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H Northoff

Publications and source records attributed to H Northoff.

At least 109 records · Page 6Linked to original sources
PubMed1987

Discrimination of hepatocyte-stimulating activity from human recombinant tumor necrosis factor alpha.

The involvement of tumor necrosis factor alpha (TNF alpha) in the regulation of acute-phase protein synthesis is currently under discussion. In this study the effect of human recombinant TNF alpha on the regulation of the 4 acute-phase proteins alpha 2-macroglobulin, albumin, alpha 1-proteinase inhibitor and alpha 1-acute-phase globulin was investigated in rat hepatocyte primary cultures. No changes in synthesis of any of the 4 proteins were observed. However, an acute-phase response similar to that in vivo could be generated by conditioned media from human monocytes containing natural TNF alpha. This response remained unchanged after neutralizing TNF alpha activity by the addition of a specific antibody to TNF alpha. It is concluded that the hepatocyte-stimulating activity synthesized by human monocytes is different from TNF alpha.

Acute-Phase Proteins↗
PubMed1987

Blood group change in a patient with blastic transformation of a myelodysplastic syndrome.

Loss of certain red blood cell antigens has been described in patients with acute myelocytic leukemia (AML). This paper describes the loss of blood group A antigen in a patient with AML. The acute leukemia in this patient was preceded by a myelodysplastic syndrome for several months. At the time of diagnosis the patient's red cells showed the 0 Rh(D)+ phenotype. After induction of complete remission with two courses of Daunorubicin, Cytosin-arabinosid, and Etoposid his blood group reverted to A2. Serological studies including saliva analysis revealed that the original blood group was very likely A.

ABO Blood-Group System↗
PubMed1987

Endotoxic activities of tumor necrosis factor independent of IL1 secretion by macrophages/monocytes.

Recombinant tumor necrosis factor (TNF) had hypothermic activity in vivo. Intravenous injection of TNF resulted in a hypothermic reaction of mice within 3 to 6 hours. This reaction was not the result of interleukin 1 (IL1) release from macrophages/monocytes. Peritoneal exudate cell cultures from endotoxin low responder mice or human peripheral mononuclear leukocyte cultures did not generate IL1 activity in the supernatant after exposure to TNF. The addition of interferon-gamma (IFN-gamma) or preexposure to IFN-gamma and then stimulation with TNF did also not result in IL1 secretion. No IL1 inhibitor was generated and TNF did not interfere with the IL1 test systems. Therefore, we conclude that the hypothermic activity of TNF is not mediated via the induction of IL1 production by mononuclear phagocytes.

Animals↗
PubMed1986

The acute-phase induction of alpha 2-macroglobulin in rat hepatocyte primary cultures: action of a hepatocyte-stimulating factor, triiodothyronine and dexamethasone.

During inflammation a number of liver-derived plasma proteins increases in concentration. In the rat these so-called acute-phase proteins are mainly proteinase inhibitors, such as alpha 1-proteinase inhibitor, alpha 1-acute-phase globulin and alpha 2-macroglobulin. At present, the mechanisms responsible for the enhanced synthesis of acute-phase proteins are poorly understood. Therefore, we have studied the induction of alpha 2-macroglobulin synthesis in rat hepatocyte primary cultures. Adrenaline, triiodothyronine, estradiol and progesterone were tested for their ability to stimulate alpha 2-macroglobulin synthesis. Only triiodothyronine induced alpha 2-macroglobulin synthesis markedly. However, the presence of dexamethasone was a prerequisite for alpha 2-macroglobulin induction indicating a permissive action of glucocorticoids. Besides glucocorticoids and triiodothyronine a non-dialyzable factor (HSF) derived from rat Kupffer cells or human peripheral blood monocytes was found to be able to stimulate alpha 2-macroglobulin synthesis in hepatocytes. Equal amounts of HSF activity were found in conditioned media from lipopolysaccharide-stimulated and unstimulated rat Kupffer cells as well as in human monocytes. Since the supernatants of unstimulated rat Kupffer cells or human monocytes did not exhibit interleukin 1 activity, HSF activity distinct from interleukin 1 must exist. No HSF activity was found in media conditioned by rat Kupffer cells which had been treated with dexamethasone. Hepatocyte primary cultures were incubated with [35S]methionine-labeled proteins secreted by rat Kupffer cells. A 30 kDa polypeptide was found to be bound to or internalized by rat hepatocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

A patient, mosaic for Rh and Fy antigens lacking other signs of chimerism or chromosomal disorder.

A patient who shows two populations of RBC, differing in their Rh and Fy antigens, was investigated but no other sign of chimerism or mosaicism in a variety of other antigenic systems, including serum and enzyme polymorphisms and HLA antigens, was observed. His karyotype, as investigated on lymphocyte and fibroblast cultures, was normal. Possible explanations of the observed phenomenon are discussed.

Alleles↗
PubMed1984

[Lymphokine production in vitro by blood lymphocytes from patients with a defective or hyperactive immune system].

Blood lymphocytes from 8 patients with common variable immunodeficiency (CVID), 5 patients with signs of polyclonal activation of the immune system (1 SLE, 3 AILAP, 1 NHL) and 6 patients with various granulomatous diseases were examined for their capacity to produce lymphokines in vitro. Lymphocytes from 16 healthy individuals served as controls. To induce interleukin-2 (IL-2) and gamma-interferon (gamma-IFN) production lymphocytes were stimulated for 24 hrs with ConA or PHA or for 72 hrs with ConA + PMA + urea. alpha-IFN production was induced with Herpes simplex virus I (HSV) and the mycoplasma infected murine leukemia line L1210. Cell-free culture supernatants were harvested and IL-2 activity was determined by means of its growth promoting activity for a murine T-cell line (M-2). IFN activities were measured in a conventional virus plaque reduction assay. Besides lymphokine production the isolated cells were also examined for lymphocyte markers, mitogen responsiveness and NK activity. As compared to the control group, CVID lymphocytes exhibited a slightly enhanced IFN production and a moderately reduced IL-2 production. Three day preincubation in FCS containing medium enhanced the IL-2 production of control and patient lymphocytes. By contrast, preincubation of lymphocytes in medium supplemented with autologous serum no longer enhanced IL-2 production of CVID lymphocytes whereas it still did so for control lymphocytes. A striking finding was the impairment of IL-2 and IFN production in cultures of lymphocytes from patients with a polyclonally activated immune system. Notably lymphocytes from the three patients with angioimmunoblastic lymphadenopathy (AILAP) failed to produce significant amounts of lymphokines. Patients with granulomatous diseases (3 Morbus Behçet, 1 tuberculosis, 2 chronic granulomatous diseases) showed little alterations of their lymphokine production capacity. The results are compared with other lymphocyte parameters and are discussed in view of recent reports in the literature on lymphokine production in various diseases.

Adult↗
PubMed1983

An ABO-blood group abnormality leading to the detection of a colon-carcinoma.

A patient who had been admitted to hospital for surgical treatment of inguinal hernias was found to have group phenotype of A1B in the presence of a non-auto-anti-B. No previous records of the patient's blood group were available. The serological workup including absorption and saliva inhibition studies yielded a high probability for an acquired B-antigen which is known to be often associated with carcinoma of the colon. Subsequent coloscopy revealed the presence of a carcinoma of the sigmoid, unaccessable to palpation. To our knowledge this is the first report in the literature that the serological diagnosis of an acquired B-antigen led to the detection of a hitherto undetected carcinoma.

ABO Blood-Group System↗
PubMed1983

Inhibition of mitogen-induced lymphocyte proliferation by ouabain: interference with interleukin 2 production and interleukin 2 action.

Since the discovery of IL 2 it has been possible to dissect the mitogenic activation of T lymphocytes into two steps: first, the production of IL 2; and second, the response of IL 2-dependent T cell blasts to IL 2. We investigated the influence of ouabain, a known inhibitor of T cell activation, on the production of and the response to IL 2 in mouse T lymphocytes. Ouabain dose-dependently inhibited DNA synthesis in Con A activated C57BL/6 spleen cells; inhibition below background levels occurred at a concentration of 5 X 10(-4) mol/liter. The action of IL 2 was assayed on a mouse T cell line, named M 2, derived from C57BL/6 spleen cells and maintained in continuous IL 2-dependent culture for more than 21 mo. Ouabain dose-dependently inhibited the response of these cells to mouse IL 2 with optimal inhibition at 10(-3) mol/liter ouabain. The production of IL 2 by Con A-stimulated C57BL/6 spleen cells was also totally inhibited by 10(-3) mol/liter ouabain; 10(-4) mol/liter ouabain inhibited IL 2 production partially, and 10(-5) mol/liter and 10(-6) mol/liter ouabain had no inhibitory effect. The ouabain-mediated inhibition of IL 2 production and of IL 2 action was not due to a nonspecific toxicity, because the preincubation of spleen cells with 10(-3) mol/liter ouabain for 24 hr did not impair their ability to produce IL 2, nor was the response of M 2 cells to exogenously added IL 2 abrogated by the preincubation of the cells with 10(-3) mol/liter ouabain. The data suggest that ouabain acts on two steps during the induction of T cell activation.

Animals↗
PubMed1982

The effect of phorbol-myristate acetate and concanavalin A on the growth of interleukin-2-dependent T-cell lines.

We tested the effect of phorbol myristate acetate (PMA) and of Con A on the growth of two Il-2 dependent T cell-lines. Il-2 dependent growth, as measured by 3H-TDR incorporation or viable cell counts was enhanced by PMA (5-100 ng/ml) and inhibited by Con A. These effects were only reproducible in the presence of intermediate concentrations of Il-2 containing supernatant. The enhancing effect of PMA was probably due to a positive influence on the replication rate since the drug had no visible effect on cell survival and since no evidence was found for the induction of Il-2 production by the cell-lines.

Animals↗
PubMed1981

Depressed mediator release by inflammatory exudate cells in immunized rats following antigen challenge.

The aim of the present study was to characterize leukocytes present in a local inflammatory reaction with respect to production of prostaglandin E (PGE) and the release of factors affecting lymphocyte function, which are produced by macrophages (interleukin-1) or stimulated lymphocytes (interleukin-2). Lewis rats immunized against bovine serum albumin (BSA) were challenged by intraperitoneal injection of antigen. The PGE release by peritoneal cells (PEC) was tested in vitro and found to be enhanced in immunized rats before BSA challenge. However, PEC harvested after the injection of antigen showed a marked reduction in prostaglandin production during the first 24 hr. When these cells were tested for the secretion of lymphokines (IL-1, IL-2) the same depression was found.

Animals↗
PubMed1981

Microtubules: are they involved in the initiation of lymphocyte activation?

Purified human blood lymphocytes were stimulated with concanavalin A or phytohemagglutinin. DNA synthesis was measured with 2-h pulses of [3H]thymidine between 48 h and 73 h after stimulation. Colchicine, at concentrations between 0.1 muM and 10 muM, suppressed consequent DNA synthesis without affecting viability of the cells when added at any time up to 18 h before incorporation of [3H]thymidine was assessed. In concanavalin-A-stimulated lymphocytes, removal of the mitogen by methyl alpha-mannoside only prevented proliferation when added initially, but was without any effect when added after 20 h of stimulation, regardless of when DNA synthesis was measured. Thus, there was a period after 20 h of concanavalin A stimulation, when DNA synthesis was still sensitive to colchicine, but no longer required the presence of the mitogen. Colchicine also suppressed incorporation of [3H]leucine into protein, in resting as well as mitogen-stimulated lymphocytes. Similarly, colchicine decreased amino acid transport, as determined by uptake of alpha-amino-isobutyrate, which appeared to be the rate-limiting step in the incorporation of amino acids into protein in colchicine-treated cells. When the rate of protein synthesis was followed by the relative distribution of ribosomal particles, especially the increase of polysomes in activated lymphocytes, colchicine was without any detectable effect. The early increase in the incorporation of [14C]oleate into phospholipids was identical in the presence or absence of the microtubule-active drug. The data strongly suggest that microtubules are not involved in the initiation of lymphocyte growth or mitogenesis.

Biological Transport↗
PubMed1980

Inhibition of concanavalin A-induced human lymphocyte mitogenic factor (Interleukin-2) production by suppressor T lymphocytes.

Supernatants of fresh human MNL stimulated with concanavalin A (Con A) generally contain little or no lymphocyte-derived mitogenic factor (LMF or Interleukin-2). However, preincubation of MNL in culture medium for 2 to 5 days before stimulation with Con A rendered them capable of producing increasing LMF. The production of LMF by reincubated MNL was inhibited by readdition of autologous fresh MNL or E-rosetting (T) lymphocytes. The producing cells were T lymphocytes; however, the production of LMF was monocyte dependent. LMF eluted from a Sephadex G150 column in 2 peaks at 12 to 27,000 and 50 to 70,000 daltons. Both species of LMF were mitogenic for mouse (C3H/HeJ) thymocytes and for human T and B cells. LMF production was not affected by x-irradiation (less than or equal to 2500 R) before preincubation; it was, however, abolished by the addition of 10(-7) M hydrocortisone during the preincubation period. LMF production by fresh MNL could be moderately enhanced by the addition of cimetidine, a drug that is known to interfere with histamine H2 receptors on suppressor T cells. Presumably, preincubation of MNL reduces the activity of Con A-induced suppressor cells. We conclude that human peripheral blood contains suppressor T cells that when activated by Con A regulate the production of LMF by other T cells in response to Con A.

Cell Adhesion↗