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Biomedical subjects

S Koshikawa

Publications and source records attributed to S Koshikawa.

At least 91 records · Page 5Linked to original sources
PubMed1987

Effect of sodium cromoglycate on an experimental model of IgA nephropathy.

Recently, we reported on an experimentally-induced model of IgA nephropathy in mice, in which the lesions were very similar to those found in human IgA nephropathy. This model was achieved by long-term oral immunization and intravenous injection of colloidal carbon in order to achieve reticuloendothelial (RES) dysfunction. In this paper, we investigated the effects of sodium cromoglycate (SCG), an anti-allergic agent, on this model. Mice were treated with a small amount of colloidal carbon three times to block the RES, in addition to receiving oral administration of lactalbumin, as a food antigen. Open renal biopsy was performed at 18 weeks after the RES blockade, and mice were divided into 2 groups. One group received orally administered SCG and lactalbumin [SCG(+)], and the other group received lactalbumin only [SCG(-)] from 19 to 30 weeks. At 30 weeks, all mice were sacrificed for histopathological observation of renal tissue and blood sampling. IgA nephropathy had developed in all mice of the SCG(-) group, but had not developed in 7 out of the 9 mice in the SCG(+) group, at 30 weeks. Serum IgA levels obtained on sacrifice were significantly higher in the SCG(-) group. It was concluded that SCG effectively inhibited, not only the onset, but also the progression of IgA nephropathy in our original model. The effective mechanisms of this drug may act to suppress the local immunity produced through sensitization of gastrointestinal mucosa by food antigens.

Animals↗
PubMed1986

Modification of immune complexes deposited in glomeruli in tissue sections treated with sulfonized gamma-globulin.

The modification of immune complexes (IC) deposited in renal tissues obtained from the patients with membranous nephropathy (MN), membranoproliferative glomerulonephritis (MGPN), systemic lupus erythematosus (SLE), IgA nephropathy, and rabbits with chronic serum sickness was investigated by an immunofluorescent technique. Following treatment with sulfonized gamma-globulin (S-GG), IgG deposited in glomeruli disappeared. However, the deposition of other immunoglobulins, complement and protein A, and the fixation of guinea pig complement were not influenced in spite of the disappearance of IgG deposits. In addition, deposition of antigen was demonstrated following treatment with S-GG in experimental animals. By elution with 0.02 M citrate buffer at pH 3.2, the intensity of these deposits markedly decreased or disappeared completely. The data suggests that the phenomena of IgG-dispersion from IC following the treatment with either S-GG or acid buffer are essentially different. The exact mechanisms of selective IgG-dispersion by the treatment with S-GG are unclear, but an antiglobulin activity (rheumatoid factor or anti-idiotypic antibody) of deposited IC may play an important role.

Animals↗
PubMed1986

Experimental IgA nephropathy in mice.

Based on a hint from an immunological abnormality found in human IgA nephropathy, we tried to make up an experimental IgA nephropathy in mice by administration of a food antigen for a long term with blockage of the reticuloendothelial system (RES). Mice were divided into three groups: group 1 had oral administration of lactalbumin (Lalb); group 2 was treated with colloidal carbon to block RES in addition to oral administration of lactalbumin; and group 3 was treated only with colloidal carbon for RES blockage. Renal biopsy was performed at 18 weeks after RES blockage and the animals were sacrified at 30 weeks for histopathological observation of renal tissue. The deposits of IgA in the mesangial area were not found in animals of groups 1 and 3 but 17.6% of group 2 at 18 weeks following RES blockage, also in no animal of group 1 but 91.7% of Group 2, and 15.4% of group 3 at 30 weeks. They were highly frequent in group 2 at 30 weeks (p less than 0.001). Observation under electron microscope also revealed a significant increase (p less than 0.001) of mesangial dense deposits in group 2 at 30 weeks, and formation of large dense deposits similar to those seen in human IgA nephropathy. Through observation over a period of time, an increase of mesangial IgA deposition and histopathological aggravation were confirmed. Serologically, serum level of IgA was significantly higher in group 2 (p less than 0.001) and was correlated with the intensity of mesangial IgA deposition. It was concluded that lesions very similar to human IgA nephropathy could be prepared in mice by inducing a dysfunction of RES as continuous oral immunization.

Animals↗