Synergistic effects of calcium‐mobilizing agents and adenosine on histamine release from rat peritoneal mast cells

Maurer, Klaus; Klotz, Karl‐Norbert; Schwabe, Ulrich

doi:10.1111/j.1476-5381.1989.tb12689.x

Cited by 11 publications

(6 citation statements)

References 26 publications

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“…To date, adenosine, and not adenine nucleotides, has received considerable recognition for a potential role in human allergies and asthma (37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49). The findings of the current study show for the first time that extracellular ATP and related adenine nucleotides markedly potentiate histamine release from immunologically stimulated mast cells.…”

Section: Discussionmentioning

confidence: 58%

“…Because ATP is degraded to adenosine by ectoenzymes (3), and adenosine modulates histamine release from rat and human mast cells and basophils (38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49), we also determined the effect of adenosine on histamine release from HLMC. In six dose-response experiments (Figure 3), previous observations (37) were confirmed: Adenosine alone did not directly induce histamine release from HLMC, but exerted a bimodal modulatory effect on anti-IgE-induced histamine release; adenosine at 10 Ϫ3 M inhibited anti-IgE-induced release of 10.3 Ϯ 3.0% to 5.3 Ϯ 1.9% (P Ͻ 0.05).…”

Section: Adenosine Effectsmentioning

confidence: 99%

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ATP Modulates Anti-IgE–Induced Release of Histamine from Human Lung Mast Cells

Schulman

Glaum

Post

et al. 1999

Am J Respir Cell Mol Biol

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Adenosine 5'-triphosphate (ATP) is released from the cytoplasm under physiologic and pathophysiologic conditions and enters the extracellular space, where it acts on a group of recently cloned cell-surface receptors termed P2-purinoceptors (subtypes P2X and P2Y). We examined the effects of extracellular ATP, uridine triphosphate (UTP), the stable ATP analogues alpha,betamethylene-ATP (alpha,betamATP), beta,gammamethylene-ATP (beta,gammamATP), and 2-methylthio-ATP (2mSATP), and adenosine (10(-6)-10(-3) M) on histamine release from human lung mast cells (HLMC) induced by anti-IgE and the calcium ionophore A23187. None of the nucleotides or adenosine directly induced histamine release. Adenosine exhibited a bimodal effect, enhancing histamine release at 10(-6) to 10(-4) M (P > 0.05, NS) and inhibiting it at 10(-3) M (P < 0.05). ATP (10(-4) M) enhanced anti-IgE-induced histamine release (10.9 +/- 2.7% to 19. 2 +/- 2.9%, n = 20, P < 0.01), but not ionophore A23187-induced histamine release (n = 10). The adenine nucleotides consistently enhanced anti-IgE-induced histamine release; the rank order for this action was: ATP > 2mSATP > alpha,betamATP > beta,gammamATP, suggesting mediation by a P2Y-purinoceptor subtype. The selective P2X purinoceptor antagonist pyridoxalphosphate-6-azophenyl-2', 4'-disulfonic acid failed to influence the effect of ATP, further supporting P2Y-purinoceptor mediation of anti-IgE-induced histamine release. UTP, an agonist at P2Y-purinoceptors, also significantly enhanced anti-IgE-induced histamine release. Application of the reverse transcription-polymerase chain reaction indicated that HLMC constitutively express the messenger RNAs encoding the P2Y1- and P2Y2-purinoceptor subtypes, and not that encoding the P2X7-purinoceptor (i.e., P2Z), a subtype implicated in ATP-induced histamine release in rodent peritoneal mast cells. The data produced in the study suggest that ATP plays an important modulatory role in histamine release from HLMC, and that it may therefore be mechanistically involved in human allergic/asthmatic reactions.

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Section: Discussionmentioning

confidence: 58%

Section: Adenosine Effectsmentioning

confidence: 99%

ATP Modulates Anti-IgE–Induced Release of Histamine from Human Lung Mast Cells

Schulman

Glaum

Post

et al. 1999

Am J Respir Cell Mol Biol

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“…From our results, it cannot be excluded that adeno sine facilitated the transport of calcium into the cell. How ever, studies with rat peritoneal mast cells [23,35] showed an unchanged intracellular calcium concentration and suggested therefore as a mechanism an increase in the cal cium sensitivity of the release process. Concurring with these results in rat peritoneal mast cells [23], we found that trapping of adenosine inside the cell with the nucleoside transport inhibitor NBTI caused enhancement of hista mine release.…”

Section: Discussionmentioning

confidence: 98%

“…Thus, adenosine appears to act through a positive feed back mechanism. By increasing the sensitivity of the re lease process to free intracellular calcium, a potentiation of mediator release is achieved [35].…”

Section: Discussionmentioning

confidence: 99%

Effects of Adenosine on Histamine Release from Human Lung Fragments

Ott

Klotz

Vogt-Moykopf³

et al. 1992

Int Arch Allergy Immunol

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The actions of adenosine on histamine release of human lung fragments were investigated. Histamine release was stimulated either with the calcium ionophore A 23187 or with concanavalin A. Adenosine and its analogue 5′-N-ethyl-carboxamidoadenosine alone had no significant effect on basal release or on the release elicited by A 23187 or concanavalin A. However, in the presence of the adenosine receptor antagonist 8-[4-[[[[(2-aminoethyl)amino]-carbonyl] methyloxy]-phenyl]-1,3-dipropylaxanthine (XAC), which itself did not affect the release, adenosine increased the stimulated histamine release. On the other hand, in the presence of the nucleoside transport inhibitor S-(p-nitro-benzyl)-6-thioninosine (NBTI), adenosine caused a reduction in stimulated histamine release. NBTI itself caused a stimulation of release. Thus, a stimulatory effect of adenosine was seen in the presence of XAC, whereas an inhibitory effect was unmasked by NBTI. From these data it is concluded that adenosine exerts two opposing effects on histamine release in the human lung which neutralize each other: it inhibits release via a site antagonized by XAC, which presumably represents an A₂ adenosine receptor, and it stimulates release via a mechanism that is blocked by NBTI, suggesting that adenosine needs to reach the interior of cells to exert this effect. The slight stimulatory effect of NBTI alone demonstrates that trapping intracellularly formed adenosine inside mast cells leads to sufficient concentrations of adenosine to stimulate histamine release. These findings suggest an important bimodal role of adenosine in regulating histamine release in the human lung.

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“…Previous studies with isolated human mast cells and basophils are consistent with the existence of A 3 adenosine receptors that facilitate IgE-dependent degranulation (6) and A 2A receptors that inhibit degranulation by a cyclic AMPdependent mechanism (7). In human lung fragments adenosine inhibits histamine release via a site antagonized by XAC, but adenosine stimulates release via a mechanism that unexpectedly was found to be blocked by the adenosine uptake inhibitor NBTI (35). The authors concluded that adenosine needs to reach the interior of cells in order to facilitate mast cell degranulation.…”

Section: Discussionmentioning

confidence: 99%