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Biomedical subjects

R J Harbeck

Publications and source records attributed to R J Harbeck.

At least 37 records · Page 2Linked to original sources
PubMed1990

The immune response to short-term nutritional intervention in advanced chronic obstructive pulmonary disease.

Nine patients with advanced chronic obstructive pulmonary disease (COPD) and recent weight loss resulting in a state of mild malnutrition were entered into a refeeding program at a clinical research center. They were divided into two groups, one using a hospital diet and the other a hospital diet with supplementation. Both groups of patients gained significant weight. Refeeding and weight gain were associated with a significant increase in absolute lymphocyte count and with an increase in reactivity to skin test antigens after 21 days of refeeding. Few changes occurred in large numbers of additional serum measurements during the study period. These preliminary observations suggest that dietary and supplementary refeeding may improve the immune responses in patients with COPD.

Aged↗
PubMed1990

An apparatus for the measurement of lung volume and compliance in mice.

Pressure-volume (P-V) curves and total lung capacity (TLC) were measured in excised lung of mice using a water manometer and a closed system in which the humidity and temperature were controlled. In pathogen-free mice there are no significant differences in elastic properties of these lungs in relation to their age. The measured TLC in those normal mice was approximately 2.9 ml. This relatively simple apparatus which allows one to make sensitive and accurate measurements of pulmonary function in mice and other small animals.

Animals↗
PubMed1989

Anti-Ia antibodies inhibit the spontaneous secretion of IL-1 from silicotic rat alveolar macrophages.

Class II antigens of the major histocompatibility complex (Ia) are important components in the investigation of cell-mediated immune responses. Several reports have indicated that anti-Ia monoclonal antibodies suppress disease development in animal models. In this paper, the expression of Ia and the effect of anti-Ia on IL-1 secretion from alveolar macrophages (AM) from silica-treated rats was examined. The results obtained showed that 45% of silicotic AM, but only 5% of AM from normal control rats, express Ia antigen. Anti-Ia treatment of silicotic AM reduced IL-1 secretion by 55%. We conclude that anti-Ia immune suppression may involve the inhibition of IL-1 secretion.

Animals↗
PubMed1989

Lymphocyte populations in lung tissue, bronchoalveolar lavage fluid, and peripheral blood in rats at various times during the development of silicosis.

Inflammatory cells and lymphocyte populations were examined in the bronchoalveolar lavage (BAL) fluid, lung tissues, and peripheral blood from rats at various times after the intratracheal instillation of silica. In lavage fluid, there was a rapid initial increase in the percentage and number of polymorphonuclear leukocytes (PMN), which slowly decreased during the course of the experiment. In addition, compared to controls, there was an increased number and percentage of lymphocytes throughout the 75 days of the experiment. The lymphocytic populations, which were determined by an indirect immunofluorescence method with monoclonal antibodies to lymphocyte surface markers, showed a predominance of the T-helper phenotype from Day 14 through the end of the experiment (Day 75). The number of PMNs obtained from collagenase digest of the lung was increased over control levels up to Day 7 after silica administration and remained at a relatively constant level until Day 14, after which time they decreased slightly in number. The total number of lymphocytes peaked on Day 14, with cells of the T-helper phenotype predominating after this time. In the peripheral blood, T-helper cells from silicotic rats were significantly increased over control rats on Days 7 and 14 but returned to normal control values after this time. The lymphocyte subsets in the BAL, but not in the peripheral blood, more closely reflect the lymphocyte patterns in the lung. The results of these experiments suggest that T-helper cells may play an important role in the inflammatory-fibrotic events in the lungs of rats with silicosis.

Animals↗
PubMed1989

Increased expression of class II antigens of the major histocompatibility complex on alveolar macrophages and alveolar type II cells and interleukin-1 (IL-1) secretion from alveolar macrophages in an animal model of silicosis.

Silicosis is a chronic progressive granulomatous and fibrotic lung disease caused by inhaled silica. Although the causative agent is known, the pathogenesis, especially the immunologic response, is not well understood. We examined two important components of cell-mediated immune responses in the lungs of rats with silica-induced lung disease, i.e., class II (Ia) antigen expression and IL-1 production. The relative density of Ia was examined on isolated alveolar macrophages and type II cells with a solid-phase cellular radioimmunoassay and the percent of Ia positive cells was determined by an indirect immunofluorescent technique. There was a three-fold increase of Ia expression on the alveolar macrophages and nearly a two-fold increase on type II cells from rats with silicosis compared to normal rats. The percent of alveolar type II cells positive for Ia increased by 20%, and the alveolar macrophages increased by 40%. IL-1 in supernatants from cultured alveolar macrophage was measured by the amount of DNA synthesis in an IL-1 dependent cell line (D10). A six-fold increase in IL-1 secretion was noted in macrophage supernatants derived from silica-treated animals. We conclude that in this animal model of silicosis, a local amplification of cell-mediated immune responses may be instrumental in the pathogenesis.

Animals↗
PubMed1988

Class II molecules on rat alveolar type II epithelial cells.

Class II (Ia) molecules of the major histocompatibility complex are important in the presentation of antigen to T cells and in the regulation of the immune response. Recent studies have suggested that many epithelial cell types can express class II molecules. We examined rat alveolar type II epithelial cells, a cell which can synthesize and secrete pulmonary surface-active material, for the expression of class II antigens. Using an indirect immunofluorescent technique with a mouse anti-rat class II monoclonal antibody (OX-4), the majority of type II cells isolated from pathogen-free Sprague-Dawley rats expressed Ia antigens as determined by fluorescent microscopy and cell sorter analysis. In culture, the Ia expression was lost from type II cells. The addition of recombinant interferon-gamma to cultures of type II cells induced the expression of class II antigens. These findings suggest that class II antigen expression on type II cells may have relevance to immune responses occurring in the lung.

Animals↗
PubMed1988

Human tonsillar IgE biosynthesis in vitro. II. Analysis of T cell regulation with monoclonal antibodies.

Phenotypes of T cells regulating human tonsillar IgE biosynthesis in vitro were studied by use of Leu 2a and Leu 3a monoclonal antibodies that recognize T cell subsets. B cells cultured with Leu 3a+-enriched populations (B cells plus T3a) produced significantly more IgE and IgG in the presence of pokeweed mitogen than B cells with the Leu 2a+-enriched populations (B cells plus T2a) (p less than 0.001 for IgE and p less than 0.001 for IgG). No significant differences were observed in IgE and IgG synthesis between the cultures of B cells alone and B cells plus T2a. T2a, but not T3a cells, significantly suppressed IgE synthesis (p less than 0.05 for geometric means and p less than 0.001 for percent suppression) when the cells were added to cultures of B cells plus T3a. Suppression of IgG synthesis was not observed under conditions that suppressed IgE synthesis, suggesting qualitative and quantitative differences in regulation of production of these isotypes. When T2a cells were irradiated, the suppressor activity disappeared. When graded numbers of T3a cells were added to B cells, it was noted that IgE synthesis first increased and then decreased as the numbers of T3a were increased. When the T3a cells were irradiated, IgE biosynthesis was suppressed at lower T/B ratios (less than 1 in four of five experiments) and was enhanced at higher T/B ratios (greater than 1 in all five experiments). Similar results were observed in experiments with OKT4 and OKT8 monoclonal antibodies. It is concluded that phenotypes of helper T cells for IgE synthesis are Leu 3a+ or OKT4+ and that IgE suppressors are predominantly Leu 2a+ or OKT8+ and are radiosensitive, as reported for regulation of other isotypes. However, it is suggested that Leu 3a+ and OKT4+ cells consist of radioresistant and radiosensitive helper cells and, presumably, a minor population of suppressor cells.

Antibodies, Monoclonal↗
PubMed1987

The isolation and characterization of enriched microvascular endothelial cells from mouse adipose tissue. The induction of class II molecules of the major histocompatibility complex (MHC) by interferon-gamma (IFN-gamma).

Collagenase digestion and selective filtration have been used to establish primary cultures from mouse omentum of cells enriched for microvascular endothelium. In culture these cells exhibit a cobblestone morphology characteristic of endothelial cells, metabolize an acetylated low-density lipoprotein, and exhibit trace levels of angiotensin-converting enzyme activity. In primary cultures, the cells are negative for class II molecules (Ia) of the major histocompatibility complex (MHC) but can be induced to express these molecules by exposure to a supernatant from concanavalin A (ConA)-treated rat spleen cells or by recombinant interferon-gamma (rIFN-gamma). This procedure can provide a readily available source of enriched endothelial cells which can be used to understand the interactions between these cells and cells of the immune system.

Adipose Tissue↗
PubMed1987

Inhibition of induced acute lung edema by a novel protein kinase C inhibitor.

The effect of the protein kinase C enzyme inhibitor H-7 on the noncardiogenic lung edema induced by phorbol myristate acetate (PMA) in mice was examined. Lung edema was assessed by measurement of 125I-labeled albumin leak into the lung. The results showed that pretreatment of mice with H-7 nearly prevents the albumin leak induced by PMA, whereas post-PMA treatment with H-7 had less of an effect on the albumin leak, although it was still significant.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1987

Brain-reactive autoantibody levels in the sera of ageing autoimmune mice.

Brain-reactive autoantibodies are thought to play an important role in mediating central nervous system (CNS) disorders in systemic lupus erythematosus (SLE). In this paper the developmental occurrence of these antibodies in the sera of autoimmune mice, i.e. NZB, NZB/W, MRL/l and BXSB mice were examined. All murine strains tested, whether autoimmune or not, showed some degree of serum reactivity toward brain antigens. Autoimmune mice, however, displayed higher levels of serum brain-reactive antibodies, and at earlier ages, than non-autoimmune mice. Immunofluorescence assays against brain sections and adsorption assays, with both neural and non-neural tissue, indicated a heterogeneity in the specificity of the populations of brain-reactive antibodies present. These studies provide an important step in characterizing the appearance and diversity of brain-reactive autoantibodies, with the goal of better understanding their significance and potential role in mediating CNS dysfunction in SLE.

Aging↗
PubMed1986

The regulatory effect of histamine on the in vitro synthesis of IgE.

The effect of histamine and its H1 and H2 antagonists, chlorpheniramine and cimetidine, on the in vitro, PWM-induced, synthesis of IgG and IgE was studied. Histamine had no effect, and cimetidine had a slight inhibitory action. In contrast, chlorpheniramine induced marked suppression of both IgE and IgG synthesis. This effect could not be attributed to drug-induced cytotoxicity. These results suggest that the modulatory effect of histamine on antibody production involves predominantly H1 receptors.

Cell Survival↗
PubMed1986

Mononuclear cell pulmonary vasculitis in NZB/W mice. II. Immunohistochemical characterization of the infiltrating cells.

NZB/W mice spontaneously develop pulmonary lymphoid hyperplasia and vasculitis in an age-related fashion. The cellular infiltrates and pattern of involvement bear similarity to various forms of pulmonary vasculitis in humans. In this study the authors used monoclonal antibodies and the avidin-biotin immunoperoxidase technique to analyze the pulmonary mononuclear cell infiltrates of female NZB/W mice at various ages and levels of disease activity. T cells, T-cell subsets, B cells, and Ia-bearing cells were localized with this technique. Most cells within the infiltrates were T cells that expressed the Lyt-1 phenotype, whereas cells expressing Lyt-2 were rarely observed. Cells reacting with a monoclonal antibody which recognizes cells of the B-lineage and cells expressing Ia antigens were also observed. Before the development of vasculitis, B and T cells were randomly distributed throughout the lesion. In older animals with vasculitis, T cells expressing Lyt-1 were associated with vessel lumen and were primarily responsible for the vascular infiltration, to the apparent exclusion of other lymphoid cell types. The B cells and Ia+ cells were localized at the periphery of the lesions.

Age Factors↗
PubMed1985

Recurrent severe infections in a girl with apparently variable expression of mosaicism for chronic granulomatous disease.

A carrier of chronic granulomatous disease (CGD) has had recurrent severe purulent infections like those characteristic of CGD. The carrier state was demonstrated by the presence of both normal and CGD granulocytes in her blood; the percentage of normal granulocytes varied from 4% to 44% over 4 years. In addition, her granulocytes were partially defective in killing Escherichia coli and staphylococci and in the release of superoxide anion during stimulation. Extensive evaluation of her immune system and phagocyte function failed to reveal a second abnormality. The course in this child indicates that the carrier state for X-linked CGD cannot be considered a benign condition and might be more properly conceptualized as a continuum in expression of the full disease. Screening assays for CGD should possess the capacity to diagnose carriers of the X-linked form of the disease.

Blood Bactericidal Activity↗
PubMed1985

The regulatory effect of macrophages on the in vitro synthesis of IgE.

The effects of indomethacin or macrophage-depletion on the in vitro unstimulated and pokeweed mitogen (PWM)-induced synthesis of IgG and IgE were compared. The effect on the unstimulated synthesis of IgG and IgE was similar, namely, no effect due to indomethacin and enhancement due to macrophage depletion. In contrast, the effect on PWM-induced synthesis was dissimilar. Macrophage depletion enhanced IgG but inhibited IgE production. The effect of indomethacin paralleled that of macrophage depletion suggesting the involvement of prostaglandins. It seems that the regulatory effect of macrophages is different in the IgE system compared with the IgG system.

Antigen-Presenting Cells↗
PubMed1985

Regulatory effect of hydrocortisone on the in vitro synthesis of IgE by human lymphocytes.

The effect of different concentrations of hydrocortisone (HC) on the in vitro, pokeweed mitogen-driven synthesis of IgG and IgE by human lymphocytes was studied. HC had the same modulatory action on the production of both immunoglobulins. Two different effects were observed: the first is enhancement of Ig synthesis by low concentrations of HC (10(-7)-10(-4) M), and the second is inhibition of synthesis by higher concentrations due to lymphocytotoxic effect.

Cell Survival↗
PubMed1985

Mononuclear-cell pulmonary vasculitis in NZB/W mice. I. Histopathologic evaluation of spontaneously occurring pulmonary infiltrates.

This report describes the spontaneous occurrence of pulmonary vasculitis in NZB/W mice, a well-characterized autoimmune strain of mice. These mice develop pulmonary vasculitis in an age-related fashion. Mild perivascular and peribronchiolar lymphoid hyperplasia is first seen at 4 months of age and progresses into severe hyperplasia by 8 months. This precedes the development of angiodestructive lesions, which are first noticeable at 10 months. By 12 months of age all mice show multilobe disease characterized by transmural infiltration of the vascular walls by plasma cells, histiocytes, and mature lymphocytes. Mitotic figures and necrosis are rare to absent. Vessel lumens are markedly narrowed and obliterated in severe cases, with focal disruption of the limiting elastic membranes. In mice older than 10 months of age, there is extension of the infiltrate into the interstitium in a manner similar to that of lymphoid interstitial pneumonia. Arteries and veins are equally affected. The cellular infiltrates and pattern of involvement bears similarity to various pulmonary vasculitides in humans. This is the first report of spontaneous pulmonary vasculitis in NZB/W mice.

Aging↗
PubMed1985

In vitro synthesis of IgE in atopic and nonatopic individuals: the effects of pokeweed mitogen, Staphylococcus aureus-derived mitogens, and cycloheximide.

We studied the production of immunoglobulin (Ig)E in cultures containing mononuclear cells obtained from atopic and nonatopic subjects. The two groups did not differ in their baseline production of IgE. Pokeweed mitogen (PWM) and three different products of Staphylococcus aureus: purified protein A, heat-killed formalinized bacteria, and double-formalinized bacteria--induced a significant increase in the in vitro production of IgE. Mononuclear cells from both atopic and nonatopic individuals were stimulated to the same degree by all four mitogens. The increased production of IgE by PWM was totally abolished by cycloheximide; hence it was due to de novo protein synthesis.

Adolescent↗