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Biomedical subjects

S S Froland

Publications and source records attributed to S S Froland.

At least 19 recordsLinked to original sources
PubMed2000

Myocardial expression of CC- and CXC-chemokines and their receptors in human end-stage heart failure.

OBJECTIVES: Chemokines regulate several biological processes, such as chemotaxis, collagen turnover, angiogenesis and apoptosis. Based on the persistent immune activation with elevated circulating levels of chemokines in patients with congestive heart failure (CHF), we have hypothesised a pathogenic role for chemokines in the development of CHF. The objective of this study was to examine mRNA levels and cellular localisation of chemokines and chemokine receptors in human CHF. METHODS: We examined explanted hearts from ten patients with end-stage heart failure (all chambers) and in ten organ donors using an RNase protection assays and immunohistochemical techniques. RESULTS: Our main findings were: (i) expression of eight chemokine and nine chemokine receptor genes in both failing and nonfailing myocardium, (ii) particularly high mRNA levels of monocyte chemoattractant protein (MCP)-1 and CXC-chemokine receptor 4 (CXCR4), in both chronic failing and nonfailing myocardium, (iii) decreased mRNA levels of MCP-1 and interleukin (IL)-8 in the failing left ventricles compared to failing left atria, (iv) decreased chemokine (e.g., MCP-1 and IL-8) and increased chemokine receptor (e.g., CCR2, CXCR1) mRNA levels in failing left ventricles and failing left atria compared to corresponding chambers in the nonfailing hearts and (v) immunolocalisation of MCP-1, IL-8 and CXCR4 to cardiomyocytes. CONCLUSION: The present study demonstrates for the first time chemokine and chemokine receptor gene expression and protein localisation in the human myocardium, introducing a new family of mediators with potentially important effects on the myocardium. The observation of chemokine dysregulation in human end-stage heart failure may represent a previously unknown mechanism involved in progression of chronic heart failure.

Adult↗
PubMed2000

The role of the tumor necrosis factor system and interleukin-10 during cytomegalovirus infection in renal transplant recipients.

The effects of cytomegalovirus (CMV) infection on monocyte and T cell activation and the role of the tumor necrosis factor (TNF) system and interleukin (IL)-10 were studied in a prospective study of 25 renal transplant recipients. Ten patients developed CMV disease (group A), 5 developed asymptomatic infection (group B), and 10 did not have CMV infection (group C). During CMV disease (group A), there was evidence of both monocyte and T cell activation. All patients with CMV infection (groups A and B) showed increased activation of the TNF system, concomitant with an increase in plasma levels of IL-10. Patients with CMV disease (group A) had more marked manifestations of TNF activation and more moderate IL-10 increase than patients with asymptomatic CMV infection (group B), reflected in a higher plasma IL-10/TNF-alpha ratio in asymptomatic patients. Thus, the balance between TNF-alpha and IL-10 may be important in the development of CMV infection and CMV-related disease.

Adult↗
PubMed1999

Tumor necrosis factor (TNF) system levels in human immunodeficiency virus-infected patients during highly active antiretroviral therapy: persistent TNF activation is associated with virologic and immunologic treatment failure.

Because persistent tumor necrosis factor (TNF)-alpha activation may play a pathogenic role in human immunodeficiency virus infection, TNF component levels were assessed over 78 weeks in plasma and peripheral blood mononuclear cells (PBMC) during highly active antiretroviral therapy (HAART) in 40 HIV-infected patients. HAART induced a significant decline in plasma levels of TNF-alpha and soluble TNF receptors and was associated with a fall in the abnormally increased unstimulated and a rise in the abnormally low Mycobacterium avium complex-purified-protein derivative-stimulated TNF-alpha released from PBMC. However, concentrations of these TNF components were not normalized. Patients with virologic and immunologic treatment failure after 52 weeks had higher levels of several TNF components than other patients early after initiation of therapy, also during periods with adequate virologic response. Although TNF components significantly decreased during HAART, these results support data indicating that full immunologic normalization is not achieved during such therapy. The persistent activation of the TNF system in a subgroup of persons may be involved in treatment failure.

Adolescent↗
PubMed1998

Possible role of interleukin-10 (IL-10) and CD40 ligand expression in the pathogenesis of hypergammaglobulinemia in human immunodeficiency virus infection: modulation of IL-10 and Ig production after intravenous Ig infusion.

The mechanisms leading to polyclonal hypergammaglobulinemia in patients with human immunodeficiency virus (HIV) infection are not well understood. In light of the important role of interleukin-10 (IL-10) and the interaction between CD40 and CD40 ligand in the normal regulation of B-lymphocyte function and Ig production, we examined these parameters in 24 HIV-infected patients. Both plasma IL-10 levels and the percentage of CD4(+) and CD8(+) lymphocytes expressing CD40 ligand were significantly higher in the patients than in the 10 blood donor controls. Serum IgG correlated positively with circulating IL-10 levels and the percentage of CD4(+) lymphocytes expressing CD40 ligand. Furthermore, a single bolus infusion of intravenous Ig (0.4 g/kg) in 8 HIV-infected patients caused a further increase in IL-10 levels in plasma and an increase in both IL-10 and IgG production in peripheral blood mononuclear cell cultures. In another patient group (Wegener's granulomatosis) receiving a single bolus infusion of intravenous Ig, a similar increase in plasma IL-10 levels was found, suggesting that this may be a general effect of intravenous Ig. In patients with HIV infection, our data suggest that a vicious cycle may be operative where high endogenous Ig levels may enhance IL-10 production that, in turn, leads to higher Ig production.

Adult↗
PubMed1977

A study of the variable heavy chain (VH) region of membrane-bound Ig on human chronic leukemic lymphocytes.

Lymphocytes from 20 patients with chronic lymphocytic leukemia (CLL) were studied for membrane staining by direct immunofluorescence by employing anti-F(ab')2, anti-VHI, anti-VHII, anti-VHIII subgroup-specific antisera, as well as light chain-specific antisera. Some lymphocyte preparations were also studied in indirect immunofluorescence with an antiserum raised against a fragment (VH) corresponding to the variable region of the heavy chain of a human IgG3 myeloma protein (Kup). Lymphocytes from each CLL patient demonstrated a restriction of VH subgroups expressed on the cell membrane; six were restricted to the VHI subgroup, seven to VHII, and seven to the VHIII subgroup. This restriction gave further evidence for monoclonality of the membrane-bound Ig and the leukemic cell proliferation. Antiserum to the VH fragment stained closely similar percentages of CLL lymphocytes to that obtained with anti-F(ab')2 antiserum. Furthermore, double staining revealed that the same cells were stained with anti-VH antiserum as were stained with anti-F(ab')2 antiserum, i.e., only the B lymphocytes.

Adult↗
PubMed1976

Chronic lymphocytic leukemia: studies on the effect of drug treatment on different lymphocytic subpopulations.

In the present work the effect of drug treatment on different lymphocyte populations in chronic lymphocytic leukemia was studied. During therapy there was evidence of an increased number of cells unidentifiable by conventional surface markers, provisionally termed lymphocyte surface-marker-negative cells. In addition, evidence of increased numbers of T lymphocytes in untreated patients and further evidence of IgG chronic lymphocytic leukemia cells were obtained.

Adult↗
PubMed1976

Distribution of heavy-chain variable-region (Vh) subgroups on human lymphocytes.

Lymphocytes from 20 normal blood donors were stained with fluorescein isothiocyanate (FITC)-conjugated anti--F(ab')2, anti-VHI, anti-VHII, and anti-VHIII subgroup antisera. The means of the percentages of staining were 2.9%, 5.0% and 5.5% for the VHI, VHII, VHIII subgroups, respectively. The sum of the percentages of the lymphocytes stained with each of the VH subgroup-specific antisera corresponded well with the percentages of lymphocytes stained with an anti-F(ab')2 antiserum. In addition, it was shown by double immunofluorescence staining and in various depletion experiments and tests with thymocytes and lymphocytes from patients with hypogammaglobulinemia that the cells staining with anti-Vh antisera corresponded to the membrane Ig-positive cells--that is, the B-lymphocyte population.

B-Lymphocytes↗
PubMed1976

Measles virus-induced migration inhibition in vitro of leukocytes from patients with multiple sclerosis.

The migration inhibition in vitro induced by measles virus material on leukocytes from 17 patients with multiple sclerosis (MS) was compared with that of 8 patients with various other central nervous system diseases and that of 12 healthy blood donors. Significant differences could not be demonstrated. The results do not indicate that MS patients' leukocytes show an altered behaviour to measles virus material in the migration inhibition test.

Adult↗
PubMed1976

Measles virus-induced migration inhibition of human leukocytes in vitro: an expression of cell-mediated immunity?

Attempts were made to establish measles virus-induced migration inhibition of human leukocytes as an in vitro test of cell-mediated immunity to the virus. Crude material from cell cultures infected with two different strains of measles virus was used as antigen in the capillary modification of the test. Both virus preparations induced migration inhibition. Incubation with puromycin indicated that the inhibition was dependent on protein synthesis, which has been regarded as a characteristic feature of an immunologically specific inhibition. However, no difference was found when the migration inhibition of leukocytes from donors without clinical and serological evidence of previous measles infection was compared with that of leukocytes from donors with such evidence. It is concluded that the migration inhibition induced by crude measles virus material does not necessarily measure cell-mediated immunity to the virus.

Adult↗
PubMed1976

Nonsecretory myelomatosis without intracellular immunoglobulin. Immunofluorescent and ultramicroscopic studies.

A patient with multiple myeloma is reported with severe hypogammaglobulinaemia but without monoclonal immunoglobulin (M-component) in the serum or Bence Jones protein in the urine. In May-Grünwald-Giemsa stained bone marrow film 45% of the cells resembled plasma cells. Marrow immunofluorescent studies showed no increase of immunoglobulin containing cells. Ultrastructural studies showed a large number of cells with a well developed rough endoplasmic reticulum and other morphological features characteristic for plasma cells.

Bence Jones Protein↗
PubMed1976

Abnormal lymphocyte populations in pure red cell aplasia.

Studies of blood lymphocytes from 4 patients with pure red cell aplasia were performed with lymphocyte surface markers, and with various in vitro tests for lymphocyte functions. Pathologically low B-lymphocyte values were found. In contrast, no marked deviation from normals were seen for T-lymphocytes and Fc-receptor-bearing lymphocytes thought largely to represent non-B, non-T-lymphocytes. In 3 patients normal lymphocyte transformation was found with unspecific and specific mitogens, while the DNA-synthesis induced by unspecific mitogens was subnormal in the fourth patients. The lymphocyte-mediated PHA-induced cytotoxicity against target cells in vitro was subnormal in 2 patients, while no depression was seen in antibody-dependent cytotoxicity mediated in vitro by lymphocytes (K-cells). It is concluded that considerable immunological abnormalities are associated with pure red cell aplasia, and the possible significance of this is discussed.

Adult↗
PubMed1975

Elution and characterization of lymphocytes from rheumatoid inflammatory tissue.

Lymphocytes were eluted from the synovial tissue of 19 patients with classical rheumatoid arthritis. The tissue was minced and dissociated by treatment with crude collagenase and DNase. The cell suspension obtained was filtered and incubated in plastic culture flasks overnight at 37 degrees C. The cells that did not adhere to the plastic surface were harvested and the lymphocytes further purified by the Ficoll-Isopaque gradient centrifugation technique. The lymphocyte yield varied from 0.64 to 32 times 10(6) cells. Differential counts showed on the average 85% lymphocytes, 12% mocrophage-like cells, and variable proportions of polymorphonuclear granulocytes, unclassified cells, and dead cells. An average of 77% of the cells were viable as assessed by the trypan blue exclusion test. This cell suspension was investigated for lymphocyte populations. T lymphocytes were predominant in all experiments (mean, 73.6%). The mean percentage of B lymphocytes was 9.7%, whereas the proportion of Fc-receptor-bearing lymphocytes was on the average 6.0%.

Adult↗
PubMed1975

Case report: maldescent of the thymus in a hypoparathyroid infant with Pharyngeal Pouch Syndrome.

The clinical and pathological findings in a 6-month-old boy with III-IV pharyngeal puoch syndrome are reported. The infant had multiple congenital anomalies including absence of the parathyroid glands, maldescent of the thymus, aberrant right subclavian artery and dysfunction of the glossopharyngeal nerve. Because of persistence of the thymus in the cervical area, a thymic shadow was not found on roentgenographic examination of the anterior mediastinum. The weight and histology of the thymus were normal, as were studies of humoral and cellular immunity.

Abnormalities, Multiple↗
PubMed1975

Different lymphocyte populations in rheumatoid arthritis and their relationship to anti-Ig activities.

The anti-immunoglobulin activities of rheumatoid arthritis appear to be related not only to plasma cells and their precursors, the B-lymphocytes. Evidence for interaction of IgG with T-lymphocytes and with Fc-bearing lymphocyte-like cells has now appeared. Both these cell types can mediate cytotoxicity which may also induce inflammation in addition to that provoked by rheumatoid factors and immune complexes. Rheumatoid factors and immune complexes may act primarily through the complement system. However, active inflammation in rheumatoid patients can occur without abundant immune complexes, e.g. in B-cell-deficient patients (31). In some cases this may be due to activation of the alternate complement pathway. However, the T-cell system with its series of lymphokines may also play an active part-in the inflammatory process. And both T-lymphocytes and Fc-bearing lymphocyte-like cells, the K-cells, can mediate cytotoxicity. Also in such patients further studies are needed to work out the complex interactions between these cell types and to discover the underlying cause or agent in the chronic destructive rheumatoid inflammation.

Antibodies, Anti-Idiotypic↗