Dual effects of acetylsalicylic acid on mast cell degranulation, expression of cyclooxygenase-2 and release of pro-inflammatory cytokines

Mortaz, Esmaeil; Redegeld, Frank A.; Nijkamp, Frans P.; Engels, Ferdi

doi:10.1016/j.bcp.2004.12.018

Cited by 35 publications

(31 citation statements)

References 39 publications

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“…This indicates that the mechanisms of NSAID idiosyncrasy may also be underlying changes in the gastrointestinal barrier postulated in cofactor-induced anaphylaxis. In addition to these effects, in vitro pretreatment of mast cells with ASA directly modulated FceRI-dependent mast cell degranulation and LTC4 release following FceRI stimulation (44,45). Moreover, several studies could show that also in humans, systemic administration of ASA triggers increased skin test reactions to different allergens (30,32), supporting the concept that ASA next to modulating the intestinal absorption of allergens also directly modulates effector cell function in cofactor-induced anaphylaxis.…”

Section: Nsaidmentioning

confidence: 82%

About the role and underlying mechanisms of cofactors in anaphylaxis

Wölbing

Fischer

Köberle

et al. 2013

Allergy

178

163

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Anaphylaxis is the systemic and most severe presentation of type I allergy. A number of conditions were identified that modulate the onset of anaphylaxis such as co-or augmentation factors, which significantly lower the allergen dose necessary for triggering anaphylaxis. Next to physical exercise or alcohol consumption, co-administration of nonsteroidal anti-inflammatory drugs (NSAID) or concomitant infectious diseases are well-documented cofactors of anaphylaxis. Registries for anaphylaxis document a role for cofactors in about 30% of anaphylactic reactions. Some disease entities such as 'wheat-dependent exercise-induced anaphylaxis' (WDEIA) are explicitly characterized by elicitation of anaphylaxis only in the presence of at least one such cofactor. Using WDEIA as a model disease, studies demonstrated that exercise increases skin prick test reactivity to and bioavailability of the allergen. Additional data indicate that alcohol consumption and NSAID administration display similar effects. Modulation of the cellular activation threshold is another mechanism underlying cofactor-induced anaphylaxis, most likely also functional when infectious diseases orchestrate elicitation of anaphylaxis. Cofactors are increasingly accepted to play a fundamental role in eliciting anaphylaxis. Consequently, to improve patient management modalities, a better understanding of the underlying mechanisms is warranted. This review aims to update clinicians and clinical scientists on recent developments.

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Section: Nsaidmentioning

confidence: 82%

About the role and underlying mechanisms of cofactors in anaphylaxis

Wölbing

Fischer

Köberle

et al. 2013

Allergy

178

163

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“…Since NSAIDs inhibit the production of cytokines from lymphocytes [2,3,4], they are also used as immunomodulatory drugs [5,6]. However, in some situations, such as in food-dependent exercise-induced anaphylaxis (FDEIA) [7,8], salicylate and its acetyl derivative, aspirin, can stimulate chemokine release from mast cells, triggering adverse immunological reactions [9,10]. On the other hand, chlorpromazine, one of the most traditionally used antipsychotic drugs [11], has also been recognized as an anti-allergic agent, because it inhibits histamine release from mast cells [12,13].…”

Section: Introductionmentioning

confidence: 99%

Amphipaths Differentially Modulate Membrane Surface Deformation in Rat Peritoneal Mast Cells During Exocytosis

Kazama

Maruyama²,

Takahashi³

et al. 2013

Cell Physiol Biochem

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Background/Aims: Salicylate and chlorpromazine exert differential effects on the chemokine release from mast cells. Since these drugs are amphiphilic and preferentially partitioned into the lipid bilayers of the plasma membranes, they would induce some morphological changes in mast cells and thus affect the process of exocytosis. Methods: Employing the standard patch-clamp whole-cell recording technique, we examined the effects of salicylate and chlorpromazine on the membrane capacitance (Cm) during exocytosis in rat peritoneal mast cells. Using confocal imaging of a water-soluble fluorescent dye, lucifer yellow, we also examined their effects on plasma membrane deformation of the cells. Results: Salicylate dramatically accelerated the GTP-γ-S-induced increase in the Cm immediately after its application, whereas chlorpromazine significantly suppressed the increase. Treatment with salicylate increased the trapping of the dye on the cell surface, while treatment with chlorpromazine completely washed it out, indicating that both drugs induced membrane surface deformation in mast cells. Conclusion: This study demonstrated for the first time that membrane amphipaths, such as salicylate and chlorpromazine, may oppositely modulate the process of exocytosis in mast cells, as detected by the changes in the Cm. The plasma membrane deformation induced by the drugs was thought to be responsible for their differential effects.

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“…Via the prostaglandins' modulation of the activity of the HPA axis at the level of the hypothalamus, pituitary, and adrenal cortex [1,[35][36][37][38] , it can be hypothesized that ASA may lead to a suppression of stress-related HPA axis responses. Likewise, downregulation of cytokine production and secretion by ASA [39][40][41][42][43] might lead to reduced HPA axis activity, since proinflammatory cytokines are potent stimulators of corticotropin-releasing hormone (CRH) and thus HPA axis activity [3,38] .…”

Section: Introductionmentioning

confidence: 99%

No Effect of 5-Day Treatment with Acetylsalicylic Acid (Aspirin) or the Beta-Blocker Propranolol (Inderal) on Free Cortisol Responses to Acute Psychosocial Stress: A Randomized Double-Blind, Placebo-Controlled Study

Kudielka

Fischer²,

Metzenthin³

et al. 2007

Neuropsychobiology

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Background: The characterization of an individual’s hypothalamic-pituitary-adrenal axis stress response is a main research topic in neuropsychobiology since alterations have been causally linked to several disease states. Over the last years, several studies focused on the identification of sources of inter- and intraindividual variability, but there is still a paucity of experimental data on the effect of different pharmaceuticals on cortisol responses to acute psychological stress. Therefore, in this randomized double-blind placebo-controlled study, we investigated the effect of treatment with two popular and clinically used pharmaceuticals on stress-related cortisol responses, namely acetylsalicylic acid (aspirin), a known prostaglandin synthesis inhibitor, and the beta-blocker propranolol (Inderal), a nonselective beta-receptor antagonist. Methods: For 5 days, 73 healthy subjects (50 men, 23 women; mean age 47.3 ± 7.7 years) received either a daily oral dose of 100 mg aspirin, 80 mg propranolol (Inderal), aspirin + propranolol, or placebo. After treatment, subjects were confronted with the Trier Social Stress Test, a widely-used standardized psychosocial stress protocol. Cortisol responses were measured by six saliva samples taken before and after the stress exposure. Results: Subjects showed a significant cortisol increase after stress (p < 0.0001). The four treatment groups did not differ in their cortisol responses (group effect p > 0.44; interaction p > 0.97). Additionally, controlling for gender, age, smoking status, body mass index, mean arterial blood pressure or pre-stress cortisol levels yielded similar results in the total sample as well as in the male or female subgroups, respectively. Conclusion: Neither short-term treatment with aspirin nor propranolol altered the acute free cortisol response to psychological stress in healthy adults.

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Dual effects of acetylsalicylic acid on mast cell degranulation, expression of cyclooxygenase-2 and release of pro-inflammatory cytokines

Cited by 35 publications

References 39 publications

About the role and underlying mechanisms of cofactors in anaphylaxis

About the role and underlying mechanisms of cofactors in anaphylaxis

Amphipaths Differentially Modulate Membrane Surface Deformation in Rat Peritoneal Mast Cells During Exocytosis

No Effect of 5-Day Treatment with Acetylsalicylic Acid (Aspirin) or the Beta-Blocker Propranolol (Inderal) on Free Cortisol Responses to Acute Psychosocial Stress: A Randomized Double-Blind, Placebo-Controlled Study

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