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Biomedical subjects

D J Stechschulte

Publications and source records attributed to D J Stechschulte.

At least 55 records · Page 3Linked to original sources

Variable severity of glomerulonephritis in inbred rats infected with Trypanosoma rhodesiense. Correlation with immunoglobulin class-specific antibody responses to trypanosomal antigens and total IgM levels.

Five strains of inbred rats (ACI, BUF, F344, WF and WL) were infected with Trypanosoma rhodesiense and killed at 28 days for renal pathology and serological studies. The BUF strain demonstrated the most consistent and severe glomerulonephritis, accompanied by high titer IgM antibodies to trypanosomes and high total IgM levels. The WL strain demonstrated mild glomerulonephritis but prominent PAS (+) intracytoplasmic inclusions in proximal convoluted tubules, accompanied by low titer IgM antibodies and slightly elevated total IgM levels. All strains had low to medium titer IgG1 and IgGa antibodies to trypanosomes. Serial serologic studies in BUF rats showed peak titers of IgM, IgGa and IgG1 antibodies to trypanosomal antigens at 10 days. Immune complexes as measured by a C1q binding assay were elevated at 10 days, 3 days following the first detectable antibody responses, and remained so through the 30th day.

Animals↗

Nonspecific suppressor cell function in atopic subjects.

The status of concanavalin A (Con A)--nonspecific suppressor cell function and histamine-receptor--carrying mononuclear cells in 19 allergic and 27 nonallergic individuals was investigated. No differences were detected between the two groups with respect to suppression by Con A--activated suppressor cells of polyvalent Ig biosynthesis, IgG secretion, or mitogen-induced proliferative responses. Histamine-receptor--carrying cells of the allergic subjects were numerically equal to those of the nonallergic subjects. Mononuclear cells from the allergic group, however, required a higher dose of histamine than did those for the nonallergic group to induce suppression in vitro (p less than 0.02 for 10(-4) M histamine and p less than 0.05 for 10(-3) M histamine). Plasma from the allergic group contained higher levels of histamine activity (p less than 0.05). Plasma from either allergic or normal groups did not affect histamine activity in vitro. There are no apparent functional abnormalities of antigen-nonspecific mononuclear cells in the allergic patients with respect to non--IgE-mediated in vitro parameters. The demonstrated dysfunction of histamine-receptor--carrying cells could be attributed to high levels of circulating histamine that could result in receptor modulation in vivo. More work is needed to clarify the status of antigen-nonspecific and antigen-specific suppressor cells that regulate IgE biosynthesis in allergic states.

Adolescent↗

Proliferative glomerulonephritis, hypocomplementemia, and nucleic acid antibodies in rats infected with Trypanosoma rhodesiense.

Host immunologic responses were studied in Sprague-Dawley rats infected with a human isolate of Trypanosoma rhodesiense. Retro-orbital sinus bleedings were obtained on days 0 and 14 and at 21 or 28 days. Infected and control rats were sacrificed on day 21 or 28 of the infection. Mild glomerulitis, as assessed by increased cellcularity and/or widening of the mesangial region, was apparent in 6 of 7 infected animals. Finely granular deposits of IgM and IgGl were found in most glomeruli with less prominent deposits of IgGa and IgA. Focal cortical mononuclear interstitial infiltrates were present in 2 of 7 rats. Subepithelial or mesangial electron dense deposits were present in the glomeruli of infected rats. Hypocomplementemia was present by day 21 and involved both the classical and alternative pathways of complement activation. Antibodies to native DNA and single-stranded RNA were present by day 21. These studies indicate the feasibility of studying trypanosomal glomerulonephritis in rats and will provide a convenient model for detailed immunologic and morphologic investigation of host immune responses in African trypanosomiasis.

Animals↗

Malakoplakia: evidence for monocyte lysosomal abnormality correctable by cholinergic agonist in vitro and in vivo.

We studied monocyte function in a case of malakoplakia in an attempt to characterize the immune defect in this condition. Our patient's intracellular cyclic-GMP levels were abnormally low (mean +/- S.D. of 0.17 +/- 0.05 pmol per 10(7) malakoplakia cells, versus 0.79 +/- 0.12 in normals) p less than 0.001). After phagocytosis, his monocytes failed to release beta-glucuronidase. In the bactericidal assay, incubation of the patient's monocytes with Escherichia coli allowed growth of 542 +/- 46 colonies, normal monocytes allowed 95 +/- 22 (p less than 0.001). The percentage of monocytes with large lysosomal granules was 23 +/- 4 in the patient and 4 +/- 2 in normal controls. After in vitro incubation of the patient's cells or in vivo treatment with bethanechol chloride, the cyclic-GMP levels, bactericidal ability and lysosomal granules of the cells returned to normal levels. Low levels of cyclic-GMP could impair lysosomal function and bacterial killing in this condition. Cholinergic agonists correct the in vitro abnormalities and are beneficial in vivo.

Adult↗

Rheumatoid nodulosis: another cuase of juxtarticular nodules.

A case of rheumatoid nodulosis and the difficulties encountered in its diagnosis are presented. A positive rheumatoid factor, biopsy proved involvement of the synovium and bone at the second metacarpophalangeal joint, and regression of nodules and mild arthritic symptoms with gold therapy, supported the diagnosis of a rheumatoid disease variant. The relationship of the disease to rheumatoid arthritis, gout, and xanthomatosis is discussed.

Fingers↗

An eosinophil leukocyte chemotactic factor of anaphylaxis.

The capacity of actively or passively sensitized guinea pig lung to react with antigen to release a factor specifically chemotactic for eosinophil leukocytes (ECF-A) has been demonstrated. The release of ECF-A was also accompanied by the elaboration of both histamine and SRS-A and the appearance of all these mediators exhibited a similar response in terms of the time course of passve sensitization, the effect of antigen dose, the time course of release, divalent cation dependence and enhancement by the presence of succinate or maleate. Decomplementation by the administration of purified cobra venom factor had no effect on the antigen-induced release of ECF-A from actively or passively sensitized lung fragments. When fragments of guinea pig lung were passively sensitized with fractions of guinea pig 7S IgG, only the IgG(1)-containing fractions prepared tissue for the antigen-induced release of ECF-A. Histamine, SRS-A, bradykinin, serotonin, and the prostaglandins PGE(1), PGE(2), and PGF(2alpha) were not eosinophilotactic per se; neither was ECF-A detected following the incubation of these agents with sensitized lung in the absence of antigen. Both eosinophilotactic activity and SRS-A survived extraction in 80% ethanol and evaporation to dryness. SRS-A, however, withstood boiling in alkaline solution for 20 min, whereas ECF-A activity was abolished by this procedure. SRS-A and ECF-A could also be separated by gel filtration. ECF-A activity was completely recovered following its passage through a column of Sephadex G-25 and had an estimated molecular weight of between 500 and 1000. On the basis of size and a formation mechanism independent of the complement system, ECF-A is distinguishable from a previously described complement-dependent eosinophilotactic factor (ECF-C). Thus, ECF-A represents a hitherto undescribed agent which selectively attracts eosinophil leukocytes.

Anaphylaxis↗