Use of Steroidal Antiinflammatory Drug Provides Further Evidence for a Potential Role of PAF-Acether in Bronchial Anaphylaxis

Chignard, Michel; Couedic, J P Le; Andersson, Paul; Brange, Charlotte

doi:10.1159/000234130

Cited by 12 publications

(3 citation statements)

References 9 publications

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“…These amines are released from the mast cells, in rats. Bioactive lipids such as leukotrienes (LTs) and platelet activating factor (PAF) are formed and released from this cell type, in the presence of stimulation [3,4]. We investigated mediators contributing to PCA in rats, Abbreviations: DNP-As, dinitrophenylated Ascads suum extract; LT, leukotriene; MCM, mast cell medium; PAF, platelet activating factor; PCA, passive cutaneous anaphylaxis; PG, prostaglandin; SRS-A, slow reacting substance of anaphylaxis.…”

Section: Introductionmentioning

confidence: 99%

Lack of involvement of leukotriene and platelet activating factor in passive cutaneous anaphylaxis in rats

et al. 1988

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Possible chemical mediators contributing to 48 hour passive cutaneous anaphylaxis (PCA) in rats were investigated. Forty-eight hour PCA was inhibited considerably by mepyramine and methysergide given intravenously, a finding suggestive of a major role for histamine and serotonin in the reaction. AA-861, a selective 5-lipoxygenase inhibitor did not inhibit the PCA, and leukotriene (LT)D4 or LTE4 and the combination with prostaglandin (PG)E2 had no significant skin reaction. In addition, only small amounts of slow reacting substance of anaphylaxis (SRS-A) were detected in skin fragments, in vitro. Although CV-3988, a selective platelet activating factor (PAF) antagonist, dose-dependently inhibited the PAF-induced skin reaction, the PCA was not affected by treatment with this compound. Indomethacin also had no inhibitory activity on PCA. Thus, sulfidopeptide LTs, PAF and arachidonate cyclooxygenase metabolites probably do not contribute to PCA, at least in rats.

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Section: Introductionmentioning

confidence: 99%

Lack of involvement of leukotriene and platelet activating factor in passive cutaneous anaphylaxis in rats

et al. 1988

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“…The contraction of sensitized guinea-pig parenchyma lung strips in response to antigen is well documented (Yen & Kreutner, 1980;Songsiridej et al, 1983;Detsouli et al, 1985) but the mechanisms involved are not fully understood. Important mediators released from lung tissues during in vitro anaphylactic shock include histamine and metabolites of arachidonic acid such as leukotrienes, thromboxane and prostaglandins, together with platelet-activating factor (Paf-acether; 1-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine) (Kravis & Henson, 1975;Chignard et al, 1986;Fitzgerald et al, 1986). Nevertheless, the aforementioned mediators do not account for the entire anaphylactic response of guinea-pig lung strips, since under conditions where their formation or activity is blocked, the antigeninduced contraction of the guinea-pig lung strips is only partially affected (Detsouli et al, 1985;Pretolani et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

Blockade by methylation inhibitors of the anaphylactic response of guinea‐pig lung strips

Randon

Lefort

Vargaftig

1987

British J Pharmacology

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The combination of two methylation inhibitors 3‐deazaadenosine (10−4 or 4 × 10−4 m) plus l‐homocysteine (2 × 10−4 m) caused a time‐dependent inhibition of antigen‐induced contraction, formation of thromboxane B2 (TxB2) and release of histamine from lung parenchyma strips taken from guinea‐pigs actively sensitized with ovalbumin (OA). The methylation inhibitors also prevented the lung strip contractions induced by the mediators platelet‐activating factor (Paf‐acether, 10−6 m), leukotriene D4 (LTD4, 10−8 and 3 × 10−8 m), and in part to arachidonic acid (10−6 and 10−5 m), under conditions where the contractions to histamine (10−6‐10−4 m) were virtually unaffected. TxB2 formation induced by these mediators or by OA was more affected by the methylation inhibitors than the lung strip contractions, indicating that prostaglandin formation is more sensitive to these inhibitors than the myotropic activity. In contrast, the suppressive effect of the methylation inhibitors on histamine secretion by parenchyma lung strips induced by OA followed the inhibition of the contraction. These results show that inhibitors of methyltransferases interfere with the myotropic responses and with the release of mediators by actively sensitized guinea‐pig lung strips stimulated with antigen, and suggest a major role for a methylation process in mediating the contraction of and mediator release by the lung parenchyma.

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“…In relation to asthma both increased levels of PAF-like activity in the bronchoalveolar lavage fluid and in saliva [12] as well as increased levels of lyso-PAF after allergen provocation in plasma in patients with late phase response [13], have been reported. The antigen-induced release of PAF from sensitized lung tissue has been described [14].…”

Section: Introductionmentioning

confidence: 99%

Current status of PAF antagonists

Heuer

1992

Clin Experimental Allergy

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Use of Steroidal Antiinflammatory Drug Provides Further Evidence for a Potential Role of PAF-Acether in Bronchial Anaphylaxis

Cited by 12 publications

References 9 publications

Lack of involvement of leukotriene and platelet activating factor in passive cutaneous anaphylaxis in rats

Lack of involvement of leukotriene and platelet activating factor in passive cutaneous anaphylaxis in rats

Blockade by methylation inhibitors of the anaphylactic response of guinea‐pig lung strips

Current status of PAF antagonists

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