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Biomedical subjects

L Schrieber

Publications and source records attributed to L Schrieber.

At least 19 recordsLinked to original sources
PubMed1992

Possible mechanisms of type I collagen-induced vascular tube formation.

UNLABELLED: We investigated the effect of type I collagen on endothelial behaviour following its contact with the apical versus basal surface of cultured human endothelial cells. When endothelial cells were plated onto type I collagen they attached via their basal surface and formed a confluent monolayer. However, when type I collagen (100 micrograms/ml) was added directly to the growth medium, so that it made contact with the apical surface of endothelial cells, it induced rapid capillary-like tube formation. Possible mechanisms were assessed using a) polyclonal (anti-VLA-2) and monoclonal (AK7) antibodies to different epitopes on the alpha 2 beta 1 integrin receptor for collagen and b) drugs (chlorpromazine and trifluoperazine) that inhibit protein kinase C activity. Both anti-VLA-2 and AK7 (1-50 micrograms/ml) showed a dose-dependent inhibition of tube formation and cell attachment. At 50 micrograms/ml, anti-VLA-2 completely inhibited tube formation whereas AK7 caused only partial inhibition (less than 50%). By contrast, AK7 was a more potent inhibitor of cell attachment than anti-VLA-2. Both chlorpromazine and trifluoperazine prevented tube formation. CONCLUSIONS: 1) The alpha 2 beta 1 integrin receptor plays a role in both endothelial cell attachment and the induction of tube formation by type I collagen. 2) Protein kinase C may be involved in collagen-induced tube formation.

Cell Adhesion↗
PubMed1992

Identification of a human endothelial cell activation antigen that is co-expressed by germinal follicle centre B lymphocytes.

Endothelial cell activation antigens may play important roles in immune responses and in inflammation. This report describes the identification and characterization of a monoclonal antibody, named EAA-B, which reacts specifically with human umbilical vein endothelial (HUVE) cells pre-treated with tumour necrosis factor-alpha (TNF-alpha) but not with untreated cells. The expression of the EAA-B antigen on HUVE cells could also be induced by interleukin-1 (IL-1), bacterial lipopolysaccharide (LPS), and phorbol esters but not by interferon-gamma (IFN-gamma). By contrast, EAA-B antigen expression on neonatal foreskin and rheumatoid synovial fibroblasts, whether pre-treated with TNF-alpha or not, was not detectable. Peripheral blood leucocytes and the leukaemic cell lines U937, HL-60, Raji and Molt 4 showed no detectable expression of the EAA-B antigen. Kinetic studies demonstrated that the EAA-B antigen was rapidly expressed, peaked at 6 hr and declined to basal level by 24 hr. Western blotting revealed that monoclonal antibody EAA-B recognized a polypeptide of approximately 80,000-90,000 MW. EAA-B partially blocked the augmented adhesion of HL-60 cells to TNF-treated HUVE cells. However, it failed to inhibit the enhanced binding of peripheral blood leucocytes, U937, Raji and Molt 4 Cells to TNF-treated HUVE cells. In situ, the EAA-B antigen was detected on some vascular endothelium in tonsils, lymph nodes, psoriatic skin and rheumatoid synovium but not in normal non-lymphoid tissues. Interestingly EAA-B antigen is also expressed by B lymphocytes in germinal follicle centres (GFC) of lymphoid tissues. The co-expression of this endothelial activation antigen by GFC B lymphocytes may have significant implications for immune responses and in B-lymphocyte differentiation.

Antibodies, Monoclonal↗
PubMed1991

Isolation and purification of microvascular endothelium from human decidual tissue in the late phase of pregnancy.

Normal pregnancy demands significant structural and physiologic adaptations of the uterine microvasculature, to facilitate adequate placentation. In pregnancies complicated by pregnancy-associated hypertension (preeclampsia), this process is defective, resulting in a high incidence of intrauterine growth retardation. The microvascular endothelium, a focal point for both initiation and inhibition of coagulation and control of vascular tone, may well contribute to development and aggravation of these abnormalities. We describe a method for isolation, purification, and culture of human decidual endothelial cells from biopsies performed at the time of cesarean section. The separation procedure is technically simple, requires only a small piece of tissue, and takes approximately 2 hours to perform. Some of the unique features of these cells in culture are outlined. This technique will permit the close examination of various aspects of the function of these cells in normal pregnancy, and their comparison with cells from pregnancies complicated by hypertension.

Cell Division↗
PubMed1991

Arachidonic acid metabolites in normal and autoimmune mice do not influence lymphocyte-high endothelial venule interactions.

In peripheral lymphoid organs the number of lymphocytes and the proportion of functional lymphocyte subsets are regulated by multiple factors including the control of lymphocyte migration by selective lymphocyte-high endothelial venule (HEV) interactions. In this study, prostaglandin E2 (PGE2) levels from normal and autoimmune mouse lymph node cells were measured. The contribution of eicosanoids to lymphocyte-HEV interactions in normal (CBA/T6) and autoimmune (MRL/n) mice was examined. There was no association between PGE2 production in normal or autoimmune mice and the age of onset of disease activity in the latter strains. Arachidonic acid metabolites, in particular PGE2 and leukotriene B4 (LTB4), did not have any effects on lymphocyte-HEV binding. Likewise, lymphocytes treated in vivo and/or in vitro with arachidonic acid metabolite inhibitors (acetyl salicylic acid, indomethacin, BW755C) did not alter lymphocyte-HEV binding interactions in both normal and autoimmune mice. No clinical significance could be attributed to lymph node PGE2 production and the age of onset of autoimmune disease. In summary, these findings cast doubt on the role of arachidonic acid metabolites in lymphocyte-HEV binding interactions.

Animals↗
PubMed1991

Rheumatic manifestations of neoplasia.

Neoplasia in an important cause of rheumatic disease. The mechanisms are either direct infiltration of the bone and joint, or indirect infiltration with manifestations distant from the site of neoplastic involvement. Many of the reports reviewed in this article center on direct associations. In particular, there is a report on polymyositis and dermatomyositis and the link with neoplasia. Cases of reflex sympathetic dystrophy are also described in association with neoplasia. There is further discussion on the link of hairy cell leukemia and vasculitis. Other case reports highlight the multiple associations of musculoskeletal disease and neoplasia. These reports include patients with subcutaneous sarcoidosis, ankylosing spondylitis, polychondritis, and systemic sclerosis. Articular manifestations of benign pleural fibromas are described. The existence of these reports, however, does not constitute proof of a causal relationship and the possibility of chance occurrences of two conditions must be considered. Finally, various therapies for cancer are associated with rheumatologic manifestations. Intravesical bacillus Calmette-Guérin has been found to cause an inflammatory polyarthritis. This form of arthritis is similar to experimentally induced adjuvant arthritis in rats that follows immunization with Freund's adjuvant containing Mycobacterium tuberculosis.

BCG Vaccine↗
PubMed1990

Correlation between tests of muscle involvement and clinical muscle weakness in polymyositis and dermatomyositis.

A correlation study was performed on the degree of muscle weakness in 36 patients with dermatomyositis and 69 with polymyositis in relation to muscle biopsy findings, electromyography (EMG) abnormalities, and serum concentrations of creatine kinase (CK), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) enzymes. Statistically significant correlations were found between muscle weakness and EMG results in patients with polymyositis, and between muscle weakness and serum CK and AST levels in dermatomyositis. As expected, correlations were found between the results of the three enzyme determinations in both groups of patients.

Alanine Transaminase↗
PubMed1990

Antiphospholipid antibodies in systemic lupus erythematosus: clinical and laboratory associations in 111 patients.

An enzyme linked immunosorbent assay (ELISA) was used to evaluate the prevalence and disease associations of antibodies to a range of negatively charged phospholipids in 111 patients with systemic lupus erythematosus (SLE). The frequency of one or more isotypes of different antiphospholipid antibodies (APLs) was similar (range 33%-45%). When individual isotypes were considered alone there was considerable variation (range 5%-32%). There were significant associations between thrombosis, thrombocytopenia, and central nervous system (CNS) disease but not abortion with elevated APL. Strong associations were found between raised anti-ds-DNA (Farr assay) and a positive direct Coomb's test with raised APL. Thus, APLs are common in SLE and are associated with discrete clinical and laboratory features. However, detection of antibodies to a range of negatively charged phospholipids added little clinically useful information to that obtained by measuring anticardiolipin antibody (ACL) alone. We cannot recommend the use of APLs other than ACL for routine testing.

Adolescent↗
PubMed1990

A case-control study of congenital heart block: association with maternal antibodies to Ro(SS-A) and La(SS-B).

A case control study of congenital complete heart block (CHB) was undertaken to determine the degree of association of this condition with maternal connective tissue disease and with maternal autoantibodies, in particular those to Ro(SS-A). Mothers of cases (n = 18) and controls (n = 72) completed a self-administered questionnaire and donated 10 ml of blood. The odds of giving birth to a child with CHB were increased by a factor of 22 for women with antibodies to Ro(SS-A) and/or La(SS-B) compared with women who did not have these antibodies. Thus the association between CHB and both anti-Ro(SS-A) and anti-La(SS-B) antibodies has been demonstrated in an Australian population and indicates that anti-La(SS-B), as well as anti-Ro(SS-A) antibodies may be a risk factor for the development of CHB.

Adolescent↗
PubMed1990

The cycling of combination antirheumatic drug therapy in rheumatoid arthritis.

In this open pilot study a combination of hydroxychloroquine, prednisolone and alternating months of treatment with sulphasalazine or oral weekly pulse methotrexate has been investigated in 16 patients with rheumatoid arthritis (RA) refractory to a total of 67 disease suppressive medications. Results at 3 months indicated significant improvements in visual analogue score for pain, joint count, Ritchie index, scale of disability related to activities of daily living, ESR, rheumatoid factor and C-reactive protein. This degree of improvement, however, was not maintained 6 and 12 months after commencement of treatment. Pain score, Ritchie index and ESR were the only parameters demonstrating significant improvement at 12 months. Therapy was terminated in eight patients, half due to lack of efficacy and half because of side effects.

Activities of Daily Living↗
PubMed1990

Effect of leukotriene B4 and prostaglandin E2 on the adhesion of lymphocytes to endothelial cells.

The arachidonic acid metabolites leukotriene B4 (LTB4) and prostaglandin E2 (PGE2) may play an important role in inflammation. It is not known whether these mediators influence the binding of lymphocytes to endothelial cells, a process which is important in the extravasation of lymphocytes in inflammatory states. In the present investigation, the effect of LTB4 and PGE2 on the binding interaction between lymphocytes and endothelial cells was examined using a centrifugation cell binding assay. Although LTB4 elicited an aggregation response on human polymorphonuclear leucocytes (PMNL) and enhanced their binding to endothelial cells it had no effect on lymphocyte binding. By contrast, PGE2 caused a dose-dependent inhibition of lymphocyte binding to endothelial cells. The inhibitory effect of PGE2 had a rapid onset but was exhibited only when PGE2 was present continuously during the cell binding assay. Although the mechanism by which PGE2 acts is not clear, it may provide a negative feedback mechanism in regulating the influx of lymphocytes into inflammatory sites.

Cell Adhesion↗
PubMed1990

Binding of human endothelium to Ulex europaeus I-coated Dynabeads: application to the isolation of microvascular endothelium.

A major problem encountered when isolating human microvascular endothelium is the presence of contaminating cells such as fibroblasts that rapidly over-grow the endothelial cells. We describe here a simple, rapid technique for purifying endothelial cells derived from the microvasculature of neonatal foreskin and osteoarthritic and rheumatoid arthritic synovium. This technique is based on the selective binding of the lectin Ulex europaeus I (UEA I) to the endothelial cell surface via fucose residues. Initially UEA I was covalently bound to tosyl-activated super-paramagnetic polystyrene beads (Dynabeads) by incubation for 24 h at room temperature. Cells were isolated by extracting microvascular segments from enzyme-treated (trypsin and Pronase) cubes of tissue. The mixed population of cells obtained were purified by incubating them at 4 degrees C for 10 min with the UEA I-coated Dynabeads. Endothelium bound to the beads whilst contaminating cells were removed by five washes with HBSS using a magnetic particle concentrator. The endothelial cells thus obtained grew to confluence as a cobblestone-like monolayer and expressed von Willebrand factor antigen. The cells were released from the Dynabeads by the competitive binding of fucose (10 min at 4 degrees C). This new method is simple and reproducible and allows pure human microvascular endothelial cells to be cultured within 2 h of obtaining a specimen.

Cell Line↗
PubMed1990

Aberrant lymphocyte migration patterns in systemic lupus erythematosus (MRL/l, MRL/n) mice are independent of the micro-environment.

Mice with systemic lupus erythematosus (SLE) have unusual patterns of lymphocyte traffic characterised by diminished uptake of intravenously injected autoimmune cells into lymph nodes. This study examines the influence of the lymphocyte micro-environment on this aberrant migratory behaviour. To evaluate lymph node lymphocyte-endothelial interactions which can affect lymphocyte distribution without the in vivo influence of liver and spleen, the in vitro high endothelial venule (HEV) binding assay was used. Lymph node HEV binding of autoimmune MRL-lpr/lpr (MRL/l) and MRL(-)+/+ (MRL/n) lymphocytes was increased when compared with CBA/T6 lymphocytes and contrasted with diminished lymph node uptake noted in vivo. This was independent of the lymph node source (MRL/l, MRL/n, CBA/T6) onto which the lymphocytes were overlaid. To examine the influence of the microenvironment on in vivo traffic, 21Cr-labelled lymph node cells from normal CBA/T6 mice were injected into sex-matched MRL/l, MRL/n and CBA/T6 recipients. The distribution of cells was the same in each recipient strain suggesting that the micro-environment had little influence on the lymphocyte trafficking profiles of autoimmune mice. This study supports the view that aberrant lymphocyte migration in autoimmune mice results from defects intrinsic to the lymphocyte population and not the micro-environment.

Age Factors↗
PubMed1989

Rheumatic manifestations of neoplasia.

The important association of neoplasia and rheumatic disease was reviewed. The literature in the last year included case reports of neoplasia, particularly hematologic, causing arthritis by direct joint involvement. Immunocytologic techniques may help in the diagnosis. The evidence linking dermatomyositis and polymyositis to malignancy was reviewed, although analysis of the literature was hampered by poor documentation and lack of control subjects. HOA may occur secondary to mediastinal or pulmonary metastases from nonbronchogenic malignancies. The important association of hematologic malignancy with vasculitis was highlighted.

Arthritis↗
PubMed1989

Isolation and propagation of endothelial cells derived from rheumatoid synovial microvasculature.

Synovial angiogenesis may play an important part in the destruction of articular cartilage in patients with rheumatoid arthritis (RA). As an important first step towards developing in vitro models of synovial angiogenesis, microvascular endothelial cells have been isolated, purified, and cultured from operative synovial specimens obtained from adult patients with RA.

Arthritis, Rheumatoid↗
PubMed1989

Lymphocyte migration patterns in autoimmune MRL-lpr/lpr mice: relationship to age, disease manifestations and lymphocyte homing receptor expression.

We have previously reported that lymphoid cells from systemic lupus erythematosus (SLE) mice with established disease migrate aberrantly. This study evaluates the abnormal lymphocyte migration patterns found in MRL-lpr/lpr (MRL/l) mice in relation to age, disease manifestations and the expression of lymphocyte homing receptors. 51chromium-labelled lymph node cells from MRL/l and from normal histocompatible CBA mice of different ages were injected i.v. into age and sex-matched CBA recipients. Diminished lymph node and increased hepatic uptake of MRL/l compared to CBA cells was evident as early as 6 weeks of age. Abnormalities in lymphocyte migration antedated the appearance of elevated antihistone antibody (AHA) levels but not the development of lymphadenopathy. Using the monoclonal antibody MEL-14, no differences in the expression of lymphocyte homing receptors between MRL/l and CBA lymph node cells were found at any age. Thus abnormalities in lymphocyte migration in MRL/l mice appear as early as six weeks and are not related to changes in homing receptor expression.

Age Factors↗
PubMed1989

Enhanced interferon-gamma (IFN) production by lymph node cells from autoimmune (MRL/1, MRL/n) mice.

Interferons (IFNs) have been implicated in the aetiopathogenesis of the autoimmune disease systemic lupus erythematosus (SLE). The ability of unstimulated and Sepharose-bound concanavalin A (ConA) stimulated spleen or lymph node (LN) cells from normal CBA/T6 mice and histocompatible autoimmune strains (MRL/1, MRL/n) of various ages to produce IFN-gamma was measured. Levels of IFN-gamma produced by ConA-stimulated spleen cells from CBA/T6, MRL/1 and MRL/n mice at 6 weeks of age were not statistically different (mean +/- SEM: 786 +/- 182, 1147 +/- 282, 1024 +/- 146 IU/ml, respectively). At this age only stimulated LN cells from MRL/l mice produced detectable IFN-gamma (538 +/- 44 IU/ml) and these levels remained constant up to 6 months. IFN production by stimulated LN cells from young MRL/n mice (66 +/- 21 IU/ml at 3 months, 44 +/- 41 IU/ml at 6 months) increased at 1 year (463 +/- 97 IU/ml) corresponding to the age of disease onset. The failure of stimulated CBA/T6 LN cells to produce IFN-gamma was not due to cell-cell suppression, defective IL-2 production or the generation of soluble inhibitors. Stimulated LN cells from other normal inbred (C57Bl/6, Balb/c, A/J) outbred and FI hybrid mouse strains (Swiss, [Swiss x Balb/c] F1, (CBA/T65 x C57Bl/6]FI) produced undetectable or low levels of IFN compared to MRL/1 and MRL/n mice. These results show that autoimmune mouse LNs generate more IFN compared to normal controls and that the increase in IFN levels (at least in MRL/n) corresponds to the age of disease onset.

Animals↗