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PubMedDate not supplied

Examination of neutrophil function in a rat model of decreased host resistance following burn trauma.

The high incidence of serious opportunistic infection following human burn injury has been well documented. Investigations of the mechanisms of this acquired susceptibility have demonstrated several defects in phagocytic defenses. An established rat burn infection model was modified for study of neutrophil function in animals with a 60% burn injury. These 350-g rats received a 35-ml saline resuscitation, and when not further stressed, 80% of the animals survived to healing. Burned animals were found to have decreased inflammatory responses to intraperitoneal injections of heat-killed Pseudomonas aeruginosa, Staphylococcus aureus, and sterile sodium caseinate. These reductions could not be explained by neutropenia. Prior immunization with heat-killed Pseudomonas did not improve the inflammatory response to homologous organisms injected intraperitoneally, but levamisole treatment did improve the inflammatory response. Epinephrine injection (intravenous) showed that burned animals have a markedly reduced proportion of marginated neutrophils but an increase in total peripheral neutrophil counts. The stress hormones corticosterone and catecholamines were elevated during times of decreased inflammatory responsiveness; additionally, neutrophils from burned animals had decreased adherence to nylon fiber. Serum from burned animals decreased in vitro adherence and chemotaxis of purified normal rat neutrophils.

Animals↗
PubMedDate not supplied

The comparison of therapeutic effects of atropine and pralidoxime on cardiac signs in rats with experimental organophosphate poisoning.

Organophosphate poisoning causes disturbances in cardiac conduction and potentially fatal severe cardiac rhythm abnormalities. This study investigated the cardiac effects of atropine and pralidoxime in the treatment of organophosphate poisoning in rats. Three groups of 10 adult male Wistar rats were anesthetized with an intraperitoneal injection of ketamine 100 mg/kg and xylazine 10 mg/kg and connected to a computerized electrocardiographic monitor. Each rat was then injected intraperitoneally with the pesticide dichlorvos 70 mg/kg. Sixty seconds after the injection, 10 rats were injected with saline, 10 with pralidoxime mesylate 20 mg/kg, and 10 with atropine 10 mg/kg. During the computerized electrocardiographic monitoring, each rat's heart rate and QT(c) intervals were recorded and analyzed as the injections were administered. The heart rates in all 3 groups did not differ before the dichlorvos was administered, nor at 60 seconds afterward, but in the atropine group, the time elapsed before the first decline in heart rate was significantly longer than that in the control group (P<.05). In addition, the interval before death was significantly longer in the atropine group than in either the control group or the pralidoxime group (P<.05 for both). The QT(c) was almost identical in each of the groups. Atropine has beneficial effects on the heart rate, prolongs the time before the heart rate declines, and delays death but has no effect on the QT(c) interval. Further research about the toxic effects of organophosphate compounds on myocardial cells is warranted.

Animals↗
PubMed1989

[The effects of biotin on the metabolism of ammonia and amino acids in urease-induced hyperammonemic rats].

The effects of oral and intraperitoneal administration of biotin in urease-induced hyperammonemic rats, as well as the influence of biotin deficiency, have been studied. Biotin deficiency was produced by feeding standard diet MF (Oriental Yeast Co.) supplemented with dry egg-white (egg-white group). Egg-white + biotin group had free access to 0.0014% of biotin solution at all time. Following an intraperitoneal injection of urease, 25 U/kg (B.W.), plasma ammonia levels in egg-white + biotin group were lower than in egg-white group, especially there was significance (p less than 0.05) at 8 hours after the urease injection. Similarly, plasma ammonia levels in biotin-injected rats, in which 1 mg of biotin had been injected intraperitoneally prior to the experiment, were significantly low compared with saline-injected controls at 4 and 6 hours after urease administration. Results of plasma amino acid analysis, 9 hours after the urease injection indicated that Fischer's molar ratio (Leu + Ileu + Val/Tyr + Phe) was significantly higher in the biotin-injected rats than the saline-injected control. It suggests that biotin might decrease blood ammonia by facilitating the detoxification mechanism as follow: L-glutamate + NH3----L-glutamine.

Amino Acids↗
PubMed1993

[N-acetylcysteine decreases functional and structural, ARDS-typical lung changes in endotoxin-treated rats].

Oxygen radicals and oxygen radical mediators derived from activated granulocytes are important components in the development of acute lung injury, namely the adult respiratory distress syndrome ARDS. N-acetylcysteine (NAC) is one important substance for endogenous production of reduced glutathion, which is known to be an intra- and extracellular reducing agent also found in lung tissue. We evaluated the effect of exogenous NAC on the endotoxin induced development and course of ARDS in rats. ARDS-like injury was induced in rats via intraperitoneal injection of Salmonella enteritidis endotoxin 30 mg/kg body weight. NAC or solvent was injected intraperitoneally 30 min prior to, at the time of and 30 min after injection of endotoxin respectively with 150 mg/kg body weight each dose. Endotoxin injection in rats resulted in 80% mortality within 72 hours, increased lung wet weight, severe ultrastructural lung damage as measured by histological methods. In isolated, ventilated, with physiological salt solution perfused rat lungs vasocontractility was severely blunted, lung albumin leakage was increased, thromboxane B2 (TXB2) and 6-keto-prostaglandin-F1 alpha (6-keto-PGF1 alpha) perfusate levels were increased. NAC treatment significantly improved survival of endotoxin treated rats, ameliorated structural lung damage, diminished lung wet weight and lung albumin leakage, lowered lung perfusate TXB2 and 6-keto-PGF1 alpha levels and slightly improved vasocontractility in isolated perfused lungs. Therefore, NAC significantly ameliorates ARDS-like lung injury in rats, when given in vivo.

Acetylcysteine↗
PubMed2002

Cisplatin-induced in vivo differentiation of human embryonal carcinoma.

OBJECTIVE: To investigate the differentiation of embryonal carcinoma (EC) by cisplatin, and the underlying mechanism, as untreated metastases of nonseminomatous germ cell tumours rarely consist of fully differentiated mature somatic tissues, but such mature metastases are more common after various treatments, including chemotherapy. MATERIALS AND METHODS: The TTSC-3 human testicular EC line heterotransplanted into nude mice was used as a target. After treating tumour-bearing mice with intraperitoneal injections of varying doses of cisplatin, the histopathology of the tumours was assessed and various gene expressions in the tumours determined by cDNA-array technology. RESULTS: When cisplatin at 1 mg/kg/week was injected intraperitoneally into TTSC-3-bearing mice, there was no effect on tumour growth. However, injecting cisplatin at 5 mg/kg/week induced a marked regression of the tumour. In contrast, cisplatin at 3 mg/kg/week had a modest inhibitory effect on tumour growth and induced tumour dormancy. Histological examination showed that 5 weeks after injecting cisplatin (3 mg/kg/week), primitive mesenchymal-like cells increased, and 10 weeks afterward cartilage and well-developed glands (teratoma) were apparent; at > 15 weeks afterward there were no EC cells visible. cDNA probes from reverse-transcribed mRNAs of TTSC-3 treated with cisplatin or saline for 10 weeks were compared to identify genes differentially expressed in cisplatin-treated TTSC-3. Of 1176 different human cDNA transcripts in cisplatin-treated TTSC-3, three genes (tumour necrosis factor receptor 1, caspase 8 and Apaf1), which are associated with apoptosis, were expressed markedly more than after saline injection. CONCLUSIONS: The intermediate dose of cisplatin inhibited tumour growth of EC by inducing differentiation and enhancing apoptosis-related gene expression. These findings suggest that cisplatin may play a significant role in the differentiation of EC in vivo.

Animals↗
PubMed1980

[The effect of immunoglobulins in experimental peritonitis (author's transl)].

We measured the influence of different drugs on mortality and lung weights in a well known and standardized peritonitis model in rats. The results are: 1. Intraperitoneal injection of immune globulin in high dosage had little effect on our parameters. High mortality and interstitial pulmonary edema were observed. 2. The same results followed injection of 20% human albumin. 3. All animals injected intraperitoneally with a modern antibiotic (Securopen) survived. Interstitial pulmonary edema was observed. 4. The combined injection of an antibiotic and immune globulin (Gamma-Venin) had the best results. None of the rats came down with a lung injection or died.

Animals↗
PubMedDate not supplied

Reducing malignant ascites accumulation by repeated intraperitoneal administrations of a Viscum album extract.

BACKGROUND: Malignant ascites is a major problem in the management of advanced stages of certain malignancies. The possibility of reducing the accumulation of ascites by intraperitoneal injections of a Viscum album extract (Iscador M) was evaluated. PATIENTS AND METHODS: Twenty-three patients, with end-stage malignancies of varying histology, requiring repeated peritoneal punctures, were eligible for analysis. The time-interval between the first two punctures was measured and defined as the baseline. Following each subsequent puncture, Iscador M 10 mg was injected intraperitoneally. The intervals between later punctures were compared to previous intervals. RESULTS: Following the first injection, the median time-interval between injections increased from 7 to 12 days, reaching 13 days after the second injection. No toxicity was observed. CONCLUSION: This phase II study suggests that installation of Iscador M into the peritoneal cavity may reduce the need for repeated punctures. A randomized trial is needed to confirm these promising preliminary results.

Aged↗
PubMed1995

Tumor necrosis factor mediates zymosan-induced increase in glucose flux and insulin resistance.

Intraperitoneal injection of sterile zymosan produces an inflammatory response ultimately resulting in multiple-organ failure. The purpose of the present study was to characterize the hormonal and metabolic alterations produced as a result of this nonbacterial nonendotoxic inflammatory agent and to determine whether these changes were mediated by enhanced production of tumor necrosis factor (TNF). Rats were injected intraperitoneally with either zymosan or saline and studied 18 h later. Under basal conditions, zymosan-injected rats were euglycemic but showed a 43% increase in hepatic glucose production and peripheral glucose uptake. The enhanced glucose flux in zymosan-treated rats was associated with elevations in plasma insulin (45%), glucagon (5-fold), corticosterone (2-fold), epinephrine (34%), and norepinephrine (115%). In vivo studies using 2-deoxyglucose (2-DG) demonstrated that the zymosan-induced increase in whole body glucose disposal resulted from an enhanced uptake by skeletal muscle (68%), diaphragm (3.7-fold), liver (144%), spleen (52%), and fat (133%). Under euglycemic hyperinsulinemic conditions, zymosan-treated rats exhibited both hepatic and peripheral insulin resistance, with the latter resulting from a decreased insulin-mediated glucose uptake by skeletal muscle, heart and diaphragm. Arterial TNF levels were increased by 1 h and remained elevated throughout the experimental protocol. Pretreatment of rats with a neutralizing anti-TNF antibody before zymosan prevented the elevation in basal glucose flux and attenuated the insulin resistance. We conclude that the inflammatory state induced by zymosan enhances basal glucose turnover and impairs insulin action and that these changes appear to be largely due to the enhanced endogenous production of TNF.

Absorption↗
PubMed2005

Protective effect of dietary azuki bean (Vigna angularis) seed coats against renal interstitial fibrosis of rats induced by cisplatin.

OBJECTIVE: We investigated the effects of azuki bean (Vigna angularis) seed coats (ABSCs), which mainly contain proanthocyanidins and dietary fibers, on the infiltration of macrophages and the progression of renal interstitial fibrosis induced by cisplatin (CDDP). METHODS: Male rats were divided into two groups: controls received intraperitoneal injections of saline and the other rats were injected intraperitoneally with 3 mg of CDDP per kilogram once a week for 5 wk. The CDDP-injected animals received one of four diets: 1) control diet (commercial diet only), 2) 0.5% red ABSC (RABSC) diet, 3) 2.0% RABSC diet, and 4) 2.0% white ABSC (WABSC) diet. The saline-injected animals were given the commercial diet. Five weeks after the final CDDP injection, macrophage kinetics and interstitial fibrotic areas were examined. RESULTS: The content of polyphenols in the RABSC (76.3 g/kg of plant material) was higher than that in the WABSC (18.1 g/kg). Proanthocyanidins were detected in the RABSC (20.4 g/kg) but not in the WABSC. Histologically, the fibrotic areas consisting of fibroblastic cells and mononuclear cells developed around the dilated or atrophic tubules in the corticomedullary junction in CDDP-treated rat kidney, whereas the extent and magnitude of damage were less in the WABSC- and RABSC-treated rats. In immunohistochemical analysis, ED1-positive macrophages in CDDP-treated rats showed a significant increase in number compared with the control. The number of macrophages in CDDP plus WABSC or RABSC groups was significantly smaller than that in CDDP-treated rats. In addition, the number of macrophages in the RABSC group was significantly smaller than in the WABSC group, indicating that ABSC, especially RABSC, prevented macrophages from infiltrating into areas of interstitial fibrosis. CONCLUSIONS: These results suggest that ABSC, especially RABSC, suppress the increase of infiltrating macrophages in the damaged kidney and may lead to amelioration of interstitial fibrosis. Based on the composition of ABSC, molecules such as proanthocyanidins and/or dietary fibers may be associated with the amelioration of renal damage.

Animals↗
PubMed1992

Immune responses to colophony, an agent causing occupational asthma.

BACKGROUND: Inhalation of fumes from heated colophony (pine resin) is a recognised cause of occupational asthma, although the mechanisms by which colophony produces symptoms are unclear and specific immune responses to colophony have not been reported in sensitised workers. A study was carried out to determine whether colophony is antigenic. METHODS: The immune responses to colophony were studied in C57BL/6 mice and Dunkin Hartley guinea pigs after intraperitoneal injection of colophony conjugated to bovine serum albumin (BSA) or human IgG by a mixed anhydride procedure. Colophony and dinitrofluorobenzene were also compared in an assay of dermal sensitisation. RESULTS: Mice immunised with the colophony conjugates produced antibodies which recognised conjugates of both BSA and human IgG irrespective of which had been used as the immunogen. Solutions of unconjugated colophony inhibited the binding of antibodies to the BSA-colophony and BSA-abietic acid conjugates, confirming that the antibodies recognised one or more components in the colophony. Portuguese colophony also abrogated the antigen binding of serum from guinea pigs immunised with the BSA-colophony conjugate. Spleen cells from immunised mice proliferated in the presence of the conjugates. Although there was some cross reactivity in these responses, it was not as marked as in the antibody assays. Unconjugated colophony failed to induce an immune response when injected intraperitoneally with adjuvant. Skin sensitisation could not be induced in mice by topical application, or by subcutaneous or intradermal injection of unconjugated colophony. CONCLUSIONS: Colophony components have the potential to act as haptens and an immune component could be involved in the pathogenesis of occupational asthma in workers exposed to colophony. Colophony is not readily immunogenic unless conjugated ex vivo to proteins.

Animals↗
PubMedDate not supplied

Magnesium sulfate treatment decreases N-methyl-D-aspartate receptor binding in the rat brain: an autoradiographic study.

OBJECTIVE: We determined the effect of peripherally administered magnesium sulfate on N-methyl-D-aspartate (NMDA) receptor binding capacity in various regions of the rat brain. METHODS: Three separate experiments were performed. 1) Six rats were injected intraperitoneally with 270 mg/kg of magnesium sulfate, followed by 27 mg/kg every 20 minutes for 4 hours; controls (n = 6) received saline. 2) Six rats received intraperitoneal injections of magnesium sulfate (270 mg/kg) every 4 hours for 24 hours, while six received saline. 3) Six rats received intraperitoneal magnesium sulfate (270 mg/kg) every 12 hours for a total of 2 weeks, and six received saline. Rats were subsequently perfused and sacrificed, and their brains were dissected, rinsed, and frozen. Cryostat sections were taken, labeled by in vitro [3H]-CGP 39653, assayed autoradiographically, and mounted on Ultrofilm for 4 weeks. Optical density measurements of binding on each section were performed using an image analyzing system. Eleven brain regions were sampled: 1, 2) frontal and occipital cortex; 3-7) hippocampus--CA-1, CA-3, stratum radiatum, stratum oriens, dentate gyrus; 8) thalamus; 9) hypothalamus; 10) caudate nucleus; and 11) cerebellum. RESULTS: The NMDA receptor binding density in the hippocampus was significantly higher than in all other brain regions in all three experiments. In experiment 1, there was no significant effect on NMDA receptor binding. However, prolonged systemic administration of magnesium sulfate for 24 hours resulted in significantly reduced [3H]-CGP binding in all brain regions sampled. After chronic magnesium sulfate administration (2 weeks), the [3H]-CGP binding was still reduced in the cortex and some regions of the hippocampus; however, there was no significant change in other regions. CONCLUSIONS: Peripheral treatment with magnesium sulfate results in a significant reduction in the NMDA receptor binding capacity in the rat brain. These results support the hypothesis that magnesium central activity is mediated, at least in part, via the NMDA receptor.

Animals↗
PubMedDate not supplied

Transfer of chromic chloride to embryonic mice and changes in the embryonic mouse neuroepithelium.

Transfer of CrCl3 to embryonic mice and changes in the embryonic mouse neuroepithelium associated with Cr-induced neural tube defects were studied. A single intraperitoneal injection of 51CrCl3 was administered on the 8th day of gestation and animals were killed at various intervals for measurements of radioactivity in the maternal blood and embryos. Radioactivity per gram of fetal tissues increased during the observed period, while those of maternal blood decreased. Pregnant mice were injected intraperitoneally with a single dose of CrCl3 (non-radioactive) on the 8th day of gestation. Animals were killed at specified times after injection and embryos were removed and examined histologically. At 4, 8 and 12 h after injection many pyknotic cells were observed on the neural plate, especially at 8 h after injection. These data suggest that CrCl3 may affect embryos directly and cause neural tube defects and that pyknotic cells on the neural plate may be an early pathological finding in cases of developing exencephaly.

Animals↗
PubMedDate not supplied

In situ evading of phagocytic uptake of stealth solid lipid nanoparticles by mouse peritoneal macrophages.

Stealth solid lipid nanoparticles (SSLN) were prepared and evaluated for the effect of evading phagocytic uptake by mouse peritoneal macrophages in situ. Fluorescent SSLNs were prepared by emulsion/evaporation with rhodamine B as the fluorescent marker and polyoxyethylene stearate as stealth agent in a stearic acid matrix. Macrophages were induced chemically through intraperitoneally injecting 1% sodium thioglycolate. After 4 days of cultivation, SSLNs suspension was injected intraperitoneally and phagocytosis taken out in situ. At definite time intervals, peritoneal fluid was drawn out and analyzed by flow cytometer. Maximum uptake by macrophages was observed at 2 hr after injection of nanoparticles. At all time intervals, phagocytic uptake of Solid lipid nanoparticles (SLNs) was better than SSLNs. Longer and dense polyethylene glycol chains led to reduced uptake by macrophages. Both SSLNs and SLN had uptake by macrophages to some extent, and the in situ model was suitable for evaluating interactions between cells and nanoparticles.

Animals↗
PubMed1985

Dextran sulfate-induced peritoneal lysophospholipase activity varies among mouse strains.

Lysophospholipase (LPL) activity resulting from the intraperitoneal injection of dextran sulfate (DS) was studied in different mouse strains. AKR/J and BALB/cByJ mouse strains showed decreased LPL levels when a low molecular weight DS was injected but increased LPL activity when high molecular weight DS was injected intraperitoneally. C57BL/6 mice had increased LPL activity with low molecular weight DS but decreased LPL activity with high molecular weight DS. All three mouse strains showed increased peritoneal-cell changes when injected with DS of a molecular weight of 79,000.

Animals↗
PubMed1988

Mouse cachexia induced by trehalose dimycolate from Nocardia asteroides.

Trehalose dimycolate (TDM) isolated from Nocardia asteroides induced in mice a severely wasted condition known as cachexia. Intraperitoneal injection of mice with five 10 micrograms doses of TDM in mineral oil at intervals of 2 d killed 90% of the animals within 26 d. Death followed a precipitous weight loss and an inflammatory process in the peritoneal cavity. When mice were injected intraperitoneally with a single 10 micrograms dose of TDM, 48 h later, they had begun to lose weight and exhibited extreme hypertriglyceridaemia and hypoglycaemia. Tumour necrosis factor (or cachectin) was detected in the plasma from animals injected with TDM. This cytokine released by mononuclear phagocytes may be involved in the induction of cachexia by TDM.

Animals↗
PubMed2001

Donor-derived soluble MHC antigens plus low-dose cyclosporine induce transplantation unresponsiveness independent of the thymus by down-regulating T cell-mediated alloresponses in a rat transplantation model.

BACKGROUND: In vitro, soluble MHC (sMHC) antigens modulate and induce apoptosis in alloreactive and antigen-specific T cells, demonstrating their potency to regulate T cell-mediated immune responses. However, their efficacy to regulate immunological responses in vivo remains unclear. Here, we report that repetitive intraperitoneal injection of recombinant Lewis rat-derived MHC class I antigens in Dark Agouti (DA) rats modulates alloreactivity. METHODS: RT1.A1 (Lewis derived) genes were cloned into mammalian expression vectors, and RT1.Aa (DA derived) genes were used to transfect a rat myeloma cell line. RT1.A1 molecules were injected intraperitoneally in DA recipients that subsequently underwent transplantation with Lewis-derived cardiac allografts. RESULTS: Soluble class I antigens were secreted by the transfected cells and were shown to be heterodimeric, peptide-loaded, and conformationally folded. Injection of donor-derived soluble MHC significantly reduced the ability of recipient animals to mount a cytotoxic T-cell response to donor-derived tissue. More interestingly, this treatment significantly prolonged donor-graft survival and allowed 60% of treated animals to develop graft tolerance (>120 days), when donor sMHC were combined with a single subtherapeutic dosage of cyclosporine. Thymectomy of recipient animals before transplantation did not interfere with induction of peripheral tolerance. CONCLUSIONS: Donor-derived sMHC are potential tolerogens for down-regulating the cytotoxic T-cell response of animals that undergo transplantation. Thus, these data provide for the first time a rationale for the application of directly injected sMHC in vivo to down-regulate immunological responses and aid the induction of graft tolerance.

Animals↗
PubMed2006

[Neurogenesis of hippocampus following pentylenetrazol-induced status epilepticus in developing rats and the effect of MK-801 on neurogenesis].

OBJECTIVE: This study aimed to determine whether pentylenetetrazol-induced status epilepticus (SE) can induce dentate granule cell neurogenesis in the developing rat and the effect of MK-801, a noncompetitive antagonism of N-methyl-D-aspartate receptor (NMDAR), on neurogenesis. METHODS: Two hundred and sixteen postnatal days 7, 14, 21 or 28 Sprague Dawley (SD) rats were involved in this study. Each age group consisted of 54 rats which were randomly assigned into a SE group, a SE + MK-801 group and a Normal control group (n=18 each). SE was induced by intraperitoneal injection of PTZ (80 mg/kg). The SE + MK-801 group was injected intraperitoneally with MK-801 (1 mg/kg) at 1 hr after SE episode. All rats were given 5-bromodeoxyuridene (BrdU) intraperitonealy to label newborn cells at 6, 13 and 27 days after seizures and then were sacrificed 24 hrs after BrdU injection. The immunohistochemistry method was used to measure the expression of BrdU, TuJl (betaIII tubulin), and glial fibrillary acidic protein (GFAP) in the dentate gyrus of hippocampus of rats. RESULTS: The number of the BrdU positive cells in the SE group was significantly higher than in the age-matched normal controls at 7 and 14 days after SE episode (P <0.05 or 0.01). Approximately 82.5% and 80.3% of BrdU-labeled cells in the SE and the Control groups were co-expressed TuJ1 respectively. MK-801 treatment decreased the BrdU positive cells compared with the SE group at 7 and 14 days after SE seizures (P < 0.01). On the 28th day after SE episode there were no differences among the three groups for the BrdU positive cells. CONCLUSIONS: PTZ-induced SE can increase the dentate granule cell neurogenesis in the developing rat. NMDAR plays an important role in neurogenesis following seizures.

Animals↗
PubMed1990

The effect of immunosuppressive and immunostimulatory treatment on experimental amoebiasis.

Immunosuppressive treatments consisting of ionizing irradiation or drugs were employed in inbred and outbred mice and in golden hamsters. Following treatment, mice were challenged intracaecally or intrahepatically with virulent, axenically-grown Entamoeba histolytica. Hamsters were challenged by intraperitoneal injection of the amoebae. Many of the experimental animals died of the combined effects of treatment and challenge. Mice remained essentially refractory to infection with E. histolytica regardless of the immunosuppressive means employed. Liver infection rates in treated and control hamsters were largely similar to one another, i.e. immunosuppressive treatment had no effect on resistance to infection. Our inability to alter the susceptibility of mice and hamsters to amoebic infection by suppressing components of the immune system does not enable us to draw any clearcut conclusions as to the effect of immunosuppression on human amoebiasis. Of the various immunostimulatory materials employed in hamsters, including polysaccharides, BCG and muramyl peptides, only glucan displayed protective capacity against infection with E. histolytica, making it an effective protective agent in an extracellular parasitic infection in addition to its published effectiveness in intracellular protozoal infections. Peritoneal cells extracted from hamsters injected intraperitoneally with E. histolytica seemed capable of reducing the infectivity of virulent amoebae after coincubation in vitro, as shown by reduced infection rates in challenged hamsters. Apparently polymorphonuclear cells, which constituted the vast majority of the extracted cells 24 hours after the stimulatory injection, can, under certain conditions, diminish the infectivity of E. histolytica.

Animals↗