RESUMEN
Mice vaccinated with whole blood-stage antigens of Plasmodium yoelii develop protective, antibody-mediated immune responses to homologous challenge infection. In this model the level of protection induced by whole parasite antigen vaccination is dependent on antibody isotype, which can be influenced by adjuvant formulations. In this study the ability adjuvant formulations to affect cytokine production and protection against P. yoelii blood-stage infection was investigated. Survival of mice in groups vaccinated with P. yoelii antigens in an aqueous mix of copolymer P1005 + RaLPS was 100%. Mice vaccinated with either P. yoelii antigens alone or combined with a water-in-oil emulsion of copolymer P1005 + RaLPS demonstrated 83 or 50% survival, respectively. The fully protective aqueous vaccine group produced higher levels of interferon gamma (IFNgamma) and interleukin 4 (IL-4) than the water-in-oil vaccine group following a live parasite challenge infection. Furthermore, mice vaccinated with the aqueous vaccine displayed prolonged IFNgamma and IL-4 response as compared to mice that received the same antigens without adjuvants. These data support the hypothesis that both the Th1 cytokine IFNgamma, and the Th2 cytokine IL-4 are modulated by the vaccine vehicle and adjuvant used for vaccination, thus possibly affecting expression of protective immune responses. However, it is the long-lasting IFNgamma response following blood-stage P. yoelii parasite challenge that is associated with enhanced survival.
Asunto(s)
Antígenos de Protozoos/inmunología , Interferón gamma/biosíntesis , Vacunas contra la Malaria/inmunología , Plasmodium yoelii/inmunología , Adyuvantes Inmunológicos/farmacología , Animales , Complejo CD3/inmunología , Femenino , Inmunización , Interleucina-4/biosíntesis , Ratones , Ratones Endogámicos ICR , Vehículos FarmacéuticosRESUMEN
Pathogenesis of Legionnaires>> disease is strictly related to the ability of the legionellae to infect phagocytic cells, yet surface markers of virulence in Legionella isolates are currently unknown. Rabbit antibodies raised against purified flagella of Legionella pneumophila serogroup 1 recognized a total of 24 of 30 laboratory-maintained isolates of L. pneumophila serogroups 1-15 and 16 of 24 other Legionella species tested by rapid immunoblot and indirect immunofluorescence assay. All isolates possessing flagella detectable with these anti-flagella antibodies, regardless of species, were capable of infecting Hartmannella vermiformis. Isolates lacking immunologic cross-reactivity were shown to lack purifiable flagella. The majority of aflagellate isolates were not motile and failed to multiply intracellularly in co-culture with Hartmannella vermiformis. Some isolates characterized as aflagellate when harvested from BCYE agar were able to multiply in amoebae, and flagella were subsequently detectable by immunologic methods. These data suggest that lack of immunologic recognition of flagella in laboratory-maintained isolates of Legionella is due to their attenuation and a corresponding loss of expression of flagella. More importantly, the presence of flagella can serve as a positive predictive marker for strain virulence and is useful in determining the virulence status of Legionella isolates.
Asunto(s)
Flagelos/fisiología , Legionella/patogenicidad , Animales , Anticuerpos Antibacterianos/inmunología , Flagelos/inmunología , Hartmannella/microbiología , Legionella/clasificación , Legionella/inmunología , Legionella/ultraestructura , Conejos , Serotipificación , VirulenciaRESUMEN
Twenty weeks after moderate level infections with Schistosoma mansoni, approximately 20% of male CBA/J mice develop hypersplenomegaly syndrome (HSS) while the rest present with moderate splenomegaly syndrome (MSS). HSS and MSS mice differ pathophysiologically (degree of splenomegaly, anaemia, ascites, periportal fibrosis, portal hypertension) and immunologically with regard to antibodies (idiotypic expression, isotype levels) to schistosome soluble egg antigens (SEA), and spleen cell phenotypic profiles. This study compared in vitro proliferative responses and IL-2, IFN gamma, IL-4, and IL-10 production by spleen cells from uninfected mice and mice with acute (8 wk), MSS or HSS schistosomiasis mansoni, upon exposure to anti-CD3 epsilon or SEA, Spleen cells from uninfected mice produce Il-2 to anti-CD3 epsilon but exposure of cells from all three groups of infected mice to anti-CD3 epsilon or SEA led to only very low levels of supernatant IL-2. Anti-CD3 epsilon- or SEA-stimulated production of IFN gamma or Il-4, and anti-CD3 epsilon-stimulated production of IL-10, displayed similar patterns: highest cytokine production by cells from mice with acute infections and lower levels of production that did not differ between the two chronic groups. In contrast, while SEA-stimulated IL-10 production was again highest with cells from mice with acute infections, spleen cells from mice with MSS produced significantly more IL-10 than did those from mice with HSS. This association of low levels of antigen-induced IL-10 with severe pathology is consistent with the theory that IL-10 plays a role in the immunoregulation that occurs in chronic schistosomiasis.
Asunto(s)
Interleucina-10/metabolismo , Schistosoma mansoni , Esquistosomiasis mansoni/inmunología , Esplenomegalia/inmunología , Animales , Antígenos Helmínticos/inmunología , Linfocitos B/citología , Complejo CD3/inmunología , División Celular , Enfermedad Crónica , Interferón gamma/análisis , Interferón gamma/metabolismo , Interleucina-10/inmunología , Interleucina-2/análisis , Interleucina-2/metabolismo , Interleucina-4/análisis , Interleucina-4/metabolismo , Masculino , Ratones , Ratones Endogámicos CBA , Bazo/citología , Bazo/inmunología , Bazo/patología , Esplenomegalia/etiología , SíndromeRESUMEN
Inbred CBA/J mice with chronic (20-week) Schistosoma mansoni infections demonstrate two distinct syndromes. Hypersplenomegaly syndrome (HSS), characterized by a massive spleen, liver fibrosis, ascites, and anemia, resembles hepatosplenic human schistosomiasis, complete with portal hypertension and shunting. Moderate splenomegaly (MSS) syndrome, with less severe pathology, parallels most chronic human infections. Phenotypic analyses of spleen cells for CD44, CD62L, CD45RB, Ia, and CD25 indicate that HSS mice have more activated and memory CD4+ T cells than do MSS mice. HSS animals also have more B cells that highly express B7-2. Anti-CD3 stimulated spleen cells from 8-week or chronically infected mice produce IL-4 and IL-10 in a manner that appears not to involve the CD28/B7-2 costimulation pathway. By contrast IFN-gamma production is augmented in the presence of anti-CD28 and decreased in the presence of anti-B7-2. Infected mice make very little IL-2 to anti-CD3, even with added anti-CD28. As cytokines affect resultant B-cell responses and HSS and MSS mice display distinctive isotypes, differential regulatory or anergy hypotheses may best explain MSS/HSS differences.
Asunto(s)
Anticuerpos Antihelmínticos/sangre , Citocinas/biosíntesis , Subgrupos Linfocitarios/inmunología , Schistosoma mansoni/inmunología , Esquistosomiasis mansoni/inmunología , Animales , Linfocitos B/inmunología , Hipertensión Portal/etiología , Inmunoglobulinas/sangre , Interferón gamma/biosíntesis , Interleucinas/biosíntesis , Masculino , Ratones , Ratones Endogámicos CBA , Esquistosomiasis mansoni/patología , Esquistosomiasis mansoni/fisiopatología , Bazo/inmunología , Bazo/patología , Esplenomegalia , Linfocitos T/inmunologíaRESUMEN
Antibodies to Schistosoma mansoni soluble egg antigens (SEA) generated in outbred rabbits from two different sources were used to study cross-reactive idiotype/anti-idiotype (Id/anti-Id) interactions in S. mansoni-infected mice in two different locations. Immunoaffinity purified rabbit polyclonal anti-SEA antibody preparations (RabId) were predominantly Ig by SDS-PAGE and demonstrated anti-SEA activity by ELISA and Western blot. RabId prepared from three separate rabbits and used at 40 micrograms/ml in vitro stimulated lymphocyte proliferative responses of spleen cells from mice with eight week infections (Mean +/- SEM [E-C]) of 3869 +/- 764, 18594 +/- 3046 and 8962 +/- 1734 cpm. Spleen cells from uninfected mice exposed to the same RabId preparations in vitro had respective [E-C] values of 206 +/- 144, 494 +/- 154 and 363 +/- 180. Lymph node cells from mice infected for 8 weeks demonstrated [E-C] of 123 +/- 400, 5073 +/- 828 and 2361 +/- 656 upon exposure to these 3 RabId preparations. Lymph node cells from uninfected mice had [E-C] of 220 +/- 76, 194 +/- 82 and 143 +/- 72 when exposed to these RabId. Maximum in vitro proliferative response to Ig from unimmunized rabbits was 761 +/- 400 by spleen cells from mice with eight week infections. These data indicate the presence of cross-reactive Id on rabbit anti-SEA antibodies from different rabbits that can stimulate in vitro lymphoproliferative responses of spleen or lymph node cells from S. mansoni-infected mice.
Asunto(s)
Anticuerpos Antiidiotipos , Antígenos Helmínticos , Idiotipos de Inmunoglobulinas , Schistosoma mansoni/inmunología , Esquistosomiasis mansoni/inmunología , Animales , Reacciones Cruzadas , Femenino , Técnicas In Vitro , Ganglios Linfáticos/inmunología , Activación de Linfocitos , Masculino , Ratones , Ratones Endogámicos CBA , Óvulo/inmunología , Conejos , Solubilidad , Bazo/inmunologíaRESUMEN
Idiotypes (Id) that stimulate immunoregulatory anti-Id T lymphocyte proliferation are expressed on murine and human antibodies (Ab) to soluble egg antigens (SEA) of Schistosoma mansoni. Kinetics of early expression of these stimulatory Id have now been studied using immunoaffinity-purified serum anti-SEA Ab from mice infected with S. mansoni for 6, 7, 8, 12, or 16 weeks. Rabbit anti-Id Ab specific for mouse anti-SEA Id expressed at 8 weeks post-infection (anti-8WkId) demonstrated the strongest interactions with Id present at 7 and 8 weeks post-infection by competitive enzyme-linked immunosorbent assay. Anti-8WkId Ab reacted progressively less well with 12 WkId, 6WkId, and 16WkId. Splenocytes from mice infected for 8 weeks demonstrated the highest blast transformation responses in vitro to anti-SEA Id from mice infected for 6 weeks, while 7, 8, 12, and 16 weeks post-infection Id preparations stimulated progressively less proliferation. These data indicate that although eventual Id-associated immunoregulatory events contribute to chronicity in this disease, production of anti-SEA Ab that express stimulatory cross-reactive immunoregulatory Id comprises a substantial portion of the initial, acute anti-SEA response in mice infected with Schistosoma mansoni. Furthermore, either this particular Id-expressing response is not maintained, or its proportional presence is greatly diminished by the cumulative production of other multiple anti-SEA Ab during the establishment of chronicity, perhaps in response to its immunoregulatory influence very early in infection.
Asunto(s)
Anticuerpos Antihelmínticos/química , Antígenos Helmínticos/inmunología , Idiotipos de Inmunoglobulinas/biosíntesis , Óvulo/inmunología , Schistosoma mansoni/inmunología , Esquistosomiasis mansoni/inmunología , Animales , Anticuerpos Antihelmínticos/sangre , Reacciones Cruzadas , Idiotipos de Inmunoglobulinas/química , Activación de Linfocitos , Masculino , Ratones , Ratones Endogámicos CBA , Esquistosomiasis mansoni/parasitología , Bazo/citología , Bazo/inmunologíaRESUMEN
The purpose of these experiments was to define the significance of the microfilarial stage to the hyporesponsive condition seen in lymphatic filariasis. Two types of experiments were conducted with Brugia pahangi-infected gerbils. In one, in vitro lymphocyte blastogenesis and in vivo granuloma formation in response to parasite antigen were correlated to microfilaremia in chronically infected individuals. In a second set of experiments, the level of in vivo granuloma formation was assessed following chemotherapeutic removal of microfilariae with ivermectin. The results indicated that the microfilarial stage alone is not responsible for the maintenance of the low cellular responses seen during chronic infections in this model. Furthermore, the data suggest that the degree of downregulation of these responses may be related to parasite burden.
Asunto(s)
Brugia pahangi/inmunología , Filariasis/inmunología , Granuloma/inmunología , Enfermedad Aguda , Animales , Enfermedad Crónica , Filariasis/sangre , Filariasis/complicaciones , Filariasis/tratamiento farmacológico , Gerbillinae , Granuloma/complicaciones , Endogamia , Ivermectina/uso terapéutico , Pulmón/patología , Activación de Linfocitos , Masculino , Microfilarias/inmunología , Bazo/inmunologíaRESUMEN
The ability of oral tetracycline to inhibit the development of third-stage infective larvae (L3) of Brugia pahangi to adult worms in jirds was studied using 2 experimental protocols. Jirds treated with 1.4% tetracycline in drinking water for a period beginning 30 days before inoculation of L3 until 30 days post-inoculation (DPI) had 97% reduction in adult worm recovery compared to untreated controls. Jirds that received 1.2% tetracycline in drinking water beginning 1 day before until either 12 or 26 DPI had adult worm recoveries of 11% and < 1%, respectively. Untreated jirds and those given tetracycline beginning at or later than 13 DPI had similar adult worm recovery (27-29%). Prepatent periods were prolonged, and circulating microfilariae were reduced in jirds given tetracycline from 27 to 54 DPI compared to controls. These data indicate that tetracycline administered to jirds in drinking water inhibits B. pahangi development from L3 to adult worms and suggest that this effect occurs during early larval development. Tetracycline administered to infected jirds prior to and continuing through the onset of patency can also affect development of microfilaremia.
Asunto(s)
Brugia pahangi , Filariasis/prevención & control , Tetraciclina/uso terapéutico , Administración Oral , Animales , Brugia pahangi/efectos de los fármacos , Ingestión de Líquidos , Filariasis/sangre , Gerbillinae , Masculino , Microfilarias/efectos de los fármacos , Tetraciclina/administración & dosificación , Tetraciclina/farmacologíaRESUMEN
Granulomatous lesion formation and immune responses to Brugia pahangi infections were compared in age-matched male progeny of homologously infected and uninfected female jirds. Infections initiated in 2-week-old offspring yielded mean +/- SD adult worm recoveries of 6.0 +/- 5.7 and 4.2 +/- 5.4 in offspring from infected or uninfected mothers, respectively. Infections initiated in 4-week-old offspring resulted in an mean +/- SD recovery of adult worms of 11.3 +/- 11.3 and 10.2 +/- 5.8 in offspring from infected and uninfected mothers, respectively. The ratio of intralymphatic thrombi per intralymphatic worm was similar between infected offspring from infected or uninfected mothers within experiments. Areas of granulomas around B. pahangi antigen-coated beads embolized in the lungs were not significantly affected by maternal origin in infected or uninfected progeny. Offspring infected at 2 or 4 weeks of age from infected mothers exhibited significantly reduced titers of serum IgG antibodies to Brugia antigens at 5-8 weeks postinfection compared to infected offspring of uninfected mothers. Infected offspring from infected mothers also had significantly fewer splenic IgG plaque-forming cells to B. pahangi antigens at 5 weeks postinfection than similarly infected offspring from uninfected mothers. Western immunoblot analysis indicated qualitative and quantitative reductions in serum antibody reactivity to adult B. pahangi antigens in infected progeny of infected females compared to age-matched infected controls. Reduced homologous serum antibody responses in progeny exposed to maternal B. pahangi infection suggest that maternal immunoregulation to filarial antigens may occur. Reduced antibody responsiveness to B. pahangi antigens observed in infected offspring from infected mothers, however, had no demonstrable effect on adult worm burdens, microfilaremias, lymphatic lesion formation, or antigen-specific granulomatous inflammatory responses compared to infected progeny of uninfected mothers.
Asunto(s)
Anticuerpos Antihelmínticos/sangre , Brugia/inmunología , Filariasis Linfática/inmunología , Enfermedades Pulmonares Parasitarias/inmunología , Animales , Anticuerpos Antihelmínticos/inmunología , Células Productoras de Anticuerpos , Antígenos Helmínticos/sangre , Antígenos Helmínticos/inmunología , Western Blotting , Filariasis Linfática/parasitología , Femenino , Gerbillinae , Granuloma/inmunología , Inmunoglobulina G/sangre , Enfermedades Pulmonares Parasitarias/parasitología , Activación de Linfocitos , Masculino , Factores de TiempoRESUMEN
Male jirds (Meriones unguiculatus) were inoculated subcutaneously with 100 Brugia pahangi L3 each at 2, 6, 10, and 15 wk of age to compare their susceptibility and pathologic reactivity to infection. Adult worm recoveries (mean +/- SD) ranged from 24.1 +/- 15.1 to 36.4 +/- 13.9 at 60 days postinfection. No significant difference in susceptibility was measured among the 4 age groups. Jirds infected at 2 wk of age had significantly fewer (alpha less than or equal to 0.025) testicular and intralymphatic worms than all other age groups. Numbers of intralymphatic thrombi were significantly lower (alpha less than or equal to 0.01) in jirds infected at 2 wk of age. Lymphatic lesion severity, expressed as the number of intralymphatic thrombi per intralymphatic worm, was similar between age groups. These data indicate no differences in susceptibility or lymphatic lesion formation following B. pahangi infection in 2-wk-old male jirds, despite altered adult worm location.
Asunto(s)
Brugia/patogenicidad , Gerbillinae/parasitología , Enfermedades de los Roedores/parasitología , Envejecimiento/fisiología , Animales , Susceptibilidad a Enfermedades , Filariasis Linfática , Corazón/parasitología , Inyecciones Subcutáneas , Pulmón/parasitología , Tejido Linfoide/parasitología , Masculino , Peritoneo/parasitología , Testosterona/sangreRESUMEN
Serum IgG antibody levels to adult Brugia pahangi antigens were measured in uninfected offspring from uninfected and B. pahangi-infected female jirds. Antibody titers to B. pahangi antigens in sera of offspring from infected females mimicked the maternal titer during the suckling period. Neonate titers peaked at 2 weeks of age at levels as high as 1:4100, then decreased to levels well below maternal titers by 8-12 weeks of age. Concurrent maternal and 2-week-old neonate sera recognized identical B. pahangi antigens in Western blots. Spleen cells from 2-week-old filariae-exposed and unexposed offspring failed to produce measurable antibody to B. pahangi in vitro. Progeny of uninfected mothers nursed by B. pahangi-infected females showed circulating IgG antibody titers to adult worm antigens similar to those of homologously reared offspring. Conversely, offspring born to B. pahangi-infected females and nursed by an uninfected female had no serum antibodies to B. pahangi antigens. Blastogenic responses of spleen cells to the mitogens phytohemagglutinin and pokeweed mitogen, and adult B. pahangi antigens, were not different between offspring groups. Mean areas of pulmonary granulomas induced by the intravenous inoculation of B. pahangi antigen-coated beads also did not differ between 4- and 8-week-old progeny of uninfected or infected females. These results suggest that the circulating IgG antibodies to adult B. pahangi antigens demonstrated in offspring of infected female jirds are maternally derived via the milk and do not alter the cellular responses of uninfected offspring to B. pahangi antigens as measured by antigen-stimulated blastogenesis or pulmonary granulomatous inflammatory response.
Asunto(s)
Anticuerpos Antihelmínticos/sangre , Brugia/inmunología , Filariasis Linfática/inmunología , Inmunidad Materno-Adquirida , Inmunoglobulina G/análisis , Animales , Animales Recién Nacidos/inmunología , Animales Lactantes/inmunología , Antígenos Helmínticos/inmunología , Femenino , Gerbillinae , Granuloma/inmunología , Enfermedades Pulmonares Parasitarias/inmunología , Activación de Linfocitos , MasculinoRESUMEN
Host responses of jirds receiving a single subcutaneous inoculation of subperiodic Brugia malayi were compared with those of jirds similarly infected with B. pahangi. Parasite burdens, lymphatic lesion severity, granulomatous reactivity, antibody responses to parasite antigens, and complete blood cell counts were assessed at 60 and 150 days post-inoculation. At 60 days post-inoculation, percentages of adults recovered at necropsy and lymphatic lesion severity were greater in B. pahangi-infected jirds. At 150 days post-inoculation, lesion severity and percentages of worms recovered were similar in both infections. No significant differences were noted in either infection in reactivity to homologous or heterologous parasite antigens in any parameter measured. Similarities in the kinetics of the inflammatory reactivities of the 2 infections suggest that previous observations made in the jird-B. pahangi model could be utilized in designing studies using B. malayi. Further, the more marked lesion severity observed in B. pahangi-infected jirds and the relative ease of maintaining B. pahangi in the laboratory support the continued use of this system as a conceptual model for the study of lymphatic lesion pathogenesis.
Asunto(s)
Brugia/fisiología , Modelos Animales de Enfermedad , Filariasis Linfática/parasitología , Gerbillinae/parasitología , Animales , Anticuerpos Antihelmínticos/biosíntesis , Antígenos Helmínticos/análisis , Western Blotting , Brugia/inmunología , Electroforesis en Gel de Poliacrilamida , Filariasis Linfática/sangre , Filariasis Linfática/inmunología , Filariasis Linfática/patología , Ensayo de Inmunoadsorción Enzimática , Granuloma/patología , Recuento de Leucocitos , Pulmón/patología , Sistema Linfático/parasitología , Sistema Linfático/patología , Masculino , Testículo/parasitologíaRESUMEN
The Mongolian jird is used widely in filariasis research for studies of protective immunity, pathogenesis, and therapy. The purpose of this study was to evaluate parasite antigen detection as a means of noninvasively monitoring Brugia pahangi infection in jirds. A parasite antigen with Mr of 105-110 kDa was identified in sera from i.p.- and s.c.-infected jirds by immunoblot with a monoclonal antibody to phosphorylcholine. The same antibody was used in a direct sandwich enzyme immunoassay to measure antigen in jird sera. Parasite antigen was detectable as early as 2 wk after i.p. or s.c. injection of L3. Antigen titers increased between 2 and 12 wk and stabilized between 12 and 36 wk after infection in s.c.-infected animals. A different pattern was seen in i.p.-infected jirds with antigen titers peaking at 16 wk and falling significantly between 16 and 32 wk after infection. Parasite antigen titers correlated significantly with adult worm infection intensities in jirds with mature i.p. and s.c. infections. Antigenemia was also detectable in sera from jirds after i.p. implantation of adult parasites of either sex. However, antigen was not detected in sera from infant offspring of antigenemic infected mothers. We conclude that parasite antigen detection allows B. pahangi development and survival as well as infection intensity to be monitored in living animals with unprecedented sensitivity and accuracy. This technique should facilitate drug and vaccine studies in this important experimental filariasis model.
Asunto(s)
Antígenos Helmínticos/sangre , Brugia/inmunología , Modelos Animales de Enfermedad , Filariasis Linfática/parasitología , Filariasis/parasitología , Gerbillinae/parasitología , Animales , Brugia/crecimiento & desarrollo , Femenino , Immunoblotting , Técnicas para Inmunoenzimas , MasculinoRESUMEN
Adult Schistosoma mansoni worms were transplanted from 8 nonhuman primates with chronic infections into 8 naive recipients, in an effort to test the hypothesis that worm fecundity reduction in chronic infections is the result of host immunity or some other host effect. Techniques for perfusing living donors without the added use of anti-schistosomal drugs and for reducing the likelihood of post-operative bacterial endotoxemia and septic shock are described. Fecundity values in terms of eggs per day per female worm were obtained for the worms in their original and in their new hosts and compared. In 3 experiments, perfusions were incomplete and the donors were saved, enabling direct comparisons of fecundity to be made in subpopulations of worms in both their original and new hosts, after equal life spans. In only 1 of the 8 transplantations was there a clear increase in fecundity after surgical introduction into a naive host. Therefore, these experiments fail to support the hypothesis that reduced fecundity of S. mansoni worms in permissive nonhuman primate hosts is a reversible result of host immunity or some other host-derived factor. Despite this negation, further evidence for reduced worm fecundity in older infections was obtained. In the absence of in vivo evidence for immune-mediated antifecundity, worm senescence is the most likely explanation for this finding, with irreversible immune damage to the worms being a less attractive alternative hypothesis.
Asunto(s)
Schistosoma mansoni/fisiología , Esquistosomiasis mansoni/parasitología , Animales , Enfermedad Crónica , Femenino , Fertilidad , Macaca fascicularis , Masculino , Papio , Recuento de Huevos de Parásitos , Esquistosomiasis mansoni/inmunologíaRESUMEN
A reliable in vitro fecundity assay for Schistosoma mansoni was established. The main features that reduced variability in in vitro oviposition were pre-selection and randomization of worm pairs producing moderate numbers of eggs in initial 2-day culture, and short pre-incubation in serumless medium prior to addition of test sera to the cultures. In 4 of 6 total experiments testing the effects of serum from chronically infected baboons, significant (P less than or equal to 0.025) fecundity reduction ranging from 29 to 82% was found. Chronically infected baboon serum also caused consistently higher unpairing than normal serum. These results demonstrate the existence of serum factors which inhibit egg production and maintenance of the paired status of Schistosoma mansoni in vitro.
Asunto(s)
Papio/sangre , Schistosoma mansoni/fisiología , Esquistosomiasis mansoni/inmunología , Animales , Femenino , Fertilidad , Masculino , Oviposición , Papio/parasitología , Schistosoma mansoni/inmunología , Esquistosomiasis mansoni/sangreRESUMEN
A population of Schistosoma mansoni from Kenya was isolated in 1968 and subsequently passaged simultaneously through 2 different vertebrate hosts: baboons and mice. Recent electrophoretic studies demonstrated that genetic differences in the degree of polymorphism and in allele frequencies of polymorphic loci existed between S. mansoni populations from the 2 hosts. The present study was undertaken to assess the importance of vertebrate host-induced selection against particular alleles as mechanism to account for the observed differences. A population of S. mansoni which had originally been passaged through baboons and subsequently passaged through murine hosts for 4 generations was studied. At least 20 infected snails served as the source of parasite for each mouse passage. Allele frequencies of 4 polymorphic loci were assessed for each generation using horizontal starch gel electrophoresis. All 4 polymorphic loci (PGM-2, MDH-2, MDH-1, PGI) showed a selective trend towards allele frequencies identical with that of a strain (from the same isolate) maintained in mice for 12 yr. These data suggest that vertebrate host-induced selection results in a decrease in parasite variability due to loss of alleles as field isolates of S. mansoni are passaged in murine hosts. The use of non-human primate hosts, on the other hand, maintains a higher level of parasite variability.