Gitelman syndrome and glomerulonephritis.
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Antibodies, Bacterial↗
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Pancreatic pseudocyst in paediatric systemic lupus erythematosus.
Pancreatitis is a rare complication of paediatric systemic lupus erythematosus (SLE). We describe a child with severe form of SLE who initially developed acute pancreatitis, subsequently complicated by extensive pancreatic pseudocyst. The treatment and outcome are discussed.
Adolescent↗
Inflammatory myositis complicating hypocomplementemic urticarial vasculitis despite on-going immunosuppression.
We present a patient with previously diagnosed hypocomplementemic urticarial vasculitis syndrome, with skin, lung, and renal involvement, who presented with congestive cardiac failure. During the course of her hospitalization, she was also found to have profound proximal muscle weakness in both upper and lower limbs associated with raised creatinine kinase levels. A muscle biopsy was performed, which demonstrated evidence of an inflammatory myositis with vasculitis, which had returned despite on-going immunosuppression. This occurrence of a new autoimmune disease may well be an example of the "waste disposal" hypothesis.
Antirheumatic Agents↗
Adiponectin: systemic contributor to insulin sensitivity.
Adipocyte-specific secreted molecules, termed adipokines, have dispelled the notion of adipose tissue as an inert storage depot for lipids, and highlighted its role as an active endocrine organ that monitors and alters whole-body metabolism and maintains energy homeostasis. One of these adipokines, adiponectin (also known as Acrp30, AdipoQ, and GBP28), has gained significant attention recently as a mediator of insulin sensitivity. Many clinical reports and genetic studies over the past few years demonstrate decreased circulating levels of this hormone in metabolic dysfunction, such as obesity and insulin resistance, in both humans and animal models. Pharmacologic adiponectin treatments in rodents increase insulin sensitivity, although the primary site and detailed mechanism of action is yet to be determined. The phenotypes of adiponectin-deficient and transgenic adiponectin-overproducing animal models underscore the role of adiponectin in the maintenance of glucose and lipid homeostasis.
Adiponectin↗
Characterization of immune complex components by dot blot analysis.
A method is described for the characterization of immune complex components by dot blot analysis. After isolation by chromatographic techniques and precipitation with polyethylene glycol, immune complexes were dissociated in 0.1 M phosphate (pH 2) and bound to a nitrocellulose membrane in a dot blot unit. Biotinylated probes were then used to identify the following immune complex components: specific antigens, biologically active antibodies, antibody isotypes, antibody subclasses, antibody idiotypes, and rheumatoid factors. This nonradioactive procedure takes less than 2 h to perform and has been used to analyze immune complexes isolated from sera (rabbit and human) and synovial fluid (human).
Acids↗
Reconstitution of murine resident peritoneal macrophages for antibody-dependent cellular cytotoxicity by homologous serum Clq.
Mouse resident peritoneal macrophages (PM) were reconstituted in their response to activation for antibody-dependent cellular cytotoxicity (ADCC) for sheep erythrocyte targets (SRBC) by subhemolytic dilutions of homologous or autologous sera. ADCC-responsive inflammatory PM were largely unaffected in their activation by exogenous serum. Augmentation of resident PM for ADCC by homologous serum was correlated with the complement-activating potential of the mouse monoclonal anti-SRBC IgG isotype in that serum augmented IgG gamma 2a greater than IgG gamma 2b much greater than IgG gamma 1. The active component of mouse serum was heat-labile at 56 degrees C for 30 min and was present in both C5-deficient AKR and C5-sufficient homologous C3H mouse sera. Western blot analysis of the cell lysates for Clq confirmed that oil-elicited and thioglycollate-elicited inflammatory PM had greater levels of endogenous Clq than did resident PM which correlated with their innate responsiveness for ADCC activation. Depletion of Clq from serum by immunoprecipitation with IgG antibody to Clq or by ion exchange chromatography removed the active reconstituting activity for ADCC. Purified mouse Clq (0.4 microgram) partially replenished the ADCC augmenting activity of Clq-depleted AKR mouse serum. SRBC targets preopsonized with IgG gamma 2a and purified mouse Clq (0.075-5.0 microgram/ml) fully reconstituted the ADCC response of resident PM similar to homologous serum indicating that the major active component of serum was Clq. Thus resident PM with low endogenous levels of Clq were reconstituted for ADCC by the addition of exogenous Clq, whereas inflammatory PM with sufficiently high endogenous levels of Clq were not further enhanced by exogenous Clq. Our findings indicate that Clq may provide an essential second signal in concert with Fc receptor binding of IgG to initiate ADCC activation of macrophages.
Animals↗
Molecular cloning and characterization of the complementary DNA coding for the B-chain of murine Clq.
cDNA clones coding for the B-chain of murine Clq were isolated from a mouse macrophage library. The characterized clones include the total coding region plus a leader sequence. High homology was found with human Clq B-chain in the coding region (81%). Northern blot analysis of total RNA from different tissues of Balb/c mice showed one band of approximately 1.2 kb. The highest signal was found in RNA preparations of thioglycolate-activated peritoneal macrophages. The probe also hybridized with mRNA from spleen, thymus and heart. Extremely weak signals were found in liver, kidney, lung and intestine tissues.
Animals↗
Effect of canine surfactant protein (SP-A) on the respiratory burst of phagocytic cells.
Cells obtained from bronchoalveolar lavage, or neutrophils of peripheral blood of dog, were incubated with the canine surfactant-associated protein A (SP-A). A significant decrease of the production of superoxide anion was observed after subsequent stimulation with phorbol-12-myristate-13-acetate (PMA) as measured by the lucigenin-dependent chemiluminescence (CL). Several other proteins used for control experiments did not decrease lucigenin-dependent CL, indicating a specific effect of SP-A on phagocytes. Treatment of SP-A with collagenase prior to incubation with neutrophils destroyed the depleting effect on oxygen radical production of PMA-stimulated cells. We propose that SP-A acts as a regulatory factor of the respiratory burst of alveolar macrophages and neutrophils in the lungs. The inhibitory effect of SP-A is down-regulated by collagenase released from stimulated alveolar macrophages.
Acridines↗
Influence of pH on the detection of low- and high-avidity anti-dsDNA.
In 2 radioimmunoassays in use to detect antibodies to dsDNA, the Farr assay and the PEG assay, we observed inhibitory effects of normal human serum (NHS) on the DNA binding by SLE sera. This was found to be due by the fact that, during incubation at 37 degrees C, CO2, introduced in the incubation mixture by the serum, evaporates from the mixture. This results in increase in pH to values well above pH 8.0, which in turn leads to a decreased DNA binding by antibody. When SLE sera are tested at low dilution, this phenomenon may lead to false negative results. Proper pH control, by the use of buffers with a greater buffering capacity than PBS, completely prevented the observed inhibitory effects. However, under these conditions NHS bound significant amounts of DNA in both assays. The non-specific DNA binding by NHS was found to be heat-stable, but could be eliminated either by aerosil treatment of the sera or by addition of dextran sulphate to the incubation mixture. Lipoproteins and, to a lesser extent, the complement component C1q appear responsible for this non-specific binding. To avoid false negative results with SLE sera as well as non-specific binding by NHS, we propose the use of stronger buffers in combination with added dextran sulphate to the incubation mixture in both the Farr assay and the PEG assay.
Antibody Affinity↗
An enzyme-linked immunoassay for circulating immune complexes using solid phased goat Clq.
An ELISA procedure was developed for measuring circulating immune complexes (IC), using solid phased goat Clq. The use of purified Clq from this species significantly diminished the background uptake of the enzyme-labeled goat antibodies used in the assay, in comparison with Clq isolated from human, guinea pig or rabbit serum. The test specimen results are reported as micrograms equivalent (microgram eq)/ml of heat aggregated human immunoglobulin G (HAIgG), and are based on standard curves developed with this latter reagent for each assay. The 2 World Health Organization (WHO) reference preparations for immune complex determinations (HAIgG and a human tetanus antitoxin-toxoid immune complex) were assayed by this ELISA procedure, and the results obtained were in very good agreement with the WHO established values. All the reagents in the ELISA, including the lyophilized HAIgG standard and the solid phased Clq are stable for more than one year at 4 degrees C. The range of accurate quantitation in test serum is 2-500 micrograms/ml, when using a 1:100 specimen dilution. The total incubation is less than 2 h, with no preliminary preparation of test specimens. The average concentration of IC reactivity in 126 healthy adults was 6 micrograms eq/ml, and the normal upper limit was determined to be 12 micrograms eq/ml.
Adult↗
Exposure of binding sites for antibodies and concanavalin A on collagen by solubilization in hot urea. An immunoblot analysis.
The presence of urea during solubilization of collagenous samples for SDS PAGE had a marked effect upon mobility of collagenous polypeptides and upon binding of antibodies from certain rabbit antisera, antibodies from several human sera and binding of concanavalin A. When samples were solubilized with urea by heating at 100 degrees C the mobility of collagenous polypeptides was retarded relative to samples that had been heated without urea or exposed to urea without heating. Antibodies from the rabbit sera only bound on immunoblots to collagen that had been urea/heat-treated. Periodate oxidation and deglycosylation with trifluoromethanesulfonic acid abolished binding of the rabbit antibodies. The results indicate the presence of carbohydrate epitopes buried within collagenous polypeptides that are exposed by harsh denaturing conditions. Heating with urea appears to cause an unfolding of collagenous molecules beyond that produced by SDS solubilization without urea. These results underscore the necessity to pay close attention to conditions used to solubilize for electrophoresis samples that are subsequently used as targets for antibodies or other ligands.
Binding Sites↗
Circulating immune complexes in the seronegative spondyloarthropathies.
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Acute Disease↗
Elevation of serum beta 2-microglobulin levels during infectious mononucleosis.
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Adolescent↗
Identification of a low molecular weight, macrophage-derived chemotactic factor for fibroblasts.
Fibroblasts migrate in vitro in response to a variety of chemoattractants including cellular, humoral, and connective tissue components. This report describes a low molecular weight, macrophage-derived chemotactic substance for fibroblasts (MDCF-F). Thioglycolate-elicited peritoneal exudate cells were collected from mice 4 days postinjection. Platelets were removed and glass-adherent macrophages were selected in the absence of fetal calf serum. The macrophage culture medium was then tested for chemotactic activity for 3T3 mouse fibroblasts using a modified Boyden chamber. Chemotactic activity was observed in the macrophage medium after a 48-hr culture period and increased during the next 24 hr. The activity was sensitive to heat treatment at 56 degrees C for 30 min, could be effectively absorbed out of the culture medium by preincubation with 3T3 fibroblasts, and was not recognized by human fibroblasts. Molecular-sieve chromatography indicated a molecular weight below 10,000. This low molecular weight, macrophage-derived chemoattractant for fibroblasts may represent a rapidly diffusable substance involved in the recruitment of fibroblasts to sites of inflammation.
Animals↗
Interaction of fibronectin with DNA/anti-DNA complexes from systemic lupus erythematosus: role of activated complement Cl in modulation of the interactions.
Fibronectin (Fn) is an integral constituent of the endothelial cell surface and the basement membrane. The mechanism for binding DNA/anti-DNA complexes to Fn was examined in a solid-phase assay. In physiological buffer, a low-affinity binding of DNA was observed with Fn and optimal binding was seen at pH 6.5 and in the absence of Ca2+. Further, the interaction of DNA to Fn was inhibited when DNA was complexed to anti-DNA antibody. However, complement Clq mediated the binding of complexes to Fn at pH 7.4 and it was proportional to the extent of the dissociation of Cl. Cl inactivator (Cl-In) appeared to play a modulating role; whereas at low concentrations (Cl:Cl-In::4: less than 1) it enhanced the binding of complexes to Fn, higher concentrations inhibited the binding. Further, sera from patients with active systemic lupus erythematosus reacted with Fn, which was shown to be dependent on the presence of Clq and was minimally affected by DNase treatment of sera, indicating a relatively minor role of DNA in the direct binding of DNA to Fn. These findings support "circulating immune complex" hypothesis in the pathogenesis of lupus glomerular immune complex deposition disease.
Antibodies, Antinuclear↗
Desensitization of anaphylactic hypersensitivity specific for the penicilloate minor determinant of penicillin and carbenicillin.
A 68-yr-old man with a history of a morbilliform rash caused by intravenous penicillin required carbenicillin (CB) therapy for refractory Serratia marcescens septicemia. Skin testing showed a positive immediate skin test to the penicilloate minor determinant in the presence of negative tests to benzylpenicilloylpolylysine (BPL) and penicillin G (PG), as well as cross-reactivity between the penicilloate derivatives of PG and CB. True densensitization was accomplished by gradual administration of CB intravenously and was accompanied by a diffuse flush reaction. There was specific loss of wheal-and-flare reactivity as well as of specific serum reaginic antibody activity during the procedure, and there was no evidence of activation of serum complement. This case illustrates the usefulness of skin tests in the prediction and management of penicillin allergy and presents data pertaining to immunologic mechanisms involved in true desensitization.
Aged↗
Immune complex-mediated disease not a factor in patients on maintenance venom immunotherapy.
Although a serum sickness-like presentation has been reported as a sequela of Hymenoptera stings, the possible role of an immune complex-mediated pathologic condition in patients receiving regular venom immunotherapy has never been addressed. To evaluate this problem, 30 adult and 15 pediatric patients receiving regular monthly doses of venom (100 micrograms of antigen) were studied. All had been receiving immunotherapy for 12 to 29 mo. At the time of venom administration, a questionnaire related to symptoms of immune complex disease was completed. A urinalysis was performed 12 hr later. In addition, blood was drawn to evaluate the presence of immune complexes by Clq and Raji cell assays. Symptom surveys revealed no clinical manifestations suggestive of immune complex pathology. All urinalyses were negative for gross and microscopic hematuria. None of the specimens was elevated on the Clq assay. Only four of the 45 patients had significantly positive Raji cell assays. Prospective reevaluation showed the presence of immune complex before venom administration, with no change in acute-phase reactants or Raji cell titers 12 hr later. Monthly administration of Hymenoptera venom appears to be unassociated with immune complex-mediated disease, by either clinical or immunologic parameters.
Adolescent↗
The hypocomplementemic urticarial-vasculitis syndrome: therapeutic response to hydroxychloroquine.
We report a patient with hypocomplementemic urticarial-vasculitis syndrome. This case illustrates the continuum between urticaria and purpura characteristic of hypocomplementemic urticarial-vasculitis syndrome. Clq precipitin was demonstrated in the patient's serum and in the diethylaminoethylcellulose-ion exchange fraction containing only IgG. A skin biopsy specimen of urticarial and purpuric lesions demonstrated leukocytoclastic vasculitis and granular deposition of C3 and Clq in the basement membrane with IgA, IgM, C3, and Clq in postcapillary venules. Serial total hemolytic complement activity and Clq determinations were performed, and the response to several treatment regimens is presented. Symptomatic and serologic improvement was observed only with hydroxychloroquine.
Adult↗