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Biomedical subjects

J B Peter

Publications and source records attributed to J B Peter.

At least 55 records · Page 3Linked to original sources
PubMed1996

Elevated concentrations of interleukin-1 beta and interleukin-1 receptor antagonist in plasma of women with silicone breast implants.

Plasma from 27 women with silicone breast implants (SBIs) and 50 age-matched control women without SBIs were examined by enzyme immunoassay for the presence of interleukin-1 beta (IL-1 beta) and its naturally occurring receptor antagonist, IL-1ra. The results show that 74% (20 of 27) of women with SBIs had elevated concentrations of IL-1ra, whereas only 2% (1 of 50) of controls without SBIs had elevated concentrations of IL-1ra. In contrast to the IL-1ra results, the frequency of elevated IL-1 beta concentrations among women with SBIs was only 40% (11 of 27), but this was significantly higher than the 0% (0 of 50) in control women without SBIs. These findings suggest that there is a chronic ongoing inflammatory process in some women with SBIs, the implications of which are discussed in the context of silicone as an antigenic stimulant of the immune system.

Adult↗
PubMed1996

Precise quantitation of antinuclear antibodies on HEp-2 cells without the need for serial dilution.

Using HEp-2 cells as a substrate, we developed a method to quantitate antinuclear antibodies (ANA) by comparing the green fluorescence intensity of unknown samples with that of calibrated standards. Intensity was then converted to international units per milliliter by reference to a standard curve. This method is accurate and precise around the cutoff for positively (5 to 10 IU/ml) and therefore provides a reliable screening test for active, untreated systemic lupus erythematosus. Furthermore, the method can identify sera likely to contain autoantibodies commonly detected in ANA-positive sera (SS-A, SS-B, Sm, small nuclear ribonucleoprotein, Scl-70, and double-stranded DNA).

Antibodies, Antinuclear↗
PubMed1996

Guillain-Barré as an autoimmune disease.

Guillain-Barré syndrome (GBS) entails a demyelinating process of the peripheral nervous system. The etiopathogenesis of the syndrome is still a matter of debate although considerable progress has been accomplished in the recent years. Abundant evidence has been put forward so as to support the role of the immune system in initiating and perpetuating the ongoing damage culminating in the emergence of the clinically overt syndrome. As such, data on the involvement of the humoral immune pathways add to the information already presented with regard to cell-mediated mechanisms participating in disruption of peripheral nerve. The following review will focus on the current knowledge of these complex mechanisms and the relative significance of each in the pathogenesis of GBS.

Animals↗
PubMed1995

Purification and immunocharacterization of human brain glutamine synthetase and its detection in cerebrospinal fluid and serum by a sandwich enzyme immunoassay.

A modified procedure employing a single chromatographic step to purify glutamine synthetase from human brain is described. The enzyme was characterized by native, denaturing, and two-dimensional gel electrophoresis and immunoblotting. Yield and purity were assessed by enzyme activity assay and a newly developed sandwich enzyme immunoassay using a mouse monoclonal antibody against native sheep brain glutamine synthetase. The immunoassay detected glutamine synthetase protein in samples where the enzyme had been inactivated by repeated cycles of freezing and thawing, and in serum and cerebrospinal fluid where glutamine synthetase was undetectable by the enzyme activity assay. Native glutamine synthetase from human brain occurred as an octamer with an estimated molecular weight of 360-400 kDa. Under reducing and denaturing conditions, the enzyme dissociated into monomeric subunits with an estimated molecular weight of 44 kDa. The monomers were recognized by the monoclonal antibody on immunoblots but not in the sandwich enzyme immunoassay, suggesting that the antigenic site occurs once on each subunit. Both human and sheep brain glutamine synthetases were composed of three and four different types of subunits with isoelectric points ranging from 7.0-7.2 and 6.8-7.0, respectively.

Animals↗
PubMed1995

Multiple autoantibodies in patients with silicone breast implants.

Diverse immunologic abnormalities have been described in women who received silicone breast implants. However, most studies have focused on either a limited number of patients or a small panel of autoantibodies. We report the analysis of 20 autoantibodies in 116 women with implants and 134 controls. The patients ranged from 26- to 66-years-old, with a mean of 45.7 +/- 8.3 years; breast prostheses were in place for a mean of 15 +/- 5.6 years, with a range of 4 to 30, the chief complaints of the 116 patients included polyarthralgias, fatigue, myalgias, morning stiffness, and decreased memory. All 250 sera were tested blindly using a panel of 20 autoantigens including SS-A, SS-B, RNP, cardiolipin (CL), collagen types I, II and IV, phosphatidylserine (PS), myeloperoxidase (MPO), sulfatides (sulf), thyroglobulin (TG), gangliosides (GDIa;GM2), proteinase-3 (PR3), Jo-1, Sm, HPRPP-ribosomal phosphate, histones (H2AH2B), Scl-70 and glomerular basement membrane (NC-1). Values from individual patients were considered positive only when greater than 3 SD above the control mean. There was a statistically significant greater frequency of autoantibodies in women with implants for 15 of the 20 autoantigens; these were particularly striking for anti-H2AH2B, HPRPP, SS-A, SS-B, Scl-70, CL, PS, GM2, and NC-1. Many patients harbored several autoantibodies; 20% had four autoantibodies; 8% had six autoantibodies. The association of autoantibodies and implants suggests an adjuvant action of silicon/silicone byproducts.

Adjuvants, Immunologic↗
PubMed1995

Autoantibody profile in the sera of women with hyperprolactinemia.

Prolactin (PRL) has been implicated as an important in vivo modulator of cellular and humoral immunity. In order to elucidate the impact of elevated serum PRL levels on the immune system, we measured circulating autoantibodies in the serum of 33 hyperprolactinemic (HPRL) women and in 19 healthy women with normal PRL levels. All sera were examined for the presence of autoantibodies against 15 different antigens, including: ssDNA, dsDNA, histones (H2AH2B), Sm, RNP, SS-A/Ro, SS-B/La, cardiolipin, Scl-70, Jo1, collagen, glomerular basement membrane (GBM), pyruvate dehydrogenase (PDH), proteinase-3 (PR3) and MPO. Twenty-five of 33 (75.7%) HPRL women were found to have at least one autoantibody, while none of the 19 women with normal PRL had any. Eight HPRL women had seven or more (up to nine) different autoantibodies. Some of the autoantibodies were more frequently expressed than others, namely: anti-ss-DNA, anti-dsDNA, anti-Sm, anti-PDH and anti-SS-A/Ro. Autoantibodies to the autoantigens tested are common in a variety of autoimmune and rheumatic disorders including systemic lupus erythematosus (SLE), Sjögren's syndrome, mixed connective tissue disease (MCTD), scleroderma, primary biliary cirrhosis (PBC), polymyositis/dermatomyositis and vasculitis. Yet none of the HPRL women whose serum was found to contain high titers of autoantibodies presented with symptoms related to the respective autoimmune disorders. Our results support the role of PRL in the regulation of immune responses in man.

Adult↗
PubMed1995

Relationship between appearance of urinary red blood cell/white blood cell casts and the onset of renal relapse in systemic lupus erythematosus.

The purpose of the study was to determine the extent to which urinary sediment findings (changes in red blood cells [RBCs], white blood cells [WBCs], and the appearance of RBC and WBC casts) predict the onset of renal relapse (defined as a specific increase in proteinuria and/or serum creatinine level) in patients with systemic lupus erythematosus (SLE). Seventeen SLE patients with biopsy-proven diffuse proliferative glomerulonephritis at initial presentation were followed prospectively for 1,129 patient-months under a study protocol. Semiquantitative urinalyses were performed at 2-month intervals during periods with little or no SLE activity and, more frequently, during periods with increased SLE activity. Each urinalysis was accompanied by a clinical evaluation and a panel of screening tests relevant to the evaluation of SLE activity. During this study, 877 semiquantitative urinalyses were performed and 43 renal relapses were observed in 14 patients. No relapse occurred in three patients. Of the renal relapses, 30 were defined as proteinuria relapses (mean baseline proteinuria increased from 0.8 +/- 0.1 g/24 hr to 2.7 +/- 0.3 g/24 hr; P < 0.001) and 13 were defined as serum creatinine relapses (mean baseline serum creatinine increased from 2.7 +/- 0.4 mg/dL to 3.8 +/- 0.5 mg/dL; P < 0.001). Red blood cell and/or WBC casts (cellular casts) were observed before or at the onset of 35 of the 43 renal relapses (sensitivity, 81%). The mean and median intervals between the appearance of cellular casts and the onset of renal relapse was 10 +/- 2 weeks and 8 weeks, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Creatinine↗
PubMed1995

Bartonella (Rochalimaea) antibodies, dementia, and cat ownership among men infected with human immunodeficiency virus.

To determine the association between recent human immunodeficiency virus (HIV)-associated dementia and serum antibodies to Bartonella (Rochalimaea) henselae, we performed a nested case control study within the Multicenter AIDS Cohort Study in Los Angeles. We measured serum IgG and IgM antibodies to B. henselae with use of enzyme immunoassay in 369 HIV-seropositive and HIV-seronegative participants with and without recent neuropsychological deterioration. Data on pet ownership were also collected. IgM antibodies to B. henselae were strongly associated with neuropsychological decline or dementia (OR = 6.6;95% CI = 1.4-31.9;P = .02). Those participants with IgM antibodies to B. henselae were 1.7 times more likely to develop HIV-associated dementia (HAD) or neuropsychological decline over the next 5 years. At least 4% of the new cases of HAD and neuropsychological decline were due to bartonella infection. Cat ownership was associated with the presence of IgM antibodies to B. henselae (OR = 6.4;95% CI = 1.3-30.8;p = .02) and with neuropsychological decline and dementia (OR = 2.4;95% CI = 1.2-5.1;P = .02). This finding suggests that some cases of HAD and neuropsychological decline are associated with potentially treatable B. henselae infections.

AIDS Dementia Complex↗
PubMed1995

Prevalence of IgM antibodies to human herpesvirus 6 early antigen (p41/38) in patients with chronic fatigue syndrome.

To evaluate the association between human herpesvirus 6 (HHV-6) and chronic fatigue syndrome (CFS), 2 geographically separate groups of CFS patients (125 and 29 patients, respectively) and healthy controls (150 and 15 controls, respectively) were compared, using an EIA, for antibodies to HHV-6 early antigen p41/38 (EA). Sixty percent (93/154) of CFS patients were were positive for HHV-6 EA IgM, 40% (61/154) were positive for IgG, and 23% (35/154) were positive for both. A total of 119 (77%) of the CFS patients were positive for HHV-6 EA IgG or IgM (or both); only 12% (20/165) of the controls had IgG or IgM to HHV-6 EA. These data demonstrate that more CFS patients than controls had elevated levels of HHV-6 EA-specific IgM, perhaps indicating active replication of HHV-6 in CFS.

Antibodies, Viral↗
PubMed1995

Severity of infections in IgA deficiency: correlation with decreased serum antibodies to pneumococcal polysaccharides and decreased serum IgG2 and/or IgG4.

In order to define abnormalities of humoral immunity which determine susceptibility to respiratory tract infections in IgA-deficient adults, serum IgG subclass concentrations, and serum concentrations of pneumococcal antibodies and Haemophilus influenzae type B (Hib) antibodies sera from IgA-deficient adults with and without susceptibility to respiratory tract infections were compared. Infection susceptibility was not related to the degree of IgA deficiency, but was related to deficiency of IgG4 and, to a lesser extent, IgG2, as well as to low basal serum concentrations of pneumococcal polysaccharide antibodies. The combination of IgG2 and/or IgG4 deficiency and a non-protective basal serum concentration of antibody against two or more pneumococcal polysaccharides was present in the serum of six of 12 (50%) patients with severe infections, but only one of 44 (2%) patients without infections. Furthermore, the preservation of antibody responses against the most immunogenic pneumococcal polysaccharide type 3, but not against the less immunogenic types 7F, 9N and 14, in patients with severe infections suggested that abnormalities of pneumococcal polysaccharide antibody responses might include defects of affinity maturation.

Adolescent↗
PubMed1995

A rapid and sensitive chemiluminescence assay for evaluation of functional opsonic activity of Haemophilus influenzae type b-specific antibodies.

Luminol-enhanced chemiluminescence (CL) of heterologous neutrophils was used to assess the capacity of a 1-ng/ml concentration of Haemophilus influenzae type b (Hib)-specific antibodies to induce opsonization of Hib with autologous heat-inactivated sera from children immunized with Hib capsular polysaccharide-polyribosylribitolphosphate (Hib-PRP) conjugate vaccine. Serum samples from 15 of 36 children (42%) vaccinated with Hib-PRP conjugate vaccine had protective levels of Hib-specific antibodies of > or = 1,000 ng/ml. Ten of these 15 (67%) had poor or nonfunctional opsonic activity. Of the 10 children whose sera lacked opsonic activity, 5 (50%) presented with recurrent Hib infection. In contrast, none of the sera of 20 healthy adults lacked opsonic capability. CL intensity was proportional to the concentration of anti-Hib antibodies used for opsonization. Furthermore, the titers of Hib-PRP-specific antibody in children and adults did not correlate with opsonic activity. These results suggest that luminol-enhanced CL as described here with minute concentrations of antibody for opsonization can be used to assess functional capacity of anti-Hib antibodies after vaccination or natural infection in the evaluation of patients with recurrent infections.

Antibodies, Bacterial↗
PubMed1995

Multireactive pattern of serum autoantibodies in asymptomatic individuals with immunoglobulin A deficiency.

Selective immunoglobulin A (IgA) deficiency (sIgAD) is associated with certain autoimmune states. Increased production of autoantibodies and eventual development of overt autoimmune disease are related in part to genetic and environmental factors as well as to the immune deficiency. We surveyed serum specimens from 60 healthy subjects with sIgAD for the presence of 21 different autoantibodies by enzyme-linked immunosorbent assays. The frequencies of 16 autoantibodies were higher in sIgAD patients than in normal healthy controls. Autoantibodies to Jo-1 (28%), cardiolipin (21%), phosphatidylserine (20%), Sm (15%), asialo-GM1 (21%), sulfatide (32%), sulfoglucuronyl paragloboside (11%), and collagen type I (10%) were detected at high frequencies in comparison to those of normal healthy controls. Many of the serum samples were multireactive (i.e., exhibited binding to more than two autoantigens). Forty percent (24 of 60) of sIgAD serum samples reacted against six or more autoantigens; 10% (6 of 60) of sIgAD serum samples were not reactive with any of the 21 autoantigens. Three percent (7 of 209) of consecutive serum samples submitted for autoimmune antibody analysis that were positive for autoantibodies were from patients with IgA deficiency. Our finding of an increased frequency of autoantibodies in sIgAD patients supports the notion of polyclonal stimulation by repeated environmental stimuli as an etiologic mechanism. Alternatively, the increased frequency may be caused by a dysregulation of the immune response in such individuals. The mere detection of autoantibodies cannot predict whether a subject with sIgAD will develop an autoimmune disease or determine which specific disease will emerge.

Antigen-Antibody Reactions↗
PubMed1995

Autoimmune aspects of primary pulmonary hypertension.

Although primary pulmonary hypertension (PPH) is considered to be an idiopathic condition, it has been postulated that autoimmunity may play a role in the pathogenesis of the disease. This argument has been based on frequent coexisting clinical and serological rheumatic findings. Moreover, approximately in a third of the patients with PPH, and antinuclear factor can be detected. Pulmonary hypertension may appear as a secondary complication to various autoimmune conditions. In light of these findings we examined sera derived from 40 patients diagnosed as having PPH for the presence of 18 different autoantibodies by the ELISA and immunofluorescent techniques. Of the 40 patients, 62.4% had circulating autoantibodies and 47.5% presented with multiantibody responses. Autoantibodies most commonly observed were antinuclear (42.5%), anti-ssDNA (25%) and antithyroglobulin (30%) antibodies. These results may imply that in a subgroup of patients with PPH the disease may be ascribed to an immune dysregulation or alternatively that autoantibodies accompany the disease progression as an epiphenomenon.

Antibodies, Antinuclear↗
PubMed1995

Autoantibody profile of primary sclerosing cholangitis.

Primary sclerosing cholangitis (PSC) is a chronic progressive liver disease of unknown etiology. It has been suggested that genetic and immunological factors are important in its pathogenesis. The present study examined the prevalence of 23 different autoantibodies in 25 PSC sera, by ELISA, in order to better define the autoimmune profile of PSC. The results indicate that 88% of PSC patients produced at least 1 autoantibody, and 36% had reactivity to multiple autoantibodies. Moreover, 35% of the PSC patients produced anti-endothelial-cell antibodies (AECA) and 75% of the sera contained perinuclear antineutrophil cytoplasmic antibodies (pANCA), detected by indirect immunofluorescence. The prominent ANCA autoantibody was anti-cathepsin-G, demonstrated in 35% of the patients. The multiplicity of the autoantibody profile, revealed in the present study, points to the autoimmune characteristics of PSC. In addition, the association of ANCA and of AECA in PSC may suggest a pathogenic role for these antibodies in PSC.

Antibodies, Antineutrophil Cytoplasmic↗