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J C Foreman

Publications and source records attributed to J C Foreman.

At least 109 records · Page 6Linked to original sources
PubMed1977

Spontaneous histamine secretion from mast cells in the presence of strontium.

1. Histamine secretion from rat peritoneal mast cells occurs spontaneously in the absence of an external stimulus. Spontaneous secretion increases as the concentration of Sr in the extracellular medium is raised from 1 to 10 m-mole/l. Ca 0.1-10 m-mole/l. does not increase spontaneous secretion.2. Spontaneous histamine secretion in the presence of Sr occurs slowly compared with evoked histamine secretion, reaching a maximum only after more than 120 min incubation with Sr 10 m-mole/l. at 37 degrees C and pH 7.6. Phosphatidyl serine, 10 mug/ml., increases the rate of spontaneous secretion in the presence of Sr.3. The spontaneous secretion occurring in the presence of Sr is highly dependent on the extracellular H ion concentration. Maximal secretion occurs at pH 8.4 and only a very limited secretion is detected at pH below 7.6. The rate of spontaneous secretion is also greater at higher pH. Inhibition of secretion caused by lowering the pH can be reversed by raising the Sr ion concentration over a limited range.4. Intact glycolytic and oxidative metabolism is required for the spontaneous secretion of histamine in the presence of Sr. Removal of extracellular glucose inhibits the secretion by about 80%, and the further addition of inhibitors of oxidative phosphorylation almost abolishes the secretion.5. Ca, Mg and Mn all inhibit the spontaneous secretion of histamine which occurs in the presence of Sr. The antagonism of the effect of Sr by Mg appears not to be competitive.6. Dibutyryl cyclic AMP, 10 mumole/l. to 3 m-mole/l. and theophylline, 30 mumole/l. inhibit spontaneous secretion in the presence of Sr. Cyclic AMP, AMP, and cyclic GMP 10 m-mole/l. are without effect on the spontaneous secretion. The inhibitory effect of dibutyryl cyclic AMP and of theophylline are dependent on pH: greater inhibition being achieved at lower pH.

Adenine Nucleotides↗
PubMed1977

Movement of strontium ions into mast cells and its relationship to the secretory response.

1. Non-stimulated mast cells take up (89)Sr and (45)Ca. There is a rapid phase of uptake of both labels which is complete in 1 min and the (89)Sr uptake is similar in magnitude to the (45)Ca uptake. A further slower phase of uptake occurs in the period from 1 to 30 min of incubation. The magnitude of this slower phase is about 6 times greater for (89)Sr than for (45)Ca.2. Non-stimulated and antigen-stimulated mast cells accumulate Sr which can be measured by atomic absorption spectroscopy. There is a direct relationship between Sr accumulation and histamine secretion which is independent of whether or not the cells are stimulated. 10% histamine secretion is associated with Sr accumulation of 0.25 f-mole/cell.3. The time course of (89)Sr uptake is similar to the time course of histamine secretion in non-stimulated cells.4. The uptake of (89)Sr is linearly related to the external Sr concentration in the range 0.5-16 m-mole/l. for both stimulated and non-stimulated cells.5. Ca, 10-1000 mumole/l. inhibits (89)Sr uptake in non-stimulated cells.6. Inhibition of glycolysis and oxidative phosphorylation prevents spontaneous histamine secretion in the presence of Sr without blocking the accumulation of Sr by the cells.7. Dibutyryl cyclic AMP, 10 m-mole/l. produces only 18% inhibition of (89)Sr uptake whereas histamine secretion is inhibited by 45% by the same concentration. The antigen-stimulated Sr uptake on the other hand can be completely inhibited by dibutyryl cyclic AMP, 10 m-mole/l.8. The uptakes of (89)Sr and Sr by unstimulated mast cells after 60 min incubation are dependent on extracellular H ion concentration. Both uptakes increase with increasing pH over the range pH 7-8.5.

Animals↗
PubMed1974

Desensitization in the process of histamine secretion induced by antigen and dextran.

1. Antigen challenge of sensitized rat peritoneal mast cells in the absence of calcium failed to release histamine. The release when calcium was added subsequently declined rapidly, this desensitization being almost complete in 4 min.2. Phosphatidyl serine (10 mug/ml.) reduced the rate of desensitization so that decay of the response to added calcium was not complete after 16 min.3. Exposing normal cells to dextran resulted in a slow rate of desensitization, the response to phosphatidyl serine added with calcium having decayed by only 27% within 10 min.4. Phosphatidyl serine added with dextran prevented desensitization so that the response to subsequently added calcium did not decay even after an interval of 20 min.5. Cells activated by dextran and calcium became rapidly desensitized as shown by decay of the response to added phosphatidyl serine which was almost complete by 5 min.6. Histamine release by the calcium ionophore (A 23187) added to cells at intervals before the addition of calcium did not show significant decay.7. Desensitization of the cells to antigen did not change their response to the ionophore.

Animals↗
PubMed1973

The action of lanthanum and manganese on anaphylactic histamine secretion.

1. In the concentration range 1 nM to 1 muM, lanthanum inhibited the calcium-dependent component of anaphylactic histamine release, but was without effect on the component which was independent of calcium.2. The inhibition of anaphylactic histamine release by lanthanum can be reversed by increasing the calcium ion concentration. The pA(2) for the lanthanum-receptor interaction was found to be 7.6.3. Lanthanum also inhibited the activation of anaphylactic histamine release by strontium ions.4. The inhibition of anaphylactic histamine release by lanthanum was reversed by eluting the lanthanum from the cells.5. In the concentration range 1 to 300 nM, lanthanum had no effect on the histamine release induced by compound 48/80 in a calcium-free medium, but the effect of calcium on the istamine release by compound 48/80 was antagonized by lanthanum in this range of concentrations.6. At concentrations of 10 muM and greater, lanthanum induced a release of histamine in the absence of antigen.7. In the concentration range 0.5 to 4.0 mM, manganese inhibited the calcium-dependent component of anaphylactic histamine release, but was without effect on the component which is independent of calcium. The inhibition of anaphylactic histamine release by manganese could be reversed by increasing the calcium ion concentration.

Animals↗
PubMed1973

The interaction of calcium and strontium with phosphatidyl serine in the anaphylactic secretion of histamine.

1. Spontaneous histamine release from isolated mast cells was found to be independent of calcium in the concentration range up to 1 m-mole/l. Phosphatidyl serine did not change the effect of calcium on spontaneous release.2. Spontaneous histamine release was found to vary with the strontium ion concentration. Graded increase in the release occurred as the concentration of strontium was raised from 1 to 10 m-mole/l. Phosphatidyl serine potentiated this action of strontium; the potentiation showed a graded increase as the phosphatidyl serine concentration was raised from 1 to 100 mug/ml.3. The activation of anaphylactic histamine release by calcium was potentiated by phosphatidyl serine; the degree of potentiation showed a graded increase as the calcium concentration was raised from 0.1 to 1.0 m-mole/l.4. The activation of anaphylactic histamine release by strontium showed little, if any, potentiation by phosphatidyl serine.5. The response of the mast cells, in terms of anaphylactic histamine release, to calcium, in the presence of optimal concentrations of phosphatidyl serine, was found to be similar to that observed in the presence of strontium alone.6. These observations are discussed in terms of the concepts of affinity and efficacy of the ions at their receptor sites.

Anaphylaxis↗
PubMed1972

The role of the alkaline earth ions in anaphylactic histamine secretion.

1. Anaphylactic histamine release from rat peritoneal mast cells is dependent on the presence of calcium ions. Graded increase of histamine release occurs as the calcium ion concentration is raised from 0.1 to 1.0 m-mole/l.2. Magnesium antagonizes the effect of calcium. The dissociation constant of the Mg-receptor complex was found to be 9.4 m-mole/l.3. Strontium will replace calcium ions in the activation of anaphylactic histamine release. Graded increase of histamine release occurs when the strontium ion concentration is raised from 1.0 to 10.0 m-mole/l.4. Magnesium also antagonizes the effect of strontium. The dissociation constant of the magnesium-receptor complex was found to be 11.0 m-mole/l.5. The log concentration-effect curve for strontium has a greater maximum and steeper slope than the curve for calcium.6. Measurements of the interaction of calcium and strontium ions are in agreement with the hypothesis that strontium possesses a higher efficacy but a lower affinity than calcium, for the ;calcium receptor' in mast cells.7. Barium will replace calcium in the activation of anaphylactic histamine release.

Anaphylaxis↗
PubMedDate not supplied

Stimulatory effects of anti-rheumatic drugs on human neutrophil functions.

Auranofin (AF), D-penicillamine (D-pen) and thiola are prescribed as disease-modifying drugs in the treatment of rheumatoid arthritis (RA). We have shown here that auranofin, 10(-8) to 10(-6) M, D-penicillamine, 10(-6) to 10(-3) M, thiola, 10(-7) to 10(-3) M, and the tripeptide thiol, glutathione, 10(-6) to 10(-3) M, enhanced f-met-leu-phe-induced lysosomal enzyme release and the phagocytic uptake of bacteria by up to 40%. The previously reported inhibitory effects of AF were only observed at concentrations in excess of those likely to be available to effector cells in vivo. The stimulatory effects of thiola and D-pen occurred at concentrations likely to be available to effector cells in vivo and, therefore, may be of greater clinical relevance. There is evidence that the drugs used in this study exert their effects via a thiol moiety and their therapeutic effect is preceded by an elevation of intracellular thiol levels.

Anti-Inflammatory Agents↗