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R H Cypess

Publications and source records attributed to R H Cypess.

At least 55 records · Page 3Linked to original sources

Immunological sequelae of Trichinella spiralis infection in mice: effect of viability and route of BCG administration on nematode-induced immunopotentiation.

Mice were infected with 200 Trichinella spiralis 22 days preceding administration of 4 times 10-6 viable or heat-killed BCG. The effect of the route of BCG administration on the subsequent delayed hypersensitivity response to old tuberculin was investigated by injecting the bacteria either intravenously, intraperitoneally, or subcutaneously. Animals of the various groups were tested for delayed hypersensitivity footpad responses 28 days after BCG inoculation. Infection with T. spiralis was found to potentiate the ability of mice to respond to both viable and heat-killed BCG. In the case of heat-killed BCG, this potentiation appeared to be route dependent, since it could not be demonstrated when the bacilli were injected subcutaneously.

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Immunological sequelae of Trichinella spiralis infection in mice: effect on the antibody responses to sheep erythrocytes and Japanse B encephalitis virus.

Immunosuppression of the antibody response to Japanese B encephalitis (JBE) virus and sheep erythrocytes (SRBC) was observed in mice infected with Trichinella spiralis. This suppression was paralleled by the presence of fewer antibody-forming cells to SRBC in the spleens of parasitized mice. Both primary and secondary complement-fixing antibody responses to JBE virus were suppressed, but the development of immunological memory was not affected. Parasitized mice demonstrated a normal blastogenic response to phytohemagglutinin and normal serum clearance rate of injected (125)I-labeled immunoglobulin G(2b), although the size of the extravascular fluid compartment was significantly increased. The data presented here and in previous reports suggest that sequential antigenic competition is a possible explanation for the humoral immunosuppression to heterologous antigens caused by T. spiralis infection.

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Effect of infection with Trichinella spiralis and BCG on thymic histology.

The histology of mouse thymic tissue was examined following infection with Trichinella spiralis and/or BCG. ICR/CD-1 mice were orally infected with 200 T. spiralis 56 days preceding intravenous administration of 4x10-6 viable BCG. Following assessment of delayed hypersensitive foot pad reactions to BCG, the mice were bled and sacrificed. The thymus was removed from each animal, fixed in 10% neutral buffered formalin, embedded in paraffin and cut in 4 mum sections. Examination of serial sections indicated that T. spiralis and T. spiralis-BCG infections induced distinct anatomical changes within the thymic cortex and medulla, which may be related to previously described functional alterations of the immune system.

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Failure of neutrophilia to increase the number of neutrophils entering a peritoneal exudate in mice.

Neutrophilia, produced by bleeding or by parasitic infection, did not result in a larger than normal number of cells migrating into endotoxin-induced peritoneal exudates. These results fail to support but do not disprove the concept that neutrophil loss from the blood may be controlled primarily by changes in the fractional turnover rate rather than by blood pool size. They indicate that the failure of exudate neutrophils to increase in proportion to blood neutrophils in patients with chronic myeloid leukemia may not be an abnormality as interpreted previously.

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Quantitative study of the effect of previous Trichinella spiralis infection on sarcoma 180 ascitic tumor formation in mice.

Tumor development in HaM/ICR mice inoculated intraperitoneally with Sarcoma 180 (S-180) can be easily quantitated by linear regression analysis of non-destructive measurement of total body mass. This procedure readily separated the postinoculation period into incubation and clinical phases. The former was dependent on S-180 dose, while the latter was not. Trichinella spiralis infection 28 days prior to S-180 challenge produced small but statistically significant increases in the length of both the incubation period and survival time, but did not affect the clinical phase. Administration of tumor cells 56 days followoing the helminthic infection had no detectable effect on any parameter of tumor development studied. The results are consistent with the hypothesis that T. spiralis infection temporarily altered the host reaction to S-180, possibly at the level of non-specific macrophage activity.

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Heligmosomoides polygyrus (=Nematospiroides dubius): the development of self-cure and/or protection in several strains of mice.

Strains of outbred (ICR/CD1 and S--W) and inbred (BALB/C and C57BL/6) mice vaccinated subcutaneously (SQ) with 500, 1,000, or 2,000 exsheathed Heligmosomoides polygyrus larvae developed varying levels of protection upon subsequent oral challenge with larvae. In contrast, the inbred C3H/HEJ strain failed to develop protection at any dosage level tested. ICR/CD1 mice vaccinated intraperitoneally with exsheathed larvae developed a high level of resistance but exhibited extensive adhesions of the viscera. When ensheathed larvae were used for vaccination, ICR/CD1 mice developed a moderate level of protection; but 1% of the vaccine dose was recovered in the intestine as adult stages. Both the inbred and outbred strains given multiple oral infections developed a protection response similar to that strain's response following parenteral vaccination. The specificity of this protection was demonstrated using various complex foreign antigens. In contrast, the self-cure response was observed only in the S--W strain.

Ancylostomatoidea↗

Immunological sequelae of Trichinella spiralis infection in mice. II. Potentiation of cell-mediated response to BCG after infection with Trichinella spiralis.

Mice were infected with 200 Trichinella spiralis 14 days after intravenous administration of 4 x 10(6) viable BCG cells. Individual groups were tested for delayed hypersensitive footpad responses at 14, 20, 29, 57, or 85 days after T. spiralis infection. An initial suppression in the 14-day test group was observed; however, mice tested at later time intervals exhibited potentiation of the 24-h footpad reaction to old tuberculin over that elicited by appropriate controls. This suggested that T. spiralis induces a potentiation of the cellular immune response to BCG. Adoptive transfer studies support the cell-mediated nature of the observed footpad reaction and indicated that the initial suppression was not due to physiological factors preventing the expression of the footpad swelling reaction.

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