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Therapy of rapidly progressive glomerulonephritis with immunosuppressive agents.

Rapidly progressive glomerulonephritis is a kidney disease leading to sudden and definitive damages of the renal parenchyma and progressive impairment of its function until the complete failure. Histological findings of the changes are characterized with dominant glomerular lesions with crescentic formations. Early and intensive immunosuppressive therapy with pulse doses of steroids (Solumedrol 1.5 to 2.5 g), followed by Prednisolone 1 mg/kg every other day and cytostatic drugs (cyclophosphamide 1-2 mg-kg/every other day) discontinues the processes of specific and non-specific inflammation in the kidney and could enable regeneration of the kidney tissues with favorable outcome of the disease. Immunosuppressive therapy should be gradually lowered after two months, and applied for at least three to six months.

Acute Kidney Injury↗
PubMed1990

The effect of immunosuppressive agents on the induction of nuclear factors that bind to sites on the interleukin 2 promoter.

Cyclosporin A (CSA), FK506, and glucocorticosteroids all inhibit the production of lymphokines by decreasing lymphokine gene expression. Previous experiments have defined six different sites that may contribute to the transcriptional control of the interleukin 2 (IL-2) promoter, and for each, active nuclear binding factors are induced upon mitogenic stimulation. While dexamethasone markedly blocks the increase in IL-2 mRNA in stimulated human blood T cells, we found that the drug does not block the appearance of factors that bind to the transcriptional control sites termed AP-1, AP-3, NF-kB, OCT-1, B site, and NF-AT. In contrast, both CSA and FK506 have similar effects: the drugs cause modest decreases in AP-3 and NF-kB, and markedly decreases in the activity of AP-1 and NF-AT. Therefore, CSA and FK506, while chemically different, seem to act upon a similar pathway that leads to IL-2 gene expression, whereas glucocorticoids do not affect this pathway.

Anti-Bacterial Agents↗
PubMed1989

Pharmacological properties of YM-11124, a selective immunosuppressive agent for cell-mediated immunity.

Effect of YM-11124 on cell-mediated immune responses, type I to type III allergic reactions and inflammatory reaction was determined in mice, rats and guinea pigs. YM-11124 inhibited picryl chloride- and methylated bovine serum albumin-induced delayed-type hypersensitivity reactions by the treatment during both the sensitization and the elicitation phases in mice. Bilateral adrenalectomy did not prevent the suppression of DTH response by YM-11124. YM-11124 significantly prolonged the survival time of allogenic skin grafts in mice. Furthermore, YM-11124 inhibited the passive Arthus reaction in guinea pigs and the reversed passive Arthus reaction in rats. However, YM-11124 did not affect the passive cutaneous anaphylaxis reaction in rats, Forssman shock in guinea pigs and paw edema in rats. These results indicate that YM-11124 suppresses not only cell-mediated immune responses (type IV allergic reactions) but also type III allergic reactions without influence on types I and II allergic reactions as well as acute inflammation.

Animals↗
PubMed1990

Effects of a new immunosuppressive agent, FK 506, on the efferent limb of the immune responses.

The effects of a novel immunosuppressant, FK 506, on the efferent limb of the immune response were studied in the experimental autoimmune uveoretinitis (EAU) in the rat, using two different treatment schedules. First, rats actively immunized with S-antigen were treated with FK 506 only after the onset of EAU. FK 506 (1 or 3 mg kg-1 day-1) reduced the intensity of EAU as compared to that of non-treated rats. Especially, a daily dose of 3 mg kg-1 completely suppressed further development of EAU. It is, therefore, suggested that FK 506 treatment is effective in suppressing the ongoing process of the immune response, even after the disease has been initiated. Second, FK 506 (0.3 mg kg-1 day-1) was given only to the recipient rats which received IRBP-sensitized lymphocytes. None of FK 506-treated recipients developed EAU, while all control recipients developed the disease approximately 4 days after the cell transfer. The immune responses of FK 506-treated rats in the two experiments were also significantly suppressed. The antibody levels to S-antigen, the antigen-specific proliferative responses of lymphocytes, and even the proliferative responses to Con A were markedly suppressed in the rats in which FK 506 was given only during the efferent limb of the immune response.

Animals↗