concanavalin-a and Schistosomiasis-mansoni

Colonic lesions are predominant in patients with schistosomiasis. However, carbohydrate alterations in colonic schistosomiasis remain unclear. Lectin-ligands allow us to identify changes in the saccharide patterns of cells.. Biopsies of descending and rectosigmoid colon of patients were submitted to WGA and Con A lectin histochemistry.. WGA stained stroma and gland cells of descending colon and rectosigmoid tissues in a granular strong cytoplasmatic pattern in schistosomiasis specimens differing from normal control and Con A failing to recognize all samples analyzed.. WGA ligands are expressed differently in patients with hepatosplenic schistosomiasis and no evidence of egg-granuloma system.

Topics: Biomarkers; Biopsy; Colon, Sigmoid; Concanavalin A; Humans; Immunohistochemistry; Schistosomiasis mansoni; Splenic Diseases; Wheat Germ Agglutinins

Reinfection with Schistosoma mansoni following chemotherapy often results in an ameliorated granulomatous reaction and hence a mild disease. This study examined some of the immunological mechanisms that could be associated with this residual protection. BALB/c mice were infected with either a single dose (group A) of 100 S. mansoni cercariae or with 10 doses of 10 cercariae each (group B) given at 3-day intervals. The mice were treated with praziquantel 8 weeks postinfection and, 2 weeks later, together with another group of naive mice (group C), they were infected with a single dose of 100 cercariae each. All the animals were killed 8 weeks later and schistosome egg antigen (SEA)- and soluble adult worm antigen preparation (SWAP)-induced cytokine recall responses in splenocytes, as well as serum immunoglobulin levels, were quantified and hepatic granuloma sizes measured. Group A animals had higher levels of SEA-induced interferon-gamma (IFN-gamma) but lower levels of interleukin (IL)-5 than groups B and C (P < 0.01). Group B animals had low SEA-induced IFN-gamma levels and elevated IL-5 levels, although these were lower than group C. SEA-induced IL-10 was low in both groups A and B as compared to group C (P < 0.01). SWAP was less effective as an inducer of splenocyte cytokine production than SEA but both SWAP-induced IFN-gamma and IL-5 were detected in groups A and C. SEA- and SWAP-specific immunoglobulin E (IgE) and immunoglobulin G (IgG) titres were not significantly different between the three groups. Granuloma diameters were larger in group C (mean 297 +/- 51.3 microm) as compared to groups A (174 +/- 49 microm, P < 0.01) and B (247.5 +/- 44 microm, P < 0.05). Taken together, these results demonstrate that granuloma size is reduced during a reinfection exposure compared with a primary infection. This reduction is associated with a T helper 1 response in mice exposed to a single large dose of cercariae in the primary infection and with a predominantly T helper 2 response in those infected with multiple small doses.

Topics: Animals; Antibodies, Helminth; Antigens, Helminth; Cells, Cultured; Concanavalin A; Culture Media; Cytokines; Female; Granuloma; Liver Diseases, Parasitic; Mice; Mice, Inbred BALB C; Praziquantel; Recurrence; Schistosoma mansoni; Schistosomiasis mansoni; Spleen; Th1 Cells; Th2 Cells

Synchronized liver granulomas were induced by injecting Sepharose beads to which SEA soluble egg antigen (SEA) or the concanavalin A binding fraction of SEA had been coupled into a mesenteric vein in naive, single-sex (35 days) and bisexually (28 days) Schistosoma mansoni-infected and Plasmodium berghei-immunized mice. Stereological analysis revealed that peak granuloma formation was already reached 8 days after injection in single-sex infected mice compared with 16 days in naive animals. No difference in granuloma formation between naive and P. berghei-immunized animals and between unisexually and bisexually S. mansoni-infected mice was observed. This suggests that the positive immunomodulatory effect on the granulomogenesis is worm specific and not likely to be due to arousal of the immune system by unrelated factors, nor is it influenced by the gender or degree of maturation of female worms. At all stages in time, the concanavalin A binding-fraction-induced granulomas reached only 65 to 70% of the volume of SEA-induced granulomas. Immunophenotyping of extracellular matrix proteins around deposited heads revealed that fibronectin was the dominant extracellular matrix protein and that also type I and IV collagen and laminin were deposited. Temporal analysis of the expression of the adhesion molecules ICAM-1, LFA-1, VLA-4, and VLA-6 was performed. Morphological evidence is presented for the role of adhesion molecules in the initiation and maintenance of hepatic granuloma formation. The chemokine monocyte chemoattractant protein-1 was expressed in the granuloma and in hepatic artery branches. From these data, it is concluded that adult S. mansoni worms positively modulate schistosomal hepatic granuloma formation in vivo. Adhesion molecules and chemokines play important roles in schistosomal granuloma formation.

Topics: Animals; Antigens, Helminth; Collagen; Concanavalin A; Cricetinae; Disorders of Sex Development; Egg Proteins; Fibronectins; Granuloma; Immunohistochemistry; Integrin alpha4beta1; Integrin alpha6beta1; Integrins; Intercellular Adhesion Molecule-1; Laminin; Liver Diseases; Lymphocyte Function-Associated Antigen-1; Male; Mice; Mice, Inbred Strains; Plasmodium berghei; Protozoan Proteins; Receptors, Lymphocyte Homing; Schistosomiasis mansoni; Sex Factors; Spleen

Schistosomiasis causes pathology in an estimated 200 million individuals. Clinical disease is caused by a complex immunopathologic response to the parasite ova, which are deposited in the host tissues. This immunopathologic response is caused by T lymphocytes which express the high-affinity IL-2 receptor (IL-2R). DAB389IL-2 is a diphtheria toxin-IL-2 fusion toxin protein which functionally inactivates or kills cells which bear the high-affinity IL-2R. DAB389IL-2 has been used in man to suppress IL-2R-dependent immune reactivity. Therefore, we reasoned that DAB389IL-2 might suppress immunopathology in schistosomiasis. In these studies we assessed the in vitro and in vivo effects of DAB389IL-2 on the development of immunopathology in murine schistosomiasis. DAB389IL-2 suppressed IL-2, lectin mitogen (Con A), and soluble Schistosoma mansoni egg antigen-induced lymphocyte proliferation and in vitro granuloma formation. In addition, DA-B389IL-2 suppressed in vitro IL-2R expression. DA-B389IL-2 also suppressed the development of granulomas and collagen deposition in vivo in the livers of infected animals. Therefore, DAB389IL-2 may have potential for the targeted reduction of immunopathology due to schistosomiasis in man.

Topics: Animals; Antigens, Helminth; Cell Division; Concanavalin A; Diphtheria Toxin; Epitopes; Granuloma; Immunosuppressive Agents; Immunotoxins; Interleukin-2; Liver Diseases, Parasitic; Lymphocyte Activation; Mice; Mice, Inbred C57BL; Receptors, Interleukin-2; Recombinant Fusion Proteins; Schistosomiasis mansoni

Mice infected with Schistosoma mansoni mount focal granulomatous responses around each ovum that deposits in the liver and intestinal wall. The granulomas ultimately destroy the ova while absorbing the released toxic, injurious agents. The granulomas contain T cells and other cell types, all of which are under control. For example, T lymphocyte proliferation in situ within the granulomas is probably restrained by various regulatory mechanisms. Granuloma eosinophils make VIP, and granuloma T cells have VIP receptors. Yet, the function of VIP within the granulomatous response is unknown. We studied the effect of VIP on granuloma and splenic T cell proliferation in response to Con A or soluble egg antigens (SEA). [3H]Thymidine incorporation was used to assess the rate of proliferation. VIP decreased Con A- or SEA-induced, T lymphocyte proliferation. Suppression of proliferation was most evident for T cells stimulated submaximally with mitogen or antigen. Since T lymphocyte proliferation in response to antigen or mitogen requires soluble lymphokines, we investigated the capacity of VIP to alter the expression of several lymphokines as a possible mechanism for mediating suppression of T cell proliferation. VIP decreased IL-2 production, but did not effect IL-5 or IFN-gamma release. The effect of VIP on IL-2 production was dependent on the presence of a CD4+ T lymphocyte subset. VIP could no longer modulate lymphocyte proliferation if exogenous rIL-2 was added to the cultures. The addition of neutralizing anti-IL-2 mAb, but not anti-IL-4 mAb, substantially decreased granuloma lymphocyte proliferation in response to antigen or mitogen. This suggested that granuloma T cell proliferation required endogenously produced IL-2. These findings suggest that VIP may help modulate granuloma T cell proliferation through regulation of IL-2 production.

Topics: Animals; CD4-Positive T-Lymphocytes; Concanavalin A; Enterotoxins; Female; Granuloma; Interleukin-2; Lymphocyte Activation; Mice; Mice, Inbred CBA; Recombinant Proteins; Schistosoma mansoni; Schistosomiasis mansoni; Spleen; T-Lymphocytes; Vasoactive Intestinal Peptide

In murine schistosomiasis, granulomas form around ova deposited in the liver and intestines of infected mice. The granulomas have eosinophils that produce vasoactive intestinal peptide (VIP) and T cells that display VIP receptors. IL-5 is a lymphokine important for the development and maturation of eosinophils. It seemed plausible that VIP, released from eosinophils, may interact with lymphocyte VIP receptors and modulate IL-5 production as part of a feedback regulatory circuit. Thus, we determined whether granuloma T cells make IL-5 and whether VIP modulates IL-5 production. Isolated granuloma cells enriched for T lymphocytes spontaneously released IL-5. Culture of these cells in the presence of VIP increased IL-5 secretion. Spleen cells were also studied. Spleen cells from infected mice did not spontaneously release IL-5 or express IL-5 mRNA and VIP did not stimulate these resting spleen cells to produce this IL. However, these cells did express IL-5 mRNA and secreted IL-5 in response to Con A or soluble egg Ag. VIP could not appreciably modulate IL-5 release when cells were cultured with VIP and the Ag or mitogen. Spleen cells washed free of Con A ceased IL-5 secretion within 24 h. These preactivated splenic T cells resumed vigorous IL-5 secretion in response to either Con A or VIP. Yet only Con A prominently induced IL-5 mRNA expression. VIP was an effective stimulus at concentrations equal to or above the kDa of the VIP receptor on both splenic and granuloma T cells (10(-8) M). It is concluded that, in murine schistosomiasis, VIP invokes IL-5 release from activated T cells that are not undergoing immediate TCR stimulation.

Topics: Animals; Antigens, Helminth; Concanavalin A; Eosinophils; Female; Gene Expression; Granuloma; Interleukin-5; Lymphocyte Activation; Mice; Mice, Inbred CBA; RNA, Messenger; Schistosomiasis mansoni; Spleen; T-Lymphocytes; Vasoactive Intestinal Peptide

Recent studies indicate that egg granuloma formation in murine Schistosoma mansoni infection is associated with Th2-mediated immune responses. The present study was designed to analyze dynamically the Th1 and Th2 responses in S. japonicum-infected animals and compare them with the results seen with S. mansoni. C3H mice were infected with 10 to 20 cercariae of S. japonicum and sacrificed 3 to 22 weeks later. Spleen cells were stimulated with parasite antigens (egg and adult worm) or the mitogen concanavalin A. Interleukin-2 (IL-2), IL-4, IL-5, and gamma interferon (IFN-gamma) levels were measured in the culture supernatants by enzyme-linked immunosorbent assay (ELISA) or bioassays. Additionally, cytokine-producing cells were enumerated by ELISPOT. The results show that Th2 cytokine production, characterized by IL-4 and IL-5, represents the major response in the first month after egg laying begins, while the Th1 functions of IFN-gamma and IL-2 production are greatly depressed. However, by 22 weeks Th2 responses have diminished and IFN-gamma production in response to concanavalin A is apparent. IL-2 responses are minimal at all times. In vitro depletion of T-cell subsets indicates that CD4+ cells are the major subset responsible for production of IL-5 at 7 weeks of infection. These findings suggest that, as in the case of S. mansoni infection, S. japonicum-induced immunopathology is temporally associated with the host Th2 response, although other experiments indicate that IFN-gamma is also involved.

Topics: Animals; Antigens, Helminth; CD4-Positive T-Lymphocytes; Concanavalin A; Enzyme-Linked Immunosorbent Assay; Female; Kinetics; Lymphocyte Activation; Lymphokines; Mice; Mice, Inbred C3H; Schistosoma japonicum; Schistosoma mansoni; Schistosomiasis japonica; Schistosomiasis mansoni; Spleen

Previous work from this laboratory has indicated that murine memory T cells differ from virgin T cells in that the former are more resistant to agents that alter intracellular [Ca]i. We have used this difference to devise a method for separating virgin from memory T cells by centrifugation over an ionomycin-containing Percoll step gradient after brief exposure to 2 microM ionomycin. Under these conditions, those T cells that are most sensitive to ionomycin-induced changes in [Ca]i become more dense and therefore travel further into the Percoll/ionomycin gradient than cells that are more resistant to ionomycin. We show that the ionomycin-resistant cell population is enriched for cells that express high levels of Pgp-1 (CD44), and low levels of CD45RB, and thus appears to consist largely of memory T cells. Both CD4 and CD8 cells can be divided into Pgp-1hi and Pgp-1lo subsets in this way. Cells recovered from such a gradient and washed to remove the ionomycin appear normally functional, i.e., neither more nor less responsive to mitogens and costimuli than untreated cells. Limiting dilution methods show that the ionomycin-sensitive (virgin) subset contains most of the Con A-responsive precursors for cytotoxicity, and most of the cells able to produce IL-2 in responses to Con A or staphylococcal enterotoxin B. Ag-specific helper memory cells are, however, found predominantly in the ionomycin-resistant fraction of the spleen and draining lymph nodes of mice infected with Schistosoma mansoni. Changes in resistance to calcium signal development may represent a fundamental distinction between virgin and memory T cells, and could contribute to differences in activation requirements between these two cell subsets.

Topics: Animals; Antigens, CD; Calcium; CD4 Antigens; CD8 Antigens; Cell Separation; Centrifugation, Density Gradient; Concanavalin A; Cytotoxicity, Immunologic; Histocompatibility Antigens; Immunity, Cellular; Immunologic Memory; Ionomycin; Leukocyte Common Antigens; Lymphocyte Activation; Mice; Receptors, Lymphocyte Homing; Schistosomiasis mansoni; T-Lymphocyte Subsets; T-Lymphocytes, Cytotoxic

T-lymphocyte-adherent mononuclear cell interaction was analyzed in the vigorous and immunomodulated liver granulomas of Schistosoma mansoni-infected mice. Collagenase-dispersed granulomas contained 15% lymphocytes, 30% macrophages, 50% eosinophilis, and some neutrophils. Dispersed granuloma cells stimulated with concanavalin A or soluble worm egg antigens (SEA) did not proliferate unless plate-adherent, esterase-positive mononuclear cells were removed before culture. To analyze the granuloma adherent cell-mediated suppression, vigorous granuloma cell cultures partially depleted of adherent mononuclear cells were supplemented with indomethacin, catalase, superoxide dismutase, levamisole, and anti-murine alpha/beta interferon antiserum. In concanavalin A and SEA-stimulated cultures, only the addition of indomethacin or anti-alpha/beta interferon antiserum alleviated the adherent cell-mediated suppression of vigorous granuloma lymphocyte response. In contrast, these agents only minimally alleviated the suppressed response of SEA-stimulated, immunomodulated granuloma lymphocytes. Moreover, coculture of equal numbers of vigorous and immunomodulated granuloma cells partially depleted of adherent suppressor cells abrogated the alleviated response of vigorous granuloma lymphocytes. These findings indicate that, within the schistosome egg-induced vigorous granulomas, the adherent mononuclear cells exert regulation over lymphocyte responsiveness by alpha/beta-interferon and an indomethacin-sensitive, probably prostaglandin-mediated pathway. Within the immunomodulated granulomas, the adherent suppressor cell-mediated regulation of lymphocyte proliferation appears to play a lesser role.

Topics: Animals; Antigens, Helminth; Concanavalin A; Granuloma; Immune Tolerance; Indomethacin; Interferon Type I; Leukocytes, Mononuclear; Liver Diseases; Lymphocyte Activation; Lymphocytes; Mice; Mice, Inbred CBA; Schistosomiasis mansoni

These studies explore auto-anti-idiotypic mechanisms as potential regulators of the protective immune response against Schistosoma mansoni. Anti-idiotypic responses were stimulated by immunization of mice with lymphoblasts, bearing specific idiotypic receptors. These receptors were produced in vitro by stimulation of Ag-reactive T cells by soluble cercarial immunogen, keyhole limpet hemocyanin, or Con A. The animals were then exposed to irradiated cercariae, keyhole limpet hemocyanin, or SRBC. The results indicate that the soluble cercarial immunogen lymphoblast recipient mice demonstrated reduction in a number of parameters of their immune response to schistosome Ag, including resistance to challenge by parasites. These changes were immunologically specific. Anti-idiotypic antibodies and anti-clonotypic T cell reactivity was demonstrated in the lymphoblast immunized mice. The suppression of reactivity in LBM was mediated by Lyt-1-, L3T-4-, and Lyt-2+ lymphocytes. These studies suggest that idiotypically dependent pathways might be important for the regulation of resistance to schistosomiasis.

Topics: Animals; Antibodies, Anti-Idiotypic; Autoantibodies; Concanavalin A; Epitopes; Hemocyanins; Immunity, Cellular; Immunity, Innate; Immunoglobulin Idiotypes; Larva; Lymphocyte Activation; Mice; Mice, Inbred C57BL; Phenotype; Schistosoma mansoni; Schistosomiasis mansoni; T-Lymphocytes

Antigen- or mitogen-stimulated CD4+/CD- lymphocytes produced factors able to induce normal human platelets into cytotoxic effectors toward the young larvae of Schistosoma mansoni. The neutralization by monoclonal anti-IFN-gamma antibody of the induction of the platelet killer effect, the presence of IFN-gamma in the CD4+/CD8- lymphocyte supernatant, and, finally, the direct inducer effect of recombinant IFN-gamma clearly demonstrated that IFN-gamma was one of the factors responsible for the induction of platelet cytotoxic functions.

Topics: Adult; Blood Platelets; Concanavalin A; Cytotoxicity, Immunologic; Humans; Interferon-gamma; Larva; Lymphocyte Activation; Lymphokines; Schistosoma mansoni; Schistosomiasis mansoni; T-Lymphocytes

The lymphoproliferative blastogenic responses to mitogens, PHA and Con A, and to schistosome-derived antigens. S. mansoni worm and egg, were tested in 35 schistosomal patients and 10 healthy controls. Of the former group, 18 patients had intestinal mansoniasis and 17 had mansoniasis with hepatosplenomegaly. The test was repeated 2 weeks and 1 and 2 months after treatment with praziquantel. The delayed intradermal test for schistosomiasis was performed on 25 of the schistosomal patients and was repeated 1 month after treatment. Statistical analysis of results of lymphoproliferative blastogenic responses showed no significant differences between the control and the two schistosomal groups in response to mitogens. The group with intestinal mansoniasis responded significantly to both schistosomal antigens, compared to the control and hepatosplenic groups. Their proliferative responses showed a significant rise 2 weeks after treatment, then a gradual drop at 1 and 2 month intervals. The hepatosplenic group responded significantly to worm antigen before treatment; their proliferative responses to both schistosomal antigens showed a significant rise 2 weeks after treatment and remained raised thereafter. No relationship was established between either of the two schistosomal groups for age, intensity of infection or positive delayed intradermal reaction.

Topics: Adolescent; Adult; Antigens, Helminth; Child; Concanavalin A; Humans; Immunity, Cellular; Lymphocyte Activation; Middle Aged; Phytohemagglutinins; Praziquantel; Schistosoma mansoni; Schistosomiasis mansoni

Antibody and lectin binding characteristics of Schistosoma mansoni schistosomula maturing in vivo and in vitro were quantitatively assessed and compared in order to investigate the basis of the reduced surface antigenicity of host derived larval schistosomes. Quantitative indirect immunofluorescence assays showed that schistosomula recovered from mice at 24 h and 5-10 days post infection bound low or insignificant amounts of a variety of anti-schistosome antibodies including those from chronically infected and radiation attenuated cercariae-vaccinated mice, a vaccinated rabbit and rabbits hyper-immunized with non-living larval and adult schistosome antigen preparations. In contrast, parasites maturing in vitro continued to bind highly significant levels of each of these antibody preparations until at least 10 days post transformation. To investigate the basis of the decreased surface antigenicity of parasites maturing in vivo, 6-day-cultured parasites were injected intravenously into mice and recovered from the lungs at various times thereafter and examined for their ability to bind both anti-parasite and anti-host antibodies. After 30 min in vivo, cultured schistosomula exhibited a significantly decreased capacity to bind anti-parasite antibodies and concanavalin A (Con A), and by 16 h had lost their binding sites for fucose binding protein (FBP) as well. That this reduction in antigenicity was due to shedding of surface antigens was suggested by the observation that the reduced ability of these parasites to bind anti-parasite antibodies coincided closely with the loss of 125I-labelled surface proteins. Furthermore unlike 6 day schistosomula which had developed wholly in vivo, 6-day-cultured parasites recovered after 30 min in vivo failed to bind anti-host antibodies suggesting that in these organisms parasite antigens were not masked by host molecules. These data argue that surface antigen shedding may explain the reduced surface antigenicity of schistosomula developing in vivo. While this surface modulation apparently occurs independently of host antigen uptake, it is dependent upon an as yet unidentified host factor.

Topics: Animals; Antibodies; Antigens, Helminth; Antigens, Surface; Concanavalin A; Epitopes; Fluorescent Antibody Technique; Larva; Lectins; Mice; Mice, Inbred C57BL; Plant Lectins; Rabbits; Schistosoma mansoni; Schistosomiasis mansoni; Soybean Proteins

The induction of schistosomulicidal activity of peritoneal macrophages by concanavalin A-stimulated supernatants from long-term T-cell clones and by interferon-gamma (IFN-gamma) was investigated in detail. Optimal conditions of in vitro macrophage activation by T-cell clone supernatants were established. Macrophages from 13-week S. mansoni-infected mice responded to lymphokine activation as well as resident macrophages from uninfected mice. IFN-gamma was shown to play an essential role in induction of schistosomulicidal macrophage activity: recombinant IFN-gamma at high concentration could induce schistosomula killing, and an anti-IFN-gamma antiserum inhibited the induction of schistosomulicidal activity by T-cell clone supernatants. Our data also indicate that macrophage activation could be obtained by IFN-gamma in synergy with other lymphokines in the supernatant of long-term T-cell clones. Macrophages from mice injected with T-cell clone supernatants were primed in vivo and triggered to kill schistosomula in vitro in the presence of lipopolysaccharide (LPS). The data demonstrate that lymphokines produced by T-cell clones and, in particular, IFN-gamma can participate in the activation of schistosomulicidal macrophages.

Topics: Animals; Clone Cells; Concanavalin A; Interferon-gamma; Lipopolysaccharides; Lymphocyte Activation; Lymphokines; Macrophage Activation; Macrophages; Mice; Mice, Inbred C3H; Mice, Inbred DBA; Schistosoma mansoni; Schistosomiasis mansoni; T-Lymphocytes

We investigated the role of T cell-derived lymphokines for macrophage activation in vivo. We show for the first time that macrophages from casein-pretreated mice can be primed in vivo by intraperitoneal injection of immune interferon (IFN-gamma) and can be triggered by lipopolysaccharide (LPS) in vitro to kill schistosomula of S. mansoni. Similar results were obtained for the activation of tumoricidal macrophages. Injection of casein-pretreated mice with concanavalin A (Con A)-induced supernatant of a long-term T cell clone containing IFN-gamma and macrophage cytotoxicity inducing factor 2 (MCIF2), however, induced macrophage activation in vivo without further addition of LPS in vitro. These experiments show that macrophages can be activated by lymphokines in vivo. In addition, the data suggest that a combination of IFN-gamma with MCIF2 might be more effective than IFN-gamma alone. These data may be relevant for the strategy of treating cancer and infectious diseases with lymphokines.

Topics: Animals; Concanavalin A; Cytotoxicity, Immunologic; Female; Immunity, Cellular; Interferon-gamma; Lymphokines; Macrophage Activation; Macrophages; Male; Mice; Mice, Inbred DBA; Schistosomiasis mansoni; T-Lymphocytes

Eosinophil chemotactic activity in sera from mice undergoing an acute stage of schistosomiasis japonica and mansoni was examined. Eosinophilotactic activity in the serum was dependent on the dose and time of infection. Eosinophilotactic activity in sera from S. japonicum-infected mice was higher than that from S. mansoni-infected mice when they were compared at the comparable dose and time of infection. After gel chromatography on Sephadex G-200, eosinophilotactic activity in sera from mice infected with 30 cercariae of S. japonicum for 5 weeks was detected in the high molecular weight component. On the other hand, when sera from mice infected with 30 cercariae of S. japonicum for 8 weeks was chromatographed through Sephadex G-200 columns, eosinophilotactic activity was segregated into high (greater than 455,000) and low (less than 13,000) molecular weight components. High molecular weight ECF in sera from mice infected with 30 cercariae of S. japonicum for 8 weeks had high affinity to Con A, and was stable to heating or pronase digestion, but was sensitive to periodate oxidation, indicating its polysaccharide or glycoprotein nature. This high molecular weight ECF could be adsorbed by, and eluted from immunoaffinity beads coated with rabbit IgG anti-S. japonicum adult worm antibody. Thus, at least some part of circulating high molecular weight ECF would be derived from adult parasites.

Topics: Animals; Chemotactic Factors; Chemotactic Factors, Eosinophil; Chromatography, Affinity; Chromatography, Gel; Concanavalin A; Electrophoresis, Polyacrylamide Gel; Male; Mice; Mice, Inbred BALB C; Molecular Weight; Schistosomiasis; Schistosomiasis japonica; Schistosomiasis mansoni