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At least 37 records · Page 2Linked to original sources
PubMed1980

Action of gold salts in some inflammatory and immunological models.

Several gold salts were compared in kaolin-induced rat paw oedema, u.v. erythema in guinea pigs, delayed type hypersensitivity and humoral immunity in mice, and adjuvant-induced arthritis in the rat. In the latter the additional parameters of serum gold and copper levels and lysosomal enzyme activity were determined. In addition, the in vitro inhibition of several lysosomal enzymes derived from mouse macrophages was studied. The gold compounds examined were aurothiomalate, aurothioglucose, triethylphosphine gold chloride (SK & F 36914) and its glucopyranoside derivative (SK & F D-39162), triphenylphosphine gold chloride and sodium gold chloride dihydrate. SK & F 36914 and SK & F D-39162 has significant activity after oral dosage upon paw kaolin and u.v. erythema in rats and guinea pigs, respectively. Gastric swelling also occurred. In Wistar rats, adjuvant arthritis was little affected by the gold salts but in the Lewis rats there was suppression. In both strains there was less elevation in serum copper levels with treatment by SK & F 36914 and SK & F D-39162, but not by aurothiomalate. None of the compounds had any measurable effect on delayed hypersensitivity or humoral antibody levels in mice. The in vitro activities of cathepsin B1 and cathepsin D were inhibited by all the gold compounds. Reactivity of gold compounds with glutathione and cysteine in vitro was dependent on compound solubility and the nature of the gold ligand. Considerable differences exist between the profiles of activity for the different gold salts evaluated. These observations indicate that some gold salts do possess anti-inflammatory activity with a potency similar to that of indomethacin.

Animals↗
PubMed1982

Immunological model of epilepsy. Epileptiform activity induced by fragments of antibody to GM1 ganglioside.

Antibodies to GM1 ganglioside injected into the sensorimotor cortex of the rat induce recurrent epileptiform activity. We now find that the divalent F(ab')2 and monovalent Fab' fragments derived from antiganglioside IgG molecules are able to induce epileptiform seizures. This result supports the view that the binding of antibodies to ganglioside receptors in the synaptic membrane is sufficient in itself to initiate changes in membrane processes which lead to epileptiform spiking. These changes do not appear to be dependent on linking of ganglioside receptors or on the presence of serum factors such as complement.

Animals↗
PubMed1998

An immunological model connecting the pathogenesis of stress, depression and carcinoma.

Recently there has been considerable conjecture in the literature concerning a possible relationship between stress, depression and bereavement, and carcinoma. We shall propose a causal model in which the relationship between stress, depression and carcinoma is clarified. This relationship is grounded on dysregulation of the inflammatory cytokines in stress and depression. Stress is associated with increased expression of interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha), and reduced expression of IL-2, interferon-gamma (IFN-gamma), major histocompatability complex (MHC) class II molecules and natural killer cell activity (NKA). Depression is associated with elevated IFN-gamma and IL-1 beta, downregulated IL-2, and reduced NKA. Most organ-related carcinomas are associated with elevated TNF-alpha, which inhibits the activity of protein tyrosine phosphatase (PTPase), the enzyme that initiates activation of the MHC class I pathway. Sustained elevation of TNF-alpha inhibits the activity of PTPase which results in diminished expression of the MHC class I antigen on the cell surface and thus, malignant cells escape immune surveillance. Therefore, stress and depression can foster tumor progression by means of inhibiting the expression of MHC class I and II molecules and through the reduction of NKA.

Cytokines↗
PubMed1999

Pargyline conjugate-induced long-term activation of monoamine oxidase as an immunological model for depression.

We describe an animal model of long-term depression based on active immunization of albino rats against BSA-conjugated inhibitor of monoamine oxidase, antidepressant, pargyline. Immunization resulted in anti-pargyline antibody formation and significant activation of monoamine oxidase A in brain. Immunized rats demonstrated potent decrease of motor, orientation and exploratory activity, increase of the immobility time ("despair") in Porsolt test, as well as notable signs of fear and anxiety in elevated plus maze. The cognitive processes were not significantly affected: the speed of learning with negative and positive reinforcement was not diminished. Complex effect on craving for alcohol (long-term suppression after short-term increase) was also demonstrated. The long-term (more than 45 days) depression achieved in this model makes it potentially important tool for testing new antidepressant pharmaceuticals.

Animals↗
PubMed1988

Immunologic modeling of a 75-kDa malarial protein with carrier-free synthetic peptides.

A protein of 75 kDa is produced in large quantities by the human malarial parasite Plasmodium falciparum and is present on the surface of the merozoite, whose function is to infect erythrocytes. Based on nucleotide sequence coding for 40% of this protein, two nonoverlapping model peptides 13 and 19 residues long were synthesized, coupled to a keyhole limpet hemocyanin carrier, and used to immunize rabbits. Although both antisera had high titers of anti-peptide antibodies, only that raised against the 13-residue peptide showed good reactivity against the original protein. Although the 19-mer adopted the helical secondary structure predicted for the corresponding protein region, antisera against this peptide reacted with the native protein weakly or not at all. Concluding that the poor anti-protein reactivity was due to modification of lysine-containing epitopes by glutaraldehyde conjugation, we used a carrier-free 28-residue peptide presented as a 56-residue disulfide-bonded dimer to model the same region. This peptide, in contrast to the conjugated 19-mer, stimulated the production of IgG antibodies that reacted at high dilution with the authentic protein in immunoblots, ELISA, and radioimmunoprecipitation assays. These data indicate that large carrier-free peptides may be successfully used as immunogens. In addition, our results show that this strategy may greatly improve the ability of conjugation-sensitive peptides to stimulate antibodies reactive with the original protein and therefore has substantial practical application.

Animals↗
PubMed1999

Immunological models of type 1 diabetes.

Type 1 diabetes mellitus is a serious health problem that affects several million new people each year. Although it is recognized that type 1 diabetes results from an autoimmune destruction of the insulin-producing beta-cells in the pancreatic islets of Langerhans, its etiopathogenesis is still not well understood. A certain genetic phenotype seems to be required, but it is not sufficient per se to trigger diabetes development. Numerous studies have pointed to the role of infectious agents as important environmental factors in breaking 'self'-tolerance and triggering activation of autoreactive T cells. Activated T cells, in turn, destroy target cells harboring the corresponding tissue-specific self-antigen, causing organ damage and loss of function. Several theories have been proposed to explain how environmental factors can initiate and/or perpetuate autoimmunity towards pancreatic beta-cells.

Amino Acid Sequence↗
PubMed1987

Demyelinating disease: an immunological model for studies of neural antigens.

Studies have shown that the parent myelin basic protein (MBP) is a more potent antigen than its disease-inducing fragments. Based on equimolar ratios, 10-15 times more peptide is required to induce experimental allergic encephalomyelitis (EAE) with the same severity as that induced by the intact MBP. In this report, we show that 2 epitopes are required for EAE in Lewis rats; that which induces T cell-mediated immunity requires the expression of a B cell epitope for the development of full spectrum of clinical and histopathological signs of disease. Thus, the development of disease may be related to the magnitude of the humoral and cellular responses to particular B and T cell epitopes. Whether more than 1 epitope, over 30 of which have been located in the MBP, contribute to the development of MBP-induced disease is not clear; but what is clear is that the EAE-inducing peptide sequence, unlike the MBP, is restricted in terms of the number of recognizable epitopes.

Amino Acid Sequence↗
PubMed1999

A novel immunological model for the study of prostate cancer.

The Dunning R-3327 rat prostatic adenocarcinoma is a widely accepted model for in vivo experimental studies of prostate cancer. We have previously derived phenotypically distinct cell lines from a s.c. tumor resulting from the inoculation of the R-3327-5 subclone into Copenhagen rats. In this study, we report studies using a gelatin sponge model for the delivery of tumor cells and the retrieval of tumor-specific leukocytes responsive to different prostatic cell lines. S.c. preimplanted sponges were inoculated with tumor cells previously selected for differential properties of tumor formation and metastasis and examined for leukocyte content at time points of 1, 3, and 5 weeks after tumor cell inoculation. Cytospin and flow cytometric analyses revealed fewer tumor-associated leukocytes present in sponges inoculated with tumorigenic R-3327-5' and R-3327-5'B lines, with lesser sponge degradation, than in experiments with the nontumorigenic R-3327-5'A line, suggestive of a tumor cell-induced immunomodulatory mechanism. Morphological studies indicate an intermittent tumor growth pattern that gradually disappears in sponges inoculated with the nontumorigenic R-3327-5'A cells but a robust growth pattern in sponges inoculated with the tumorigenic cell lines. Cytokine analyses show the secretion of higher levels of active transforming growth factor-beta by the more invasive and metastatic lines. Total transforming growth factor-beta levels are higher in the epithelial, tumorigenic R-3327-5'B line. Additionally, the more tumorigenic lines secrete interleukin 10, a potent immunosuppressive molecule. In this report, we demonstrate the ability to retrieve viable leukocyte populations from a prostate tumor line bearing sponges, which offers an important model for further in vitro and in vivo manipulations and holds promise for testing adoptive immunotherapeutic strategies.

Adenocarcinoma↗
PubMed1984

The living skin-equivalent as a structural and immunological model in skin grafting.

The living skin equivalent is a tissue formed when self-assembled collagen fibrils are contracted by fibroblasts. The rate and extent of volume contraction is proportional to the number of cells incorporated into the lattice. The fibroblasts are biochemically active in the lattice, synthesizing collagen and adding it to the matrix. This compacted lattice provides a substrate allowing attachment of keratinocytes and the formation of a multilayered keratinized epidermis with a basement lamella. When a skin equivalent grafted to a recipient animal is wounded, it is capable of wound contraction and repair. Because of the simplified character of the skin equivalent it may offer a useful model for studying wound healing. During the initial healing of the grafted skin equivalent, fibroblasts from the skin equivalent move freely into the surrounding tissue. Karyotyping of fibroblasts grown from skin surrounding the skin equivalent graft shows that fibroblasts from the graft migrate at least 6-9 mm from the graft edge. At 3-6 mm from the graft edge about 50% of the fibroblasts present are of donor origin. Fibroblasts also migrate from allogenic skin grafts before these grafts are rejected. At 3-6 mm from the scar left by the rejected graft 36% of the fibroblasts are of donor origin 2 months after grafting. The skin equivalent model provides a well-defined system for studying transplantation reactions. Results obtained on persistence of allografted fibroblasts support our theory that in the rat, the fibroblast is antigenically neutral.

Animals↗
PubMedDate not supplied

[The rabbit's appendix: an immunological model applied to the study of epithelial immunity (author's transl)].

The rabbit's appendix is a pecular lympho-epithelial formation as it includes both areas of thymus-dependent lymphocytes (the interpolated sieved lamina) and non-thymus-dependent lymph nodes. The epithelium joining the intestine lumen and the lymphatic tissue contains cells that become permeable at the contact of lymphocytes. These "tranformed" enterocytes are crossed by antigenic molecules, bacteria, yeasts and evolutive forms of coccidia. Lymphocytes within--as well as reticular cells below the epithelium--catch large molecules, especially antigens, thus having a share in humoral immunity. Just as those of the intestine, the enterocytes of the appendix glandular area are informed at the level of the areas of epithelial mitosis and become resistant to certain infections such as coccidosis. This particular form of immunity we have named "epithelial immunity". Thick sections provide ultrastructural views physically showing information exchanges. Intercellular exchange by contiguous endoplasmic reticular canaliculi at the interface of two cells have thus been demonstrated. They have been as clearly observed between two epithelial cells at between two cells of connective origin and again between an epiethelial cell and a lymphocyte.

Animals↗