PubMed Health⌕ Search

Biomedical subjects

H Zoellner

Publications and source records attributed to H Zoellner.

12 recordsLinked to original sources
PubMed1994

Association of amyloid P protein with pathology in periodontal tissues.

The lesion of chronic periodontitis is characterized by the persistence of perivascular collections of degenerate plasma cells. In this study, immunohistochemical demonstration of amyloid P (AP) component was used to define the distribution of this protein in established periodontitis lesions and in biopsies of non-destructive marginal gingivitis. Quantitative assessment of AP indicated significantly higher levels in periodontitis than in gingivitis for all regions of the tissue. This was associated with pathology as determined by the intensity of plasma cell accumulation and the extent of connective tissue matrix degradation. AP was concentrated in the deep connective tissue areas but perivascular accumulation was also noted, as was deposition associated with nerve bundles and, occasionally, in the extracellular matrix of the lining epithelium. These findings have potential significance in relation to the pathology of chronic periodontitis as AP has been shown to interact in a calcium-dependent manner with a number of ligands including fibronectin, elastic fibres, C-4 binding protein and amyloid fibrils.

Adult↗
PubMed1994

Extraction of amyloid-like fibrils from chronically inflamed periodontal tissues.

Immunohistological studies have established an association between the deposition of the amyloid P protein and disease status in chronically inflamed periodontal tissues. The aim of this study was to determine if amyloid-like fibrils could be extracted from these tissues. Biopsies were homogenised and extracted exhaustively in saline before serial extraction in distilled water. Electrophoretic analysis revealed the presence of previously undetected protein bands in the fifth water extraction. These were probed and were found to react with antisera to kappa and lambda immunoglobulin light chains but not with antisera to mu, gamma or alpha heavy chains. Electron microscopic study indicated fibrils of 9.7 nm diameter. These bound Congo Red and exhibited green birefringence under polarised light. The results supported the presence of an amyloid-like matrix composed of immunoglobulin light chains in the lesions of chronic periodontitis. This could explain the persistence of foci of degenerate plasma cells and the paucity of granulation tissue formation in the disease process.

Amyloid↗
PubMed1994

The vascular response in chronic periodontitis.

The role of vascular endothelial cells (EC) in periodontitis was investigated in a series of histological studies. Expansion of the vasculature was found to occur with development of gingivitis and periodontitis. This was thought to contribute to the characteristic tissue degradation in the developing disease. Vascular expansion could also play a role in the formation of a previously unreported perivascular hyaline material (PHyM). Polymorphonuclear leukocytes (PMN) are known to be protective in periodontitis, and the location, incidence and extent of PHyM suggested a role for PHyM in periodontitis by inhibiting PMN emigration. PMN emigration was found to occur from specialized high EC (HEC) lined post capillary venules. This was unexpected, as such vessels have previously been found to exchange lymphocytes almost exclusively. Detailed histochemical, ultrastructural and biosynthetic studies of these specialized blood vessels led to the suggestion that HEC may be specially adapted for the synthesis of cytokines in periodontitis. A negative association between expression of the membrane bound ectoenzyme, alkaline phosphatase, and HEC suggested a role for this enzyme in leukocyte emigration. These observations compel re-evaluation of the role of EC in chronic inflammation, and in periodontitis in particular. The direction of current and future work is discussed.

Chronic Disease↗
PubMed1994

Stimulation of PAI-1 expression in endothelial cells by cultured vascular smooth muscle cells.

Regulation of endothelial cell (EC) plasminogen activator inhibitor type-1 (PAI-1), the primary physiological inhibitor of tissue-type plasminogen activator (TPA) and urokinase-type plasminogen activator (UPA), by various stimuli has been well characterized. We report the upregulation of secreted and intracellular PAI-1 in human umbilical ECs when cocultured with human smooth muscle cells (SMCs) on amniotic membranes or incubated with SMC conditioned medium (CM) under serum-free conditions as determined by enzyme-linked immunosorbent assay. Cocultured human umbilical vein ECs and SMCs, or human umbilical artery ECs and SMCs, displayed a 73% and 68% increase, respectively, in released PAI-1. SMC-derived stimulatory factor release showed tissue specificity, since only human aortic, umbilical vein, and umbilical artery SMCs upregulated PAI-1 synthesis, whereas SMCs from human mammary artery, pulmonary artery, and saphenous vein did not. Stimulation of EC PAI-1 by SMC CM was both time and concentration dependent, with as much as five- and fourfold increases in supernatants and lysates, respectively. PAI-1 synthesis and activity in ECs from other vascular beds were also upregulated by SMC CM. Northern blot analysis paralleled the protein results, showing as much as a 2.7-fold increase in specific EC PAI-1 mRNA expression after incubation with SMC CM for 8 hours. PAI-1 stimulatory activity in SMC CM was completely abolished by boiling or incubation with protamine sulfate and was reduced by transient acidification or heparin-Sepharose pretreatment by 33% or 48%, respectively. The stimulatory factor(s) appeared to have a molecular mass of 23 kD as determined by gel filtration.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Communication↗
PubMed1994

Interferon-alpha 2 counteracts interleukin-1 alpha-stimulated expression of urokinase-type plasminogen activator in human foreskin microvascular endothelial cells in vitro.

We investigated the effect of interferon-alpha 2 (IFN-alpha 2) on interleukin-1 alpha (IL-1 alpha)-induced up-regulation of urokinase type plasminogen activator (u-PA) expression in human foreskin microvascular endothelial cells (HFMEC) and human umbilical vein endothelial cells (HUVEC) in vitro. When IFN-alpha 2 and IL-1 alpha were added to the cells simultaneously, IFN-alpha 2 inhibited IL-1 alpha-induced up-regulation of u-PA antigen in a dose- and time-dependent fashion in HFMEC, whereas in HUVEC no effect of IFN-alpha 2 on IL-1 alpha-induced u-PA was seen. IL-1 alpha-induced up-regulation of PAI-1 antigen in HFMEC was not counteracted by IFN-alpha 2. When IFN-alpha 2 was added to HFMEC 1 or 2 h after IL-1 alpha a significant inhibition in u-PA synthesis was seen, whereas when IFN-alpha 2 was added to the cells 8 h after IL-1 alpha no effect on the induction of u-PA synthesis by IL-1 alpha was seen. IFN-alpha 2 also inhibited significantly the IL-1 alpha stimulated up-regulation of specific u-PA mRNA expression. In conclusion, our data show that IFN-alpha 2 can counteract the IL-1 alpha-induced up-regulation of u-PA in a similar way as IFN-gamma. This effect, which seems to be specific for microvascular endothelial cells, could contribute to the modulation of endothelial cell-mediated extravascular proteolysis in processes such as wound healing, neovascularisation, and endothelial cell migration.

Cells, Cultured↗
PubMed1993

Thrombin stimulates expression of tissue-type plasminogen activator and plasminogen activator inhibitor type 1 in cultured human vascular smooth muscle cells.

The effect of thrombin on the fibrinolytic potential of human vascular smooth muscle cells (SMC) in culture was studied. SMC of different origin responded to thrombin treatment with a dose and time dependent increase in tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor type-1 (PAI-1) levels in both cell lysates and conditioned media with maximum effects achieved at 10-20 IU/ml thrombin. PAI-1 antigen levels also increased in the extracellular matrix of thrombin treated SMC. PAI-2 levels in cell lysates of such SMC were not affected by thrombin. The effect was restricted to active thrombin, since DFP-thrombin and thrombin treated with hirudin showed no increasing effect on t-PA and PAI-1 levels in SMC. Enzymatically active thrombin also caused a four-fold increase in specific PAI-1 mRNA and a three-fold increase in t-PA mRNA. Furthermore we demonstrated the presence of high and low affinity binding sites for thrombin on the surface of SMC with a KD = 4.3 x 10(-10)M and 9.0 x 10(4) sites per cell and a KD = 0.6 x 10(-8) M and 5.8 x 10(5) sites per cell respectively. Thrombin could come in contact with SMC in case of vascular injury or following gap formation between endothelial cells. Our data support the idea that besides its known proliferative effect for SMC, thrombin could also modulate their fibrinolytic system.

Antigens↗
PubMed1992

Human arterial smooth muscle cells synthesize granulocyte colony-stimulating factor in response to interleukin-1 alpha and tumor necrosis factor-alpha.

Vascular smooth muscle cells (SMC) are a major cell type comprising the walls of blood vessels. We report the synthesis of granulocyte colony-stimulating factor (G-CSF) by cultured human SMC obtained from the internal mammary artery and thoracic aorta. Interleukin-1 alpha (IL-1 alpha) greatly increased in a dose-dependent manner the amount of this cytokine produced by the SMC, with tumor necrosis factor-alpha (TNF-alpha) being less effective. Newly formed G-CSF could be detected in culture supernatants within 6 hours after IL-1 alpha or TNF-alpha treatment. Northern blot analysis of SMC stimulated with IL-1 alpha and TNF-alpha showed an increase in the amount of mRNA for G-CSF as compared with control cells. Enhanced G-CSF mRNA levels were observed when SMC were treated with cycloheximide in the absence or presence of added cytokine. In vasculitis, the walls of blood vessels become inflamed as evidenced by a leucocytic infiltrate usually dominated by polymorphonuclear neutrophil leukocytes (PMNs). G-CSF is known to stimulate PMNs, and our findings raise the possibility that G-CSF made by SMC contributes to the development of vasculitis lesions.

Aorta↗
PubMed1992

Gamma-interferon counteracts interleukin-1 alpha stimulated expression of urokinase-type plasminogen activator in human endothelial cells in vitro.

The effect of gamma-interferon (gamma-IFN) on the interleukin-1 alpha (IL-1 alpha) induced stimulation of urokinase-type plasminogen activator (u-PA) expression in human foreskin microvascular endothelial cells (HFMEC) and in human umbilical vein endothelial cells (HUVEC) was investigated. When gamma-IFN and IL-1 alpha were added to the cells simultaneously, gamma-IFN inhibited the IL-1 alpha induced increase in u-PA antigen production in both HFMEC and HUVEC in a dose dependent fashion, with a maximum inhibitory effect achieved between 2.0 and 20.0 U/ml of gamma-IFN. Pretreatment of HFMEC with gamma-IFN for 1 hour before addition of IL-1 alpha resulted in a significant reduction in u-PA synthesis. However, when HFMEC were pretreated for 8 hours with gamma-IFN before the addition of IL-1 alpha the reduction in u-PA production was even more significant. When gamma-IFN was added to HFMEC 1 hour after IL-1 alpha, a significant inhibition in u-PA synthesis was seen. In contrast only a slight inhibition in IL-1 alpha induced u-PA production was seen when gamma-IFN was added to the cells 8 hours after IL-1 alpha. gamma-IFN also inhibited significantly the IL-1 alpha induced increase in u-PA specific mRNA in HUVEC and HFMEC.

Blotting, Northern↗
PubMed1991

Chronic adult periodontitis and burst progression may reflect local neutrophil defects due to perivascular hyaline deposits.

Chronic adult periodontitis (CAP) is a common disease of the supporting tissues of teeth, and is a major cause of tooth loss. This disease is distinguished from more rare rapidly progressing forms of periodontitis, in which a variety of neutrophilic polymorphonuclear leukocyte (PMN) defects have been identified. PMN dysfunctions have, however, not been observed in CAP. In CAP, destructive episodes of the disease occur sporadically and independently in different parts of the mouth. In this paper, it is proposed that CAP is due to highly localized defects in PMN function. Impaired PMN function is suggested as resulting in the formation of a virulent bacterial plaque, which is capable of initiating periodontal pocket formation. A previously reported perivascular hyaline material may account for localized PMN defects, by reducing the number of PMNs entering affected sites. The proposed model may explain both the presence of CAP in otherwise normal patients, and the sporadic pattern of tissue destruction seen in this disease.

Adult↗
PubMed1991

Vascular expansion in chronic periodontitis.

Animal studies have demonstrated expansion and remodelling of gingival blood vessels in inflamed gingival tissues. However, there is a paucity of information, regarding the vascular response in human gingivitis and periodontitis. In this study, gingival biopsies were obtained from 51 separate patients. Fifteen minimally inflamed, 16 gingivitis and 20 periodontitis specimens were studied. Gingival biopsies were divided into five fields, and a quantitative survey of vascular changes was performed. In fields adjacent to the bacterial plaque irritant, vessel profiles were increased in number with the development of the advanced periodontal lesion. The diameter of blood vessels throughout the entire thickness of gingival biopsies was found to increase with advancing periodontal disease. It is concluded that considerable remodelling of the gingival vasculature occurs in chronic periodontitis, and that this may contribute to the tissue destruction seen in this disease.

Adult↗
PubMed1989

Perivascular hyaline deposits in inflamed gingival tissues.

A perivascular hyaline material (PHyM) was found in gingival biopsies from patients with periodontitis, gingivitis and minimally inflamed gingiva. PHyM was found only in association with the sulcular or pocket epithelium. The extent and frequency of the deposits was quantitatively associated with inflammation of the gingival tissues, as well as with the apical region of periodontal pockets. Evidence for angiogenesis was found in association with the deposition of PHyM. The ultrastructure of the PHyM indicated that the material, which was of an amorphous hyaline appearance at the light microscope level, was composed of multiple basal lamina impregnated with irregular collagen fibrils, fine fibrils and cellular debris. The basal lamina material was degraded at many sites. Immunohistochemistry confirmed the abundance of type IV collagen, supporting the basal lamina origin for PHyM. It is proposed that the deposition of the hyaline matrix is related to the effect of angiogenic and injurious agents on the vascular endothelium. PHyM could contribute to the development of periodontitis by impairing the emigration of polymorphonuclear leukocytes into the gingival sulcus.

Basement Membrane↗