmentioning

confidence: 99%

Elimination of a primary schistosome infection from rats coincides with elevated IgE titres and mast cell degranulation

Cutts

Wilson

1997

Parasite Immunology

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Schistosomes are eliminated from laboratory rats around 28 days post-infection, whilst they are still resident within the hepatic portal distributaries of the liver. We have previously shown that their presence in this location is accompanied by an intense mastocytosis. We have investigated the potential relationships between IgE responses, the allergenicity of schistosome antigens, mast cell responsiveness, and worm elimination. Total and specific IgE were measured using an ELISA and a functional assay based on 3H serotonin release from activated rat basophilic leukemia cells (RBL-SRA), respectively. Both assays revealed that infected rats produced elevated IgE titres relative to naive animals. At days 28 and 35, mixed-sex infections stimulated a higher total IgE than male-only infections. IgE was affinity purified from rat infection serum and used to probe a fractionated soluble worm antigen preparation (SWAP) by Western blotting. Two allergenic products were detected of M(r) 67 and 36-38 kDa, the former having the same molecular weight as a previously identified secretory protein. IgE from mixed-sex schistosome infections bound strongly to the 36-38 kDa molecule, compared to the relatively weak binding exhibited by IgE from male-only infection serum. Since eggs were not recovered from the infected rats, this reactivity was attributed to the greater release of allergens from female worms. Results from the RBL-SRA showed that female SWAP was a more effective trigger of mast cell degranulation in vitro, for equal amounts of protein. This enhanced allergenicity was ascribed to the relative abundance of carbohydrate moieties. Our results support a role for IgE, and mast cell degranulation in the elimination of a primary schistosome burden from rats.

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“…This study confirms the possibility of the concomitant immunity (CI) as one of these features. Previous experimental studies on CI indicate that this feature is an immunological process and is called 'self-cure phenomenon' (14,15). It was observed between the 4 th and the11 th week, as measured by the liver perfusion technique, or by the lung recovery method (16)(17)(18)(19).…”

Section: Discussionmentioning

confidence: 97%

“…Previous experimental studies on CI indicate that this feature is an immunological process and is called 'self-cure phenomenon' (14,15). It was observed between the 4 th and the11 th week, as measured by the liver perfusion technique, or by the lung recovery method (16)(17)(18)(19). The exact mechanism of CI as a phase of acquired immunity is still unclear, The number of cercariae used for primary / challenge infections was 100 (20)(21)(22).…”

Section: Discussionmentioning

confidence: 99%

Concomitant Immunity to Schistosoma mansoni in Mice

Salim

Al-Humiany²

2013

TurkiyeParazitolDerg

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Objective: The aim of the present study was to confirm observations on the concomitant immunity to Schistosoma mansoni in mice and assess its effects on the resistance of mice to a challenge infection. Methods: Cercariae from infected Biomphalaria glabrata were used to infect mice. Twenty mice were infected with a single dose of S. mansoni cercariae. The animals were randomly divided into two groups: experimental group (Group A) and control group (Group B). Group A mice were challenged with the same number of cercariae six weeks after the primary infection. Perfusion of all mice was done 9 weeks after infection in order to obtain worm burdens in relation to their initial cercarial dose. The livers of all mice were obtained for parasitological and pathological assessments. Results: Our results showed that all the exposed animals became infected with S. mansoni. After a challenge infection, Group A mice had a 54.66% worm reduction rate, 41.45% liver egg reduction rate, and 51.76% granuloma size reduction rate compared to their respective controls. This study shows that mice with persistent adult S. mansoni infection are able to mount a very strong regulatory response to a challenge infection. It is concluded that concomitant immunity does occur in mice. Conclusion: These results describe novel imaging methods that permit visualization of live schistosomes within their living hosts and may help to elucidate mechanisms of infection and also be of value not only for epidemiological investigations, but also in designing government control programs for schistosomiasis. (Turkiye Parazitol Derg 2013; 37: 19-22) . Grup A fareleri birincil enfeksiyondan altı hafta sonra aynı sayıda serkarya ile sınandı. Başlangıç serkarya dozlarıyla ilişkili kurtçuk yükünü elde etmek için tüm farelere enfeksiyondan 9 hafta sonra perfüzyon yapıldı. Bütün farelerin karaciğerleri parazitolojik ve patolojik değerlendirmeler için alındı. Bulgular: Sonuçlarımız maruz kalan tüm hayvanların S. mansoni ile enfekte olduğunu gösterdi. Karşılaşılan bir enfeksiyondan sonra ilgili kontrolleriyle kıyaslandığında, Grup A farelerde kurtçuk azalma oranı %54.66, karaciğerdeki yumurta azalma oranı %41.45, granülom boyutundaki azalma oranı %51.76 idi. Bu çalışma göstermektedir ki persistant yetişkin S. mansoni enfeksiyonu olan fareler, meydan okuyan bir enfeksiyona çok güçlü bir düzenleyici cevap oluşturabilmektedir. Farelerde konkomitant bağışık oluştuğuna karar verilmiştir. Sonuç: Bu bulgular canlı şistozomların yaşayan konaklarında görüntülenmesini sağlayan yeni görüntüleme metotlarını tanımlamaktadır ve enfeksiyon mekanizmalarını açıklamaya yardımcı olabilir. Ayrıca bu bulgular, sadece epidemiyolojik araştırmalar için değil, şistozomiyaz için devlet kontrol programları tasarlamak için de önemlidir. (Turkiye Parazitol Derg 2013; 37: 19-22)

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The cellular and humoral immune response to Schistosoma mansoni infections in inbred rats

Cited by 78 publications

References 36 publications

Schistosoma mansoni host-exposed surface antigens characterized by sera and recombinant antibodies from schistosomiasis-resistant rats

Schistosoma mansoni host-exposed surface antigens characterized by sera and recombinant antibodies from schistosomiasis-resistant rats

Elimination of a primary schistosome infection from rats coincides with elevated IgE titres and mast cell degranulation

Concomitant Immunity to Schistosoma mansoni in Mice

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