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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inbred rats were thymectomized, irradiated, and reconstituted with T cell-free bone marrow cells. Thymectomized-reconstituted (B rats) and control rats were infected with Schistosoma mansoni cercariae and the number of worms recovered was determined at various times after infection. The extent of immunosuppression was assessed by two criteria: 1) response to an injection of sheep erythrocytes (plaque assay, hemagglutination, hemolysis); 2) response to schistosome antigens (passive hemagglutination). Humoral responses to worm antigens were completely suppressed in almost all instances and anti-sheep erythrocyte responses showed a more variable but always very definite depression in B rats. The number of worms in B rats was about 4 times higher than in control animals at 5 weeks and about 3 times higher at 6 weeks. In a different experiment, rats were perfused at 4, 6, and 9 weeks after infection and the number of worms was found to be consistently higher in B rats, by a factor of about 2 at 4 weeks to a factor of about 4 or 6 at subsequent times. Although B rats had more worms than controls even at 9 weeks, a slow drop in their worm burden was noticeable with time in both experiments. Moreover, the size of worms in B rats was smaller than in controls and even 9-week-old worms failed to develop to normal size and appearance and could not be shown to produce fertile eggs. These experiments show a definite involvement of the immune system in the "self-cure" phenomenon, but may at the same time suggest that other non-immune mechanisms are involved in determining the pattern of S. mansoni infection in the rat.
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PMID:The course of Schistosoma mansoni infection in thymectomized rats. 77 68

It has been recognized that Schistosoma mansoni infection causes depression of T-cell responsiveness. In this study we have evaluated whether immunodepression associated to schistosomiasis could be reverted by specific treatment. T-cell immune response was assessed by means of intradermal tests using recall antigens in a group of 22 patients with hepatosplenic schistosomiasis, one year after treatment with oxamniquine and compared with a group of untreated hepatosplenic patients. Only 27% of treated patients presented complete anergy to all tested antigens, in marked contrast to 80% unresponsiveness showed by hepatosplenic patients without treatment. Although most of the treated individuals showed some response to the tested antigens, in some individuals this unresponsiveness still persisted after treatment. Anergy was not found in any normal individual of the control group. It was concluded that Schistosoma mansoni infected patients may recover their normal immune responsiveness after the elimination of the worm by treatment.
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PMID:Specific treatment of hepatosplenic schistosomiasis can increase T-lymphocyte reactivity. 184 33

The morphology of Schistosoma mansoni eggs in intestinal tissues (oograms), and egg hatching in faeces, were studied after parenteral administration of praziquantel (PZQ) to infected mice. PZQ was given parentally in doses of 60 mg kg-1 for one day, five days or 10 days. Eleven days after initiation of therapy, oograms from all groups receiving PZQ showed more dead eggs than controls; a dose response was also observed. Depression of faecal egg hatching occurred within 24 hours of PZQ administration. Our observations suggest that PZQ kills most S. mansoni eggs in host tissues when administered in higher doses than are routinely recommended for treatment of intestinal schistosomiasis mansoni. In order to reduce the lifespan of metabolically active eggs in sensitive tissues, prolonged courses of PZQ could be used when treating central nervous system schistosomiasis.
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PMID:Effect of praziquantel on the eggs of Schistosoma mansoni, with a note on the implications for managing central nervous system schistosomiasis. 251 14

Peritoneal exudate cells from mice infected with Schistosoma mansoni (S-PEC) can kill a small proportion of schistosomula in vitro in the presence of immune serum. S-PEC produce a low level of respiratory burst. However, schistosomula mortality in their presence is not reduced when exogenous antioxidants are added, suggesting that with S-PEC, oxidative killing may not be important. Hydrogen peroxide (H2O2) and superoxide production by S-PEC, and cells from Bacillus Calmette-Guerin (BCG) and thioglycollate (THGL) injected mice, nonspecifically stimulated with opsonized zymosan, were measured. Levels of H2O2 produced by S-PEC were significantly lower than BCG or THGL PEC, and were below the threshold for schistosomula killing. This correlated with lower levels of cell-mediated killing of schistosomula in vitro by S-PEC than by BCG-PEC. Superoxide levels, however, were similar between the 3 cell populations. It therefore appears that the efficiency of PEC to kill schistosomules in vitro correlates with H2O2 rather than superoxide levels. It was found that there was a sharp concentration threshold in H2O2 mediated killing of schistosomula. A depression in the levels of H2O2 produced may be a mechanism by which the parasite can partially evade the host immune system.
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PMID:Depression of hydrogen peroxide dependent killing of schistosomula in vitro by peritoneal exudate cells from Schistosoma mansoni infected mice. 253 85

Antigen antibody complexes are suspected to play a role in the pathogenesis of some of the lesions that result from schistosomiasis. To examine the effect of immune complexes on the immune system of mice experimentally infected with Schistosoma mansoni, we measured antibody-dependent cell-mediated cytotoxicity (ADCC) and complement-mediated serum hemolysis in normal and infected animals. ADCC activity in infected mice was depressed compared to control mice. However, preincubation of spleen cells for 24 h in medium followed by washing restored ADCC activity. This suggested that a soluble factor(s), presumably immune complexes, was bound to the Fc receptors with resultant block in ADCC activity and this was removed in vitro during the 24-hour preincubation. Furthermore, the complement activity of mouse serum was markedly depressed in mice infected for 3 or 6 weeks. Again, the presence of immune complexes could explain this depression since immune complexes bind complement. We attempted to confirm and extend these findings with an immunoperoxidase-staining technique using antibody to S. mansoni antigen. Most of the granuloma formations identified in portal tracts and intestinal mucosa were composed of macrophages and epithelial cells surrounding a central nidus of schistosome egg. In addition, schistosome antigen was seen diffusely bound to some of the lymphoid elements in the lamina propria and many of these cells appeared plasmacytoid. Furthermore, large amounts of schistosome antigen were sequestered in the medullary cords of the mesenteric lymph nodes and in the Billroth cords of the spleen. This suggests that the antigen is conveyed to the lymph nodes and the spleen through the systemic circulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parasitic modulation of host immune mechanisms in schistosomiasis. 311 52

The effect of neonatally initiated injections of anti-mu serum on immunity to reinfection with Schistosoma mansoni in the rat was investigated in vitro and in vivo. Anti-mu treatment resulting in a profound depression of immunoglobulin synthesis dramatically decreased immunity to reinfection assessed by worm recovery technique. Complement-dependent antibody, IgG2a antibody-eosinophil-mediated and IgE-macrophage cytotoxicity reactions were in parallel markedly reduced. These results show the prominent role played by antibody-dependent mechanisms in immunity to schistosomes in the rat.
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PMID:Effect of neonatal injection of anti-mu antibodies on immunity to schistosomes (S. mansoni) in the rat. 676 87

The immune responsiveness of mice infected with 90 cercariae of Schistosoma mansoni has been investigated. Post-infection kinetics of antibody responses, delayed hypersensitivity and mitogen responsiveness show that there are profound disturbances of these immunological parameters starting 2 weeks after the infection. Although the final outcome is immunodepression the S. mansoni infection can produce immunostimulation. We have observed differences in the kinetics of the depression of humoral antibody responses in two strains of mice. It seems that the worms and not the eggs are of major importance in determining the observed alterations of immune responsiveness.
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PMID:Modification of immune responsiveness in murine Schistosomiasis mansoni. I. Time course after cercarial exposure. 700 Jun 79

The response of hepatic and haemotopoetic functions to treatment with praziquantel was studied using healthy and schistosome-infected mice. Female CF1 mice harbouring an 18 week old infection with Schistosoma mansoni and healthy uninfected mice of the same age were orally treated with 1 x 250 mg praziquantel/kg. The respective uninfected controls received the vehicle only. Blood samples were taken one, five, 14 and 28 days after treatment. Parameters studied were: activity of GOT, GPT and AP, concentration of glucose, blood clotting time, haemoglobin content, erythrocyte and leucocyte counts, PCV and body weight. The data were analyzed to reveal the effect of the three independent variables involved: infection, treatment and time after treatment. Infection of mice with S. mansoni for 18 weeks resulted in a depression of body weight, in a decrease of plasma GOT activity and of PCV and in increases of plasma GPT and AP activities, leucocyte counts and clotting time. Plasma glucose concentrations remained unaffected. The effects of treament with praziquantel were confined to the infected group. Changes attributable to the variable time were also more pronounced or even restricted to the infected treated group. Treatment of infected mice with praziquantel resulted in a temporary elevation of plasma GOT and GPT activities on Day 1 after treatment. Values had returned to normal on Day 5. Treatment further resulted in a slight but prolonged elevation of AP activities, a high leucocyte count on Day 5 after treatment and a normalization of the underweight and anaemic state of the infected mice. The nature of the effects observed after treatment with praziquantel is discussed in the light of corresponding data on the effect of treatment with hycanthone and SQ 18.506 in schistosome infected mice and Mastomys. It is concluded that the changes observed can be regarded as secondary, reflecting host responses to damaged parasites and healing processes.
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PMID:Effect of praziquantel on clinical-chemical parameters in healthy and schistosome-infected mice. 743 2

Naive CBA/Ca mice and mice vaccinated with gamma-irradiated cercariae of Schistosoma mansoni were challenged percutaneously with normal cercariae and depleted of L3T4+ T helper cells through the administration of a specific monoclonal antibody. Three regimes were utilized to target known phases of parasite migration. The in vivo depletion of L3T4+ cells resulted in a significant reduction in immunity (up to 65%) in vaccinated/challenged mice, provided the monoclonal antibody was targeted towards skin-resident schistosomula. When antibody was targeted towards lung phase challenge larvae, however, there was a significant reduction in worm recovery, but no correspondingly significant reduction in vaccine immunity. In contrast, the administration of monoclonal to naive mice, via all three treatment regimes, had no effect on the primary schistosome worm burden. Histopathological studies complemented these worm recovery data. Skin tissue biopsied from vaccinated/challenged mice treated with monoclonal to L3T4+ T cells rarely showed the inflammatory foci which normally characterize untreated vaccinated/challenged mice. This was true when antibody was given either before challenge, or just after challenge, and correlated with the recorded depression in vaccine immunity. Lung tissue collected from monoclonal-treated vaccinated/challenged mice (for all three treatment regimes) exhibited no changes in morphology compared to that from untreated vaccinated/challenged mice. This was not altogether surprising since in the NIMR vaccine mouse model, the lungs represent a poor site for challenge attrition and appear normal in morphology with the exception of a few, small inflammatory reactions. When the monoclonal was given to naive/infected mice, there was no change in the morphology of the pulmonary tissue, as compared to corresponding untreated cohorts. Immunohistochemical studies revealed that Thy-1+ cells dominated the subdermal inflammatory foci of vaccinated/challenged mice. Of the T cells identified, the T helper subset was the most common, with T suppressor cells being only weakly represented, and in some cases not at all. The proportion of macrophages (Mac-1+) varied between reactions.
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PMID:The role of T cells in vaccine immunity in the murine model of schistosomiasis mansoni. 849 7

The biogenic monoamines, serotonin (5-HT), dopamine (DA) and L-dopa were measured using high performance liquid chromatography with electrochemical detection (HPLC-ED) in the extracts of the central nervous system (CNS) and plasma of uninfected freshwater snails, Biomphalaria glabrata, and in snails at 7, 14, 21 and 28 days postexposure (PE) to the miracidia of the human blood fluke, Schistosoma mansoni. Relative to age-matched uninfected snails, a general depression of biogenic amine levels was observed in the plasma (cell-free haemolymph) and the CNS of infected snails, especially during the latter phase of the prepatency period. Significant decreases were first observed in the CNS of infected snails beginning at Day 14 PE for DA and 5-HT and Day 21 PE for L-dopa. Parasite-exposed snails also exhibited an early and persistent suppression of plasma 5-HT concentrations, starting at 7 days PE and continuing throughout the infection test period. In order to determine the effect of 5-HT on reproduction and, thereby, establish a possible relationship between the observed parasite-induced reduction in 5-HT levels and parasitic castration, the effect of exogenous 5-HT on individual infected and uninfected B. glabrata was investigated. Repeated treatment with 10 microM 5-HT promoted both ovulation and oviposition in B. glabrata. Snails treated with 5-HT consistently layed more eggs than did sham-treated controls. Infected snails that were treated with 5-HT exhibited similar egg-laying rates as those of both serotonin-treated and untreated, uninfected snail groups, thus reversing the castrating effects of larval infection. These findings suggest that 5-HT acts as a stimulant for egg production in B. glabrata, and that parasitic castration may be due, at least in part, to larval-induced suppression of 5-HT in the snail's CNS and plasma during the course of infection with S. mansoni.
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PMID:Biogenic monoamines in the freshwater snail, Biomphalaria glabrata: influence of infection by the human blood fluke, Schistosoma mansoni. 875 45


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