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Biomedical subjects

F L Pearce

Publications and source records attributed to F L Pearce.

At least 37 records · Page 2Linked to original sources
PubMed1989

Non-IgE-mediated mast cell stimulation.

The effect of a variety of non IgE-mediated stimuli on histamine release from mast cells from different locations is described. Sensory neuropeptides are shown to resemble other polycationic compounds in preferentially activating mast cells from the rat while having a limited effect on human mast cells, except possibly those from skin. Similar results were obtained with the putative non-adrenergic, non-cholinergic neurotransmitter ATP, thereby questioning the role of neuronal mast cell activation in allergy and inflammation. Bradykinin also acted selectively against rat cells while complement-derived and formylmethionyl peptides were effective against human basophils and cutaneous mast cells. The latter results may indicate a role for the skin cell in local inflammatory responses involving complement activation and in host resistance to bacterial infection. Rat mast cells and human basophils were most responsive to hyperosmolar challenge but significant effects were obtained from human pulmonary mast cells obtained by bronchoalveolar lavage. The latter cells may thus be implicated in exercise-induced asthma. The plasma substitute dextran was a specific secretagogue for the rat while morphine sulphate largely induced histamine release from human cutaneous mast cells. The latter result may account for anaphylactoid reactions to the opiate. In total these data emphasize the functional heterogeneity of mast cells from different locations and highlight the particular pharmacological properties of the skin mast cell in man.

Animals↗
PubMed1989

Active sensitization does not increase the responsivity of rat peritoneal mast cells to diverse chemical stimuli.

Peritoneal mast cells from specific pathogen-free rats that had been sensitized to the nematode Nippostrongylus brasiliensis released histamine in a dose-dependent fashion on challenge with antigen, anti-rat IgE, anti-rat IgG and concanavalin A. Cells from non-sensitized animals showed weak or insignificant responses to these agents. However, the two preparations did not obviously differ in their reactivity to a range of pharmacological agents including ATP, dextran, polyamines and calcium ionophores. Both populations were refractory to cholinergic stimulation. These results show that active sensitization does not per se lead to a global increase in mast cell reactivity or releasability.

Adenosine Triphosphate↗
PubMed1989

Some further characteristics of histamine secretion from rat mast cells stimulated with sodium orthovanadate.

Sodium orthovanadate induced a release of histamine from rat peritoneal mast cells. Other oxyanions of vanadium with the metal in the +V oxidation state also evoked histamine release but neither vanadyl sulphate (+IV oxidation state) nor the analogous orthophosphate anion were effective secretagogues. The release evoked by vanadate was selectively inhibited by the anion channel blocker SITS, and by theophylline and Bu2cAMP, but was unaffected by disodium cromoglycate and lanthanum ions. These results are discussed in terms of the possible mode of action of vanadate.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1989

Effects of antihistamines on isolated human lung mast cells, basophil leucocytes and erythrocytes.

Low concentrations of H1- and H2-receptor directed compounds inhibited the immunologic secretion of histamine from human lung mast cells and basophil leucocytes and protected human erythrocytes from hypotonic lysis. Higher concentrations induced a release of the amine from the histaminocytes. These results are discussed in terms of the possible membrane effects of the test compounds.

Basophils↗
PubMed1989

Divalent cation dependence of the inhibition by phenothiazines of mediator release from mast cells.

1. The divalent cations calcium, strontium and barium--and in that order of decreasing effectiveness--were capable of supporting the stimulated release of histamine from rat peritoneal mast cells (RPMC). 2. The responsiveness of mast cells to stimulation in the presence of divalent cations was, in general, markedly enhanced when the cells were first depleted of their intracellular calcium stores. 3. The putative calmodulin antagonists, chlorpromazine, promethazine, thioridazine (phenothiazines) and W-7 (a naphthalene sulphonamide) all inhibited histamine release in the presence of divalent cations in both untreated cells and in RPMC depleted of their intracellular calcium. 4. Histamine release induced by antigen, compound 48/80 and ionophore A23187 was inhibited by this class of compounds most effectively in the presence of extracellular barium, less so in the presence of strontium and least so in calcium-containing media. 5. In the experimental situation where the extracellular calcium concentration was reduced (less than 1 mM), the phenothiazines inhibited the stimulated release of histamine more effectively. 6. In toto, these results suggest that strontium and barium, as well as calcium, can support histamine release from RPMC by directly interacting with an intracellular divalent cation-binding site that may be calmodulin. As a consequence, one mechanism by which the phenothiazines and W-7 may modulate the secretory response could reflect an antagonism of a divalent cation interaction at that same site, although other additional potential sites of inhibitory action are indicated, dependent on the stimulus employed for secretion.

Animals↗
PubMed1989

Characteristics of histamine secretion induced by neuropeptides: implications for the relevance of peptide-mast cell interactions in allergy and inflammation.

A variety of basic, sensory neuropeptides induced the release of histamine from rat peritoneal mast cells. However, a wide range of other polycationic agents, such as compound 48/80, the mast-cell-degranulating peptide from bee venom and polylysine also activated this cell type. Histamine release induced by all of these agents had characteristic features in common. In each case, the process was extremely rapid, essentially independent of added calcium or phospholipids, not mediated through cell-fixed antibodies, and inhibited by antagonists of the so-called polyamine receptor. The release was also very species- and tissue-specific. All of the compounds were most active against rat serosal mast cells. Tissue mast cells of this species and peritoneal mast cells of other rodents showed graded responses while guinea pig and human mast cells were unreactive. On the basis of these results, the possible role of peptide-mast cell interactions in neurogenic models of inflammation is discussed.

Animals↗
PubMed1989

Effects of sodium cromoglycate and nedocromil sodium on histamine secretion from mast cells from various locations.

Nedocromil sodium and sodium cromoglycate inhibited histamine release from rat peritoneal mast cells. Tachyphylaxis was observed with both drugs. The 2 compounds were extremely selective in their action, being less active against peritoneal mast cells from the hamster and completely ineffective against mast cells from the mouse. Human basophil leucocytes, tissue mast cells of the guinea-pig and rat intestinal mast cells were also unresponsive. Both drugs inhibited immunological histamine release from human pulmonary mast cells obtained by bronchoalveolar lavage (BAL) and, less effectively, from lung parenchyma. Nedocromil sodium was about 1 order of magnitude more potent than sodium cromoglycate in each case. Tachyphylaxis was observed with the dispersed lung, but not with the cells obtained by BAL, and the degree of inhibition varied inversely with the magnitude of the secretory response. The possible clinical significance of these observations is discussed.

Animals↗
PubMed1988

Comparative studies on the effect of non-steroidal anti-inflammatory drugs (NSAID) on histamine release from mast cells of the rat and guinea pig.

The effects of a number of non-steroidal anti-inflammatory drugs (NSAID) on histamine secretion from tissue mast cells of the rat and the guinea pig have been examined. According to the experimental conditions and cell type, the drugs potentiated, inhibited or had no effect on histamine release. The possible mechanisms of these effects are discussed.

Animals↗
PubMed1988

Histamine secretion from mast cells stimulated with sodium orthovanadate.

Sodium orthovanadate was found to be an effective histamine liberator from peritoneal mast cells of the rat and mouse. The release process was slow, non-cytotoxic and strongly dependent on pH and extracellular calcium. The effect was highly tissue and species specific and human basophil leucocytes and tissue mast cells of the rat and guinea pig were only weakly responsive or essentially unreactive.

Animals↗
PubMed1988

Effects of phorbol ester, serine phospholipids, and calcium on histamine release from mast cells and basophils.

The effects of calcium, serine phospholipids and the phorbol ester tetradecanoylphorbol acetate (TPA), a known activator of protein kinase C, have been examined on mastocytes from different sources. A complex and differential interaction between these agents and histamine secretion was observed in human basophil leucocytes and in peritoneal mast cells from the rat, mouse and hamster. On this basis, the possible role of kinase C in histamine release is discussed.

Animals↗
PubMed1988

Histamine secretion from mast cells stimulated with somatostatin.

Histamine release from isolated mast cells stimulated with somatostatin resembled that induced by other basic agents. The process was rapid, independent of added calcium or phospholipids, non-cytotoxic, species and tissue specific, not mediated through cell-fixed antibodies or glucoreceptors, and inhibited by antagonists of the polyamine receptor. Somatostatin and other polycations may then act through a common receptor or binding site on the mast cell membrane.

Animals↗
PubMed1988

Some studies on the isolation and properties of pulmonary mast cells from the pig.

Mast cells were isolated by the enzymic dissociation of lung tissue from the pig. The responses of these cells to a variety of histamine liberators and anti-allergic drugs were examined. On the basis of these findings, the possible use of porcine pulmonary mast cells in the study of immediate hypersensitivity reactions is discussed.

Animals↗
PubMed1988

Cardiac and renal mast cells: morphology, distribution, fixation and staining properties in the guinea pig and preliminary comparison with human.

In guinea pig (GP) and human heart and kidney cell or tissue preparations fixed with Carnoy's fluid (but not with formol-saline), mast cells (MC) were extremely well preserved and could be detected after staining with alcian blue (AB). Although histamine content and distribution in GP and human heart appeared to be different, morphological and histochemical studies of MC suggested a similarity between the two species and a clear distinction from rat peritoneal MC.

Animals↗
PubMed1988

Effects of sodium cromoglycate and nedocromil sodium on histamine secretion from human lung mast cells.

Sodium cromoglycate and nedocromil sodium produced a dose dependent inhibition of histamine secretion from human pulmonary mast cells obtained by bronchoalveolar lavage and by enzymatic dissociation of lung parenchyma. Both compounds were significantly more active against the lavage cells than against the dispersed lung cells, and nedocromil sodium was an order of magnitude more effective than sodium cromoglycate against both cell types. Tachyphylaxis was observed with the parenchymal cells but not with the lavage cells. Nedocromil sodium and sodium cromoglycate also inhibited histamine release from the lavage cells of patients with sarcoidosis and extrinsic asthma.

Asthma↗
PubMed1988

Guinea pig mast cells: comparative study on morphology, fixation and staining properties.

We have studied the distribution of mast cells (MC) in different tissues of the guinea pig (GP), and certain aspects of their histochemical and cytochemical properties. In preparations fixed with Carnoy's fluid, MC were extremely well-preserved and were detected in all tissue sections and cytocentrifuge smears obtained from enzymically dispersed cells after staining with alcian blue at pH 0.5-2.2. In formol-saline-fixed preparations, there was a substantial reduction in MC counts. Most of the tissue MC were located interstitially and in the perivascular connective tissue. A small proportion of MC was located in certain organ- or tissue-specific structures. When counted manually, MC comprised 0.43-3.1% of the cell population obtained by enzymic dispersion. This proportion was higher than that obtained by the automated Technicon H6000 basophil system, but the two counting systems confirmed organ differences in MC counts. MC in different GP tissues varied in size, morphology, histamine content and degree of susceptibility to formol-saline fixation. The granules of GP connective tissue MC differed from those of rat peritoneum in failing to take the fluorescent stain berberine sulphate which has greater affinity for the highly sulphated glycosaminoglycans such as heparin, and in having some morphological and histochemical similarity to 'mucosal' MC.

Animals↗
PubMed1987

On the mechanism of dextran-induced histamine secretion from rat peritoneal mast cells.

The mechanism of histamine release induced from isolated rat peritoneal mast cells by clinical dextran was examined in detail. The putative involvement of cell-fixed IgE antibodies in the process was discounted by a number of experimental approaches. Instead, the characteristics of the release were found to be consistent with the interaction of the polysaccharide with specific glucoreceptors on the mast cell membrane.

Animals↗