Biomedical subjects

H E Jacobse-Geels

Publications and source records attributed to H E Jacobse-Geels.

6 recordsLinked to original sources

PubMed1986

Virion polypeptide specificity of immune complexes and antibodies in cats inoculated with feline infectious peritonitis virus.

Immune complexes purified from sera and ascitic fluids of cats after inoculation with feline infectious peritonitis (FIP) virus contained proteins and proteolytic fragments of the peplomer, nucleocapsid, and envelope polypeptides; in addition, host proteins were demonstrated in the immune complexes. Free (uncomplexed) antibodies against the 3 classes of virion polypeptides were detected and quantitated; the weakest and latest response was directed against the peplomer protein. Immunofluorescence titers showed the best correlation with the antibody response directed against the envelope polypeptides. Differences in reactivity were not found between sera and ascitic fluids from the same animals and between seropositive healthy cats and cats which had died of FIP. Humoral antibody and hypergammaglobulinemia showed a linear correlation, but the wide variation in antiviral titers at a given concentration of gamma-globulin indicated that additional (autoimmune) reactions occur during the pathogenesis of FIP.

Animals↗

PubMed1983

Expression of feline infectious peritonitis coronavirus antigens on the surface of feline macrophage-like cells.

Growth of feline infectious peritonitis virus in a continuous feline cell line is described and evidence for the macrophage-like character of these cells is presented. Under one-step growth conditions, cytopathic changes and giant cell formation were observed 12 h after infection; more than 99% of the virus remained cell-associated 15 h after infection. Viral proteins at the surface of infected cells were detected by immunofluorescence. The exposed antigens were localized on four proteins with molecular weights of 225.5K, 175K, 138K and 25K using radioiodination followed by immunoprecipitation. Another viral polypeptide of 44K (the nucleocapsid protein) was only labelled when the cell membranes had been disrupted. Expression of viral antigens on the cell surface may be a significant factor in the immune pathogenesis of feline infectious peritonitis.

Animals↗

PubMed1982

Antibody, immune complexes, and complement activity fluctuations in kittens with experimentally induced feline infectious peritonitis.

Humoral changes were studied in 6 specific-pathogen-free kittens during experimental infection with feline infectious peritonitis virus. Although the incubation period and the duration of the disease differed widely, a similar pattern of rectal temperatures, serum complement values, circulating immune complexes, and antibody titers was found for all kittens during the last 15 to 20 days of life. Antibody formation started 8 to 13 days before death and was accompanied by the appearance of circulating immune complexes with subsequent increased concentrations of complement followed by complement depletion. The data are discussed as evidence for an immune complex pathogenesis of feline infectious peritonitis.

Animals↗

PubMed1980

Isolation and characterization of feline C3 and evidence for the immune complex pathogenesis of feline infectious peritonitis.

Infections of cats with feline peritonitis (FIP) virus are usually inapparent but may lead to fatal polyserositis. We have recently advanced the hypothesis that immune complexes play an essential role in the pathogenesis of the condition. To support this hypothesis, the role of the third component of complement in FIP was investigated. In the present paper, the isolation of C3 from normal cat serum and some of its physical and immunologic properties are described. The final protein had an apparent m.w. of 185,000 and was composed of 2 polypeptide chains with m.w. of 128,000 and 71,000, respectively. When tested against whole cat serum, an antiserum raised in rabbits against purified C3 recognized only 1 protein whose identity with C3 was established. With the aid of this antiserum, depositions of C3 in renal glomeruli of FIP-affected cats were demonstrated by immunofluorescence. Their localizaton coincided with that of deposited IgG, thereby supporting the concept of an immune complex pathogenesis of FIP.

Animals↗

PubMed1979

Histamine 2 receptor-mediated immunomodulation in the mouse. I. Immunomodulation by the H2 agonist tolazoline.

Tolazoline, a drug used in the treatment of hypertension, has been described as a typical H2 agonist. In this study possible immunomodulating properties of tolazoline were investigated. A single injection of tolazoline 1 day before immunization caused an effect on delayed hypersensitivity that depended on the antigen dose. The response to 10(5) and 10(6) sheep red blood cells (SRBC) was decreased, whereas the response to 10(9) SRBC was enhanced. Administration of tolazoline 4 days after immunization predominantly affected the humoral response. The IgM response was inhibited in favour of the IgG response. Low doses of tolazoline, given to animals simultaneously with the elicitation for delayed hypersensitivity, lead to a more severe inflammation. The possible involvement of suppressor cells and vessels in tolazoline action is discussed. The application of tolazoline in the immunotherapy of human cancer is suggested.

Animals↗

PubMed1978

Evidence for the involvement of corticosterone in the ontogeny of the cellular immune apparatus of the mouse.

The effects of corticosterone deprivation in the cellular immune system of the mouse have been studied. Adrenalectomy was performed from three weeks after birth; at an earlier age oral administration of aminoglutethimide phosphate (AGP) had to be used. Three effects could be recognized: (1) Adrenalectomy or AGP treatment, at any age studied, resulted in an enhanced delayed hypersensitivity (DH) to sheep red blood cells (SRBC). This effect has previously been ascribed to monocytes. (2) An altered T lymphocyte distribution was observed as consequence of early adrenalectomy or continuous AGP administration. The lymph nodes were depleted whereas the thymus was increased in size and blood-leucocytes increased in number. This effect appeared reversible on restoration of adrenal function. (3) Irreversible damage to the cellular immune system following early AGP intake was observed in DH after recovery of the adrenal function. As corticosterone is the principal glucocorticoid produced by mice the effects described under (2) and (3) may be ascribed to this hormone. Our results suggest that thymic involution during life, is at least partially, under adrenal control.

Adrenal Glands↗