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Biomedical subjects

R Harbeck

Publications and source records attributed to R Harbeck.

13 recordsLinked to original sources
PubMed1994

The production of interferon-gamma in response to a major peanut allergy, Ara h II correlates with serum levels of IgE anti-Ara h II.

The current study was undertaken to examine the potential role of T cells in the pathogenesis of peanut allergy. Peripheral blood mononuclear cells (PBMCs) from patients with peanut allergy, patients with asthma, and nonatopic normal control subjects were assessed for proliferation after stimulation with a 17 kd major peanut allergen (Ara h II), ovalbumin, casein, soy, and Candida albicans. We found that Ara h II and C. albicans induced significantly higher levels of proliferation than ovalbumin, casein, and soy. Because interferon-gamma (IFN-gamma) and interleukin-4 (IL-4) play critical roles in IgE regulation, we assessed the production of these cytokines after stimulation with C. albicans and Ara h II. C. albicans stimulated similar levels of IFN-gamma in all three study groups. In contrast, after stimulation with Ara h II, culture supernatants from PBMCs of subjects with peanut allergy contained significantly lower levels of IFN-gamma than did the PBMCs of the two control groups (p = 0.02). More important, there was a significant (p = 0.05) inverse correlation between the serum IgE anti-Ara h II levels and IFN-gamma production by PBMCs from the respective peanut-allergic patients. IL-4 protein was not detected in culture supernatants of PBMCs stimulated with Ara h II. However, amplification of cytokine gene transcripts by polymerase chain reaction did demonstrate IL-4 expression in Ara h II-stimulated PBMCs from both patients with peanut allergy and control subjects. These data suggest that the level of IFN-gamma production in response to Ara h II may be an important factor in determining the development of peanut-specific IgE responses.

2S Albumins, Plant↗
PubMed1993

Presence of IgE antibodies to staphylococcal exotoxins on the skin of patients with atopic dermatitis. Evidence for a new group of allergens.

In the current study, we investigated whether Staphylococcus aureus grown from affected skin of atopic dermatitis (AD) patients secreted identifiable toxins that could act as allergens to induce IgE-mediated basophil histamine release. The secreted toxins of S. aureus grown from AD patients were identified by ELISA using antibodies specific for staphylococcal enterotoxin (SE) exfoliative toxin (ET), or toxic shock syndrome toxin (TSST-1). S. aureus isolates from 24 of 42 AD patients secreted identifiable toxins with SEA, SEB, and TSST accounting for 92% of the isolates. 32 of 56 AD sera (57%) tested contained significant levels of IgE primarily to SEA, SEB, and/or TSST. In contrast, although SEA, SEB, or TSST secreting S. aureus could be recovered from the skin of psoriasis patients, their sera did not contain IgE antitoxins. Freshly isolated basophils from 10 AD patients released 5-59% of total histamine in response to SEA, SEB, or TSST-1 but only with toxins to which patients had specific IgE. Basophils from eight other AD patients and six normal controls who had no IgE antitoxin failed to demonstrate toxin-induced basophil histamine release. Stripped basophils sensitized with three AD sera containing IgE to toxin released 15-41% of total basophil histamine only when exposed to the relevant toxin, but not to other toxins. Sensitization of basophils with AD sera lacking IgE antitoxin did not result in release of histamine to any of the toxins tested. These data indicate that a subset of patients with AD mount an IgE response to SEs that can be grown from their skin. These toxins may exacerbate AD by activating mast cells, basophils, and/or other Fc epsilon-receptor bearing cells armed with the relevant IgE antitoxin.

Allergens↗
PubMed1991

Alpha beta T-lymphocyte depleted mice, a model for gamma delta T-lymphocyte functional studies.

Adult mice can be depleted of essentially all mature alpha beta T lymphocytes by chronic treatment with the framework-recognizing, pan-specific anti-TCR alpha beta mAb, H57-597. Similar findings have been reported in rats, gamma delta cell populations remain essentially unaltered in size and reactivity. Suppression of alpha beta T-cell development results in the loss of alloantigen reactivity and of B-cell help, suggesting that gamma delta and alpha beta populations differ in their functional capabilities. Indirect effects of the antibody treatment include quantitative changes in splenic B cells, as well as reduced sizes and weights of experimental animals. alpha beta-suppressed mice and rats may provide model systems for studies on gamma delta cell function in vivo.

Animals↗
PubMed1991

Possible links between immune system and stress response: the role of gamma delta T lymphocytes.

Heterologous heat shock proteins (hsps) are antigens in many infectious diseases involving bacteria, parasites and perhaps even fungi. T and B lymphocytes recognize multiple epitopes on these proteins. Recently, lymphocytes expressing gamma delta T cell receptors (gamma delta cells) were also found to react with hsps that are members of the 60 kiloDalton (kDa) family. The response of gamma delta cells to hsp 60 differs from that of alpha beta T cells and B cells in several ways: the frequency of reactive gamma delta clones is high. Many clones recognize the same portion of this protein instead of scattered antigenic epitopes; and most gamma delta cells that react with the mycobacterial hsp-60 homolog are also stimulated by the autologous homolog. Perhaps, such (self) hsp-reactive gamma delta populations function by distinguishing stressed from not stressed states in autologous cells and tissues, rather than by discriminating 'self' and 'non-self'.

Bacterial Proteins↗
PubMed1988

Elastic properties of the excised lungs of NZB/W mice and their correlation with histopathologic changes.

Lung volume and the pressure-volume (PV) relationships of the lung were determined in excised lungs of an animal model of human systemic lupus erythematosus, which develops in NZB/W mice, and correlated with histopathologic changes. In young, 4-month-old NZB/W mice, and in nonautoimmune BALB/c mice at any age, there were minimal histologic changes or alterations in lung function. The NZB/W mice developed histologic changes with aging. Perivascular, peribronchial, and interstitial changes developed and were associated with a significant reduction in total lung capacity as well as changes in the pressure-volume characteristics of the lung, which are compatible with a restrictive process.

Age Factors↗
PubMed1976

Degradation of circulating DNA by extracorporeal circulation over nuclease immobilized on nylon microcapsules.

Studies were undertaken to determine whether deoxyribonuclease I, (DNase I) once immobilized on activated nylon microspheres, would be capable of degrading circulating DNA in vitro and in vivo in an extracorporeal circulation system in dogs. Nylon microspheres were prepared and after gentle hydrolysis and glutaraldehyde treatment, demonstrated a retention of up to 4.73 mg of Dnase I. In vitro studies showed that DNase I immobilized on microspheres degreded a significant percentage of 125I-native DNA (nDNA) within 15 min. Mongrel dogs were injected with 125I-nDNA and a variation in initial t 1/2 in individual animals was observed. Therefore, for experimental studies, 125I-nDNA was injected and decay was recorded during a control period in which untreated microcapsules were utilized in the extracorporeal system. DNase I microspheres were then introduced into the extracorporeal circuit which resulted in an acceleration of degradation of acid precipitable 125I-nDNA. When 200 mug of unlabeled DNA with 125I-nDNA was injected, a similar augmentation of DNA degradation was noted after extracorporeal circulation over DNase I microcapsules. This effect could not be attributed to release of DNase I from the microspheres since no 131I-DNase was detected in the serum or organs of the dogs at the conclusion of the experiments. 125I-nDNA:anti-DNA complexes were passively injected into dogs and after a similar control period of circulation over untreated microcapsules. DNase I microspheres were introduced. Results showed a rapid acceleration in the degradation rate of 125I-nDNA:anti-DNA complexes precipitable with (NH4)2SO4. Extracorporeal circulation over nylon microspheres resulted in no significant alteration of the host's hematocrit or platelet count, and little residual cellular debris on the microcapsules. These data suggest that DNAase immobilized on nylon microspheres may have a potential role in the specific therapy of systemic lupus erythematosus, when it is desirable to hydrolyze DNA circulating free or in combination with antibody.

Animals↗
PubMed1976

Specific removal of DNA antibodies in vivo with an extracorporeal immuno-adsorbent.

The selective removal of circulating antibody specific for DNA was affected with an immuno-absorbent consisting of DNA-cellulose incorporated into agar gel. Antisera to DNA obtained from patient with systemic lupus erythematosus was circulated in vitro through experimental and control columns by a dual channel haemodialysis pump and serial aliquots were withdrawn and assayed for antibody. A 65% reduction in DNA binding of serum was achieved at a flow rate of 210 ml/min over a 4-hr period with no release of 125I-labelled DNA from the column into the serum. For in vivo studies, 2-6-3-8 kg rabbits were actively immunized with methylated bovine serum albumin conjugated to single-stranded DNA (MBSA-ssDNA). Whole blood was pumped from the femoral artery through an immuno-adsorbent composed of ssDNA-cellulose in an agar matrix. Results showed significant reductions in ssDNA binding activity over various periods after connection of the rabbit's circulation to the immuno-adsorbent with only minimal changes in BSA binding during the same period. Little release of incorporated 125I-labelled DNA from the column as assayed in the blood and tissues of the experimental animals occurred during the procedure. The immuno-adsorbent columns showed no residual cellular debris or thrombotic material. These results suggest that this immuno-adsorbent system may be used to specifically withdraw circulating DNA antibodies in vivo. Such a system may have clinical potential for specific therapy of systemic lupus erythematosus.

Adsorption↗
PubMed1976

Specific removal of bovine serum albumin (BSA) antibodies in vivo by extracorporeal circulation over BSA immobilized on nylon microcapsules.

Studies were undertaken to determine whether BSA, once immobilized on activated nylon microspheres, would be capable of specifically removing circulating BSA antibody in vitro and in vivo in an extracorporeal circulation system in dogs. Nylon microspheres were prepared and, after gentle hydrolysis and glutaraldehyde treatment, demonstrated a retention of up to 34.5 mg of BSA. In vitro studies showed that BSA immobilized on microspheres removed a significant percentage of BSA-binding activity. For in vivo studies, an extracorporeal circulation system was established and mongrel dogs were then injected with anti-BSA and anti-HSA antibodies. After an equilibration period, BSA microspheres were introduced into the extracorporeal circulation system. After the insertion of BSA microcapsules, serum exhibited a sharp reduction in BSA binding over the next 15 min, with a more gradual diminution over the ensuing 60 to 90 min. There was no significant reduction in anti-HSA binding over the same time frame. This effect could not be attributed to release of BSA from the microspheres since no 125I-BSA was detected in the serum or organs of the dogs at the conclusion of the experiments. After extracorporeal circulation over nylon microspheres, there were only minimal changes in the host's hematocrit or leukocyte counts and no significant thrombotic material or cellular debris was recoverable on the capsules. These data suggest that antigen immobilized on nylon microspheres may specifically withdraw circulating antibodies in vivo with minimal release of its antigenic material and little alteration in the host's hematologic status.

Animals↗