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Biomedical subjects

W Schmutzler

Publications and source records attributed to W Schmutzler.

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

Glucocorticoid-induced appearance of the macrophage subtype RM 3/1 in peripheral blood of man.

The effect of intravenous administration of the glucocorticoid prednylidene on the macrophage subtype RM 3/1 in the peripheral blood of man was studied. Injection of 60 mg steroid resulted in an increase in the proportion of RM 3/1 positive monocytes 12 h after application from the basic level to about 80%. After 24 h the number of RM 3/1 positive cells decreased but remained elevated over the basis rate for a period of at least 15 days. Similar results were obtained after administration of 30 or 6 mg prednylidene even if the peak value occurred with a delay of 12 h after 6 mg. A dose- and time-dependent induction of the RM 3/1 positive subtype could also be demonstrated in vitro by the addition of prednylidene or dexamethasone to cultured purified human monocytes/macrophages. Deoxycortone or indomethacin had no effects. These results suggest that glucocorticoids exert their influence on cells of the mononuclear phagocytic lineage by inducing a distinct monocyte/macrophage subpopulation which seems to be associated with anti-inflammatory functions.

Adult↗
PubMed1989

The effects of metoclopramide and cloxacepride on human mast cells from adenoidal tissues.

Cloxacepride is an amide of the dopamine antagonist metoclopramide and has been reported to possess oral antiallergic properties in the rat PCA model. Both substances have now been tested in isolated mast cell preparations from human adenoidal tissues to determine whether any therapeutic antiallergic potential in man could be expected. Metoclopramide at concentrations 10(-5)-10(-3) M had no inhibitory effect but instead enhanced Con A-induced histamine release at concentrations greater than 10(-4) M. Cloxacepride at concentrations 10(-5)-10(-4) M significantly inhibited Con A-induced histamine release. This inhibitory effect was not diminished by increasing the preincubation time for up to 30 min. In contrast, cloxacepride concentrations greater than 4 x 10(-5) M caused a substantial histamine release. This effect could not be alleviated by an increase in the number of mast cells per sample. These results then suggest a very narrow range of therapeutic potential for cloxacepride.

Adenoids↗
PubMed1989

Study of the antiallergic component of inosine pranobex (Inosiplex, Isoprinosine).

Inosine pranobex (INPX) at concentrations greater than 10(-3) M inhibits significantly the concanavalin A or antihuman IgE induced histamine release from human mast cells. The inosine moiety of the compound does not contribute to this effect, but rather interferes with it. The other component, the salt of dimethylaminopropanol and acetamidobenzoic acid, produces a small but significant inhibition of the histamine release already at 10(-6) M. This effect is due to the acetamidobenzoic acid although the base (dimethylaminopropanol) adds to it. With increasing incubation time, the salt of dimethylaminopropanol and acetamidobenzoic acid looses its histamine release inhibiting effect.

Concanavalin A↗
PubMed1988

Synthetic retinoids inhibit histamine release from isolated human mast cells.

In view of the immunomodulating properties of the synthetic retinoids etretinate and isotretinoin, their effects on isolated human mast cells were investigated. At concentrations of 10(-6) to 10(-5) M, isotretinoin and at 10(-6) M to 5 X 10(-5) M, etretinate inhibited concanavalin-A induced histamine release dose-dependently. Effective concentrations corresponded to achievable levels under therapeutic conditions in man. Without any additional stimulant, both drugs exhibited no appreciable effects with the exception of a toxic damage at very high levels.

Concanavalin A↗
PubMed1988

Human C5a induces a substantial histamine release in human basophils but not in tissue mast cells.

The histamine-releasing effect of human C5a was compared with that of concanavalin A in blood basophils and isolated adenoidal mast cells from the same donors. In basophils, C5a (10 ng/ml) induced a significant histamine release (7.5 +/- 2.1%, corrected value). In isolated adenoidal mast cells C5a had only a marginal effect (2% histamine release), although the cells responded markedly to concanavalin A stimulation (about 13% release). The results support the view that the heterogeneity of mast cells and basophils is also reflected in the expression of anaphylatoxin receptors on their surface.

Adenoids↗
PubMed1987

Study of the inhibition of histamine release by inosine pranobex.

The effects of Inosine pranobex and its parent compounds inosine and dimethylamino-2-propanol-p-acetamidobenzoic acid (DipPacBa) on the Concanavalin A (ConA)-induced histamine release from human adenoidal mast cells were investigated. Inosine pranobex inhibited the ConA-induced histamine release at concentrations greater than 10(-3) M. Inosine itself (10(-5)-10(-2) M) enhanced the ConA-induced histamine release whereas DipPacBa inhibited the release significantly at concentrations between 10(-6) and 10(-2) M. These results are consistent with the assumption that the effect of Inosine pranobex is due to the DipPacBa moiety.

Concanavalin A↗
PubMed1987

Seasonal variation of mast cell function in human adenoid tissues.

The number of mast cells which can be recovered from human adenoid tissues varies characteristically in the course of the year. The yield was found to be highest in May and lowest in July. The average histamine content was above average in April, June, July and September. Although the spontaneous histamine release remained relatively constant, the concanavalin A-stimulated histamine release was significantly reduced from June to September.

Adenoids↗
PubMed1986

The effects of the anaphylatoxins C3a and C5a on isolated mast cells from rat and man.

Of the complement peptides comprising anaphylatoxin activity, only C5a caused a very small (less than 1.5%) but statistically significant histamine release from isolated human adenoidal mast cells. C3a and the respective des-Arg-derivatives were found to be ineffective. In rat peritoneal mast cells, neither peptide caused histamine release.

Animals↗
PubMed1986

Tolerance to monovalent dextran of human mast cells.

In the present study it was investigated if monovalent dextran (Dx 1, HR 573, Promit) possibly involving activated complement is capable of inducing mediator (histamine) release from isolated human mast cells. Dx 1 in the absence or in the presence of 20% fresh human serum did not induce a histamine release from human mast cells. The "non-release" could be established statistically using a new sequential test which provides a substantial reduction of the average sample size required to reach a prescribed test power. In contrast, concanavalin A (Con A) or ionophore A 23187 caused a marked histamine release in the absence of human serum. In the presence of human serum the spontaneous histamine release was increased but the Con A- or ionophore-induced release was inhibited.

Dextrans↗
PubMed1985

The effects of adenosine and of some adenosine analogues on the concanavalin A-or acetylcholine-induced histamine release from human adenoidal mast cells.

Histamine release induced by concanavalin A (Con A) or acetylcholine is enhanced by adenosine or the adenosine analogues PIA and NECA. The enhancement is not affected by preincubation with adenosine deaminase. The degree of the Con A-induced histamine release decreases with increasing incubation time. Under these conditions, the enhancing effect of adenosine on histamine release is either abolished or even reversed to inhibition.

Acetylcholine↗
PubMed1985

The human adenoidal mast cell. Susceptibility to different secretagogues and secretion inhibitors.

Mast cells from adenoid tissues of man do not form a homogeneous population but differ in size and ultrastructure. They degranulate on stimulation with specific antigen, ionophore A 23187, Concanavalin A and, under certain conditions, antihuman IgE or acetylcholine. Compound 48/80, dextran, purified C3a or C5a are ineffective. Adenosine exerts either an enhancing or inhibiting effect on the stimulated histamine release, depending on the actual conditions of the mast cells. The study of a range of known mast cell degranulation inhibitors revealed important differences between human adenoidal mast cells and human basophils or animal mast cell systems. The efficacies of the drugs or drug combinations so far tested correspond well with the established therapeutic effects in man.

Adenoids↗
PubMed1984

Recognition of the 'calcium paradox' and the effects of verapamil and gallopamil in human adenoidal mast cells.

Human mast cells from adenoids show when resuspended in medium containing 10(-3) M CaCl2 after their temporary exposure to Ca2+-free saline for about 20 min an irreversible reduction of responsiveness to a variety of stimuli: The histamine release induced by concanavalin A or ionophore A 23187 is only 30-50% of the one obtained in cells which were kept in 10(-3) M Ca2+ throughout the experiment. This phenomenon called 'calcium paradox' can be almost entirely avoided if the cells are temporarily exposed to 10(-4) M Ca2+ instead of Ca2+-free saline. Number yields, average histamine contents of mast cells and the rate of the spontaneous histamine release are not affected by the transitory lack of Ca2+, nor is the histamine release enhancing effect of adenosine. At 10(-3) M Ca2+ concentration the calcium antagonists verapamil or gallopamil cause a significant inhibition of the Con A-induced histamine release only at concentrations much higher (10(-4) M than those effective in smooth muscle preparations. The actions of both calcium antagonists were not affected by the presence of added extracellular adenosine.

Adenoids↗
PubMed1983

[Pharmacological aspects of immunostimulants].

Immunostimulants are chemical substances capable of increasing the overall activity of a normal immune system as well as normalizing the function of an impaired immune system (immune restauration). This review is concerned with substances of microbial or chemical origin and excludes the so-called physiological inductors or regulators, e.g. thymic factors, interferon etc. During the last decade considerable progress has been achieved with respect to the isolation of effective compounds and the elucidation of their chemical structure. However, the knowledge of their mechanism of action and their effects in the living organism is still poor because of the complexity of the immune system, lack of appropriate standardization methods, lack of internationally agreed test conditions or diseases in intact animals or conditions for controlled clinical trials in man.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1983

[Pharmacological aspects of immunostimulation].

Immunostimulants are chemical substances capable of increasing the overall activity of a normal immune system as well as normalizing the function of an impaired immune system (immune restauration ). This review is concerned with substances of microbial or chemical origin and excludes the so-called physiological inductors or regulators, e.g. thymic factors, interferon etc. During the last decade considerable progress has been achieved with respect to the isolation of effective compounds and the elucidation of their chemical structure. However, the knowledge of their mechanism of action and their effects in the living organism is still poor because of the complexity of the immune system, lack of appropriate standardization methods, lack of internationally agreed test conditions or diseases in intact animals or conditions for controlled clinical trials in man.

Adjuvants, Immunologic↗
PubMed1982

Centrifugal elutriation studies in mast cells from rats, guinea pigs and man.

Elutriation is a cell separation method based on countercurrent centrifugation. For mast cell purification it is superior to density gradient methods since no foreign protein or dense material has to be removed from the purified cells. The elutriation profiles of peritoneal rat mast cells differ considerably if the cells come from non-sensitized or actively sensitized donor animals and/or from different strains. This result is another indication of an altered morphological state of mast cells due to active immunization and is dependent on genetic factors. Cell aggregation proved to be the main obstacle to elutriation purification of guinea pig tissue mast cells. Human mast cells from adenoid tissues, however, could be brought to 70-90% purity, even if the elutriation profiles varied from donor to donor.

Adenoids↗