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Results for “Immunization, Passive”

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At least 127 records · Page 7Linked to original sources
PubMed2005

Meningoencephalitis associated with passive immunization of a transgenic murine model of Alzheimer's amyloidosis.

Immunization against the Abeta peptide reverses the pathologic and behavioral manifestations of Alzheimer's disease in murine models. Since active immunization is associated with an autoimmune meningoencephalitis in a subset of humans, passive transfer of anti-Abeta immunoglobulin is being pursued as a potentially safer alternative. We have identified cases of meningoencephalitis subsequent to peripheral and intracerebral passive immunization of Tg2576 mice. The vasocentric mononuclear infiltrate localized only to brain regions affected by Abeta amyloid deposits suggesting that the inflammatory reaction was Abeta specific. This report indicates that current passive immunization in humans should proceed with careful regard for autoimmune complications.

Alzheimer Disease↗
PubMed1992

A comparative study on the use of bovine and murine monoclonal antibodies for passive immunization in cattle.

In the present experiments the efficacy of murine and bovine monoclonal antibodies for passive immunization in cattle was compared. The in vivo immunoneutralization of pregnant mare serum gonadotrophin (PMSG) by murine and bovine antibodies after repeated administration was chosen as a model for this study. Results indicate that repeated injections of murine monoclonal antibodies against PMSG (mMCA) alone did not, or only to a small extent, elicit an anti-mouse immune response. The simultaneous administration of mMCA and PMSG resulted in relatively high levels of anti-mouse antibodies after the second injection, leading to a decrease in neutralizing activity of mMCA. The results suggest that the neutralizing activity of mMCA is inhibited more by anti-idiotypic than by anti-isotypic antibodies against mMCA. In vivo, the bovine monoclonal antibody against PMSG (bMCA) only partially neutralizes PMSG. After repeated administration of bMCA, either alone or in combination with PMSG, no anti-bMCA antibodies could be detected in our assay system. In addition, no change in plasma levels of bMCA and PMSG compared with levels after the first injection was observed. Although it has to be confirmed by further experiments whether our findings can be generalized, the present results suggest that for repeated passive immunization in cattle homologous antibodies are to be preferred above heterologous antibodies.

Animals↗
PubMed1987

Virus vaccine and passive immunization for the prevention of viral myocarditis in mice.

The effect of an inactivated virus vaccine and passive immunization was studied in an animal model of viral myocarditis. Encephalomyocarditis (EMC) virus was inactivated by 1:4000 formalin. Four-week-old CD-1 mice were injected subcutaneously and after 7 days intravenously with 0.1 ml vaccine. Seven days after the second vaccine, live EMC virus was inoculated intraperitoneally. None of ten mice with vaccine treatment died or showed myocardial lesions after challenge with EMC virus, whereas all ten mice without vaccine died 5-7 days after EMC virus inoculation and showed severe myocardial lesions. Hyperimmune rabbit serum, made by inactivated EMC virus, had a neutralizing antibody titer of 1:3000. Four-week-old BALB/c mice were injected intramuscularly with 1:10 dilution of hyperimmune rabbit serum in 6 groups (each, n = 10) on day -2, -1, 0, 1, 2, or 3, respectively, after inoculation with 10 plaque-forming units of EMC virus, and observed for 14 days. Eight mice infected with the virus without immune serum died and all ten mice showed severe myocardial lesions. No death or myocardial lesion was seen in mice with hyperimmune rabbit serum given on days -2 to 2. In this model, the virus vaccine prevented development of myocarditis, and passive immunization had a protective effect if given early after infection.

Animals↗
PubMed1978

Passive immunization with antisera to Streptococcus mutans in the prevention of caries in rhesus monkeys.

1) The immunological mechanism of protection against dental caries has been investigated by passive immunization with antisera to S. mutans in the rhesus monkey. 2) Passive immunization with separated IgG, IgM and IgA from sera of immunized monkeys supports the concept that IgG, unlike IgA or IgM antibodies are protective. 3) The role of cell-mediated immunity has been explored by the use of transfer factor. This showed that protection against dental caries can be elicited by passive transfer of whole immune serum and cellular immunity, but not by cellular immunity or immune serum alone. 4) The results of active and passive immunization suggests that immuno-regulation of T and B cell interactions plays an important part in the effector mechanism of opsonization, phagocytosis and killing of S. mutans.

Animals↗
PubMed1977

Humoral immune response to the heat-labile enterotoxin of Escherichia coli in naturally acquired diarrhea and antitoxin determination by passive immune hemolysis.

Acute- and convalescent-phase sera from 132 students attending a university in rural Mexico were assayed for antibody against the heat-labile enterotoxin (LT) of Escherichia coli by neutralization of LT activity in the Y-1 adrenal cell assay and by passive immune hemolysis of LT-sensitized sheep erythrocytes. The two titration methods produced comparable results with respect to antitoxin responses detected. An inverse relationship was found between acute geometric mean antitoxin titer and the occurrence of diarrhea associated with LT-producing E. coli, especially in newly arrived students from the U.S.A. A significant correlation (P less than 0.00 5) was found between a rise in antitoxin titer detectable by the passive immune hemolysis technique and diarrhea with LT-producing E. coli isolated. Thus, humoral antitoxin titers appear to be a useful indicator of immune status with respect to enterotoxigenic (LT) E. coli diarrhea.

Adult↗
PubMed1987

Passive immunization with monoclonal antibodies against herpes simplex virus glycoproteins protects mice against herpetic ocular disease.

The effects of passive immunization with specific monoclonal antibodies against herpes simplex virus glycoproteins gB, gC, gD, and gE on the course of herpetic keratitis, survival and the establishment of latency in an outbred mouse model are described. A total of nine monoclonal antibodies were tested in these experiments. Passive immunization at 24 or 48 hours post-inoculation had little effect on the severity of the initial epithelial infection of the cornea, but blocked dissemination of the virus to the central nervous system and periocular tissues and prevented development of blepharitis, iritis and stromal keratitis. Additional studies are needed to characterize these monoclonal antibodies in greater detail, and to define the mechanism of these protective effects.

Animals↗
PubMedDate not supplied

Passive immunization versus adhesion of Bordetella avium to the tracheal mucosa of turkeys.

Three-week-old turkeys were passively immunized with convalescent serum or treated with tracheal washings from turkeys infected with Bordetella avium. Western blot analysis of the convalescent serum and tracheal washings revealed at least two bands of interaction with outer membrane protein preparations of B. avium. Adherence of B. avium in vivo to tracheal mucosa was determined and compared in treated and untreated turkeys. Passive immunization with convalescent serum reduced adherence of B. avium to the tracheal mucosa in a dose- and time-dependent manner. Adherence was significantly inhibited (P less than 0.01) when turkeys were treated intravenously with 1 ml of undiluted serum either 1 or 6 hours previously. Incubation of the bacterial inoculum with convalescent tracheal washings or application of the washings to tracheal segments before adherence determination in vivo resulted in a significant (P less than 0.01) decrease in adherence. These results indicate that adherence of B. avium to tracheal mucosa is inhibited by substances (antibody) present in both serum and tracheal secretions of convalescent turkeys.

Animals↗
PubMed1992

Time course of hepatitis A virus antibody titer after active and passive immunization.

To investigate the antibody titer necessary to prevent hepatitis A virus infection, either 15 or 7.5 mg/kg of immune serum globulin was injected into 10 antihepatitis A virus negative volunteers and their serum antihepatitis A virus titers were observed for 28 wk. In addition, antibody titers were observed for 96 wk in a phase 1 clinical trial of a hepatitis A vaccine. The two studies were then compared to assess the immunogenicity of the vaccine and the persistence of the antibody. Serum-neutralizing antibody titers that were greater than or equal to 4 (considered as positive) persisted for 18 wk and 14 wk after the injection of 15 and 7.5 mg/kg of globulin, respectively. Hepatitis A virus vaccine recipients showed adequate neutralizing antibody titers, with the groups receiving 1, 0.5 and 0.25 micrograms/dose showing titers of 4(5.5), 4(4.7) and 4(4), respectively, at 18 mo after the third inoculation. These findings suggested that effective blood antibody titers were likely to be retained in the 1.0 micrograms or 0.5 micrograms/dose groups for at least several years. Moreover, the serum antihepatitis A virus titers demonstrated by a modified radioimmunoassay changed in parallel with the neutralizing antibody titers in the volunteers injected with globulin.

Adult↗
PubMed1995

Effects of passive immunization against parathyroid hormone-related protein: PTHrP is the responsible factor in mediating hypercalcemia in the Walker carcinosarcoma 256 rat model.

The Walker carcinosarcoma (WCS) 256 is a well-characterized rat model of humoral hypercalcemia of malignancy (HHM). We addressed the question of whether parathyroid hormone-related protein (PTHrP) is the factor responsible for mediating HHM in this model. WCS 256 cells were subcutaneously implanted in female rats. We examined the plasma at days 0, 2, 4, 6, and 8. The midregional PTHrP measured by radioimmunoassay (RIA) and the plasma calcium increased significantly. Measuring PTHrP by a two-site immunoradiometric assay (IRMA) showed comparable results. There was a strong positive correlation between plasma calcium and midregional PTHrP (r = 0.85, p < 0.0001). A strong positive correlation between tumor weight and both midregional PTHrP (r = 0.83, p < 0.0001) and plasma calcium (r = 0.87, p < 0.0001) was also found. After surgical removal of the tumor at day 5, both plasma calcium and plasma PTHrP levels fell to within the normal range. Ip administration of native polyclonal antiserum against PTHrP(53-84) led to a significant decrease of plasma calcium. Extracted WCS 256 tumor showed 5-fold increased levels of midregional PTHrP compared with liver. Immunohistochemistry and Western blot were positive for PTHrP. RNA from the WCS 256 tumor was positive for PTHrP whereas liver tissue RNA was negative. WCS 256 cells grown in vitro also secreted PTHrP into the medium. We conclude that PTHrP is synthesized and secreted by WCS 256 and that PTHrP is the factor responsible for mediating hypercalcemia in the WCS 256 rat model.

Analysis of Variance↗