Accumulation of Platelets and Eosinophils in Baboon Lung after Paf-acether Challenge: Inhibition by Ketotifen

Arnoux, B.; Denjean, A.; Page, Clive; Nolibé, D.; Morley, John E.; Benveniste, Jacques

doi:10.1164/ajrccm/137.4.855

Cited by 92 publications

(41 citation statements)

References 11 publications

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“…Additionally, it is likely that lipid mediators such as peptidoleukotrienes (Verhagen et al, 1984) and PAF (Lee et al, 1984) may, in large part, be generated by eosinophils. PAF has been reported to induce a selective accumulation of eosinophils in the airways of guinea-pigs (Aoki et al, 1988a) and primates (Arnoux et al, 1988). Hence, we have studied the dose relationship and time course of PAF-induced bronchial eosinophil accumulation in the guinea-pig and have examined the capacity of a range of anti-asthma drugs to inhibit this response.…”

Section: Introduction Antiseramentioning

confidence: 99%

Eosinophil accumulation in pulmonary airways of guinea‐pigs induced by exposure to an aerosol of platelet‐activating factor: effect of anti‐asthma drugs

Sanjar

Aoki

Boubekeur

et al. 1990

British J Pharmacology

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101

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Exposure of guinea‐pigs to aerosols of platelet activating factor (PAF) (0.01 to 100 μg ml−1) induced a dose‐dependent increased incidence of eosinophils in bronchoalveolar lavage fluid (BAL) at 48 h. Total leucocyte numbers and the percentages of lymphocytes and neutrophils were unchanged in BAL fluid. Increased numbers of eosinophils were detected in BAL 1 h after exposure to PAF but eosinophilia was not maximal until 48 h. One week after exposure to PAF, the percentage of eosinophils in BAL was within the normal range. Depletion of circulating platelets or neutrophils by intravenous injection of specific antisera did not modify accumulation of eosinophils in the airway lumen following inhalation of PAF (10 μg ml−1). PAF‐induced pulmonary airway eosinophil accumulation was inhibited by treatment with SDZ 64–412, a selective PAF‐antagonist, whether the compound was administered before, or 30 min after, inhalation of PAF. Pulmonary airway eosinophil accumulation due to inhaled PAF (10 μg ml−1) was inhibited by prior treatment with aminophylline, cromoglycate, ketotifen, dexamethasone and AH 21–132. Pulmonary airway eosinophil accumulation due to inhaled PAF (10 μg ml−1) was not inhibited by prior treatment with indomethacin, salbutamol or mepyramine.

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Section: Introduction Antiseramentioning

confidence: 99%

Eosinophil accumulation in pulmonary airways of guinea‐pigs induced by exposure to an aerosol of platelet‐activating factor: effect of anti‐asthma drugs

Sanjar

Aoki

Boubekeur

et al. 1990

British J Pharmacology

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101

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“…The physiopathological significance of the presence of IgE receptors has been linked to the cytocidal activity of platelets (Capron et al, 1986). Platelet activation and/or accumulation within the pulmonary vasculature in several animal species (Pretolani et al, 1986;Arnoux et al, 1988;Lellouch-Tubiana et al, 1988) and in man (Knauer et al, 1981) is associated with bronchoconstriction following immunological stimulation or the administration of inflammatory mediators, including platelet-activating factor (PAF) (Page et al, 1982;Lellouch-Tubiana et al, 1988). Plate-let activation may thus play an important role in hypersensitivity reactions.…”

Section: Introductionmentioning

confidence: 99%

Antigen induces leucopenia in non‐immunised guinea‐pigs injected with platelets from actively sensitized animals

Pretolani¹,

Randon

Vargaftig

1990

British J Pharmacology

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Ovalbumin administration to animals injected with 0.5–5 × 106 washed platelets μl−1 from actively sensitized animals induced a marked decrease (maximum of around 50% at 60 min) in the number of circulating leucocytes, whereas platelet counts were unaffected. The intensity of the decrease in leucocyte counts was dependent upon the concentration of the injected platelets. No drop in leucocyte counts was measured upon antigen challenge of guinea‐pigs injected with platelets from non‐sensitized animals. This phenomenon was unaffected by pretreatment of the recipient animals with a platelet‐activating factor (PAF) antagonist WEB 2086 (3 mg kg−1 i.v.) but was markedly reduced (around 50% inhibition) by the anti‐allergic drug nedocromil sodium (100 mg kg−1 i.v.). By contrast, indomethacin (5 mg kg−1 i.v.) caused a significant (P < 0.01) enhancement of the antigen‐induced leucopenia, whereas the mixed cyclooxygenase and lipoxygenase inhibitor, BW 755C (10 mg kg−1 i.v.) suppressed the drop in leucocyte counts evoked by ovalbumin administration. These results indicate that platelets from actively sensitized guinea‐pigs transferred to normal animals still responds to the specific antigen with the activation of circulating leucocytes. This phenomenon appears to be independent of the production of PAF and of cyclo‐oxygenase metabolites. By contrast, the production of the metabolites of the lipoxygenase pathway by platelets could account for the marked leucopenia observed following the immunological stimulation.

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“…In this context, it has been established that systemic administration of PAF will induce airway hyperreactivity (2) and that prophylactic anti-asthma drugs can prevent development of such airway hyper reactivity (3). More recently, it has been established that inhalation (4) or intratracheal instillation (5) of PAF can also induce a selective accumulation of eosinophils that can be prevented by ketotifen (5,6) and other prophylactic anti-asthma drugs (6). These observations raise the possibility that inhi bition of eosinophil accumulation may be a property common to anti-asthma drugs.…”

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confidence: 99%

Inhibition of PAF-induced eosinophil accumulation in pulmonary airways of guinea pigs by anti-asthma drugs.

Sanjar

Boubekeur

et al. 1989

Jpn.J.Pharmacol

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Abstract-IntraperitoneaI (i.p.) injection of platelet activating factor (PAF) in guinea pigs caused a dose-related increase in the number of eosinophils recovered from bronchoalveolar lavage fluid (BALF). The prevalence of eosinophils in BALF had significantly increased within 1 hr of i.p. injection of PAF (10 /-'g/animal) and was maximal after 24 hr. Subcutaneous osmotic mini-pumps were used to administer drugs for 5 days prior to i.p. injection of PAF (10 ,ug/animal) and for the subsequent 24 hr. The percentage increase of eosinophils in BALF, due to PAF, was inhibited in animals treated with dexamethasone, aminophylline, cromoglycate, tranilast or ketotifen, but not in animals treated with oxatomide, azelastine, amlexanox, ibudilast or AA-861. These results suggest that inhibition of pulmonary eosinophilia may be a necessary property of prophylactic anti-asthma drugs and provide indirect evidence favoring a role for PAF in eosinophilia of asthma.

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Accumulation of Platelets and Eosinophils in Baboon Lung after Paf-acether Challenge: Inhibition by Ketotifen

Cited by 92 publications

References 11 publications

Eosinophil accumulation in pulmonary airways of guinea‐pigs induced by exposure to an aerosol of platelet‐activating factor: effect of anti‐asthma drugs

Eosinophil accumulation in pulmonary airways of guinea‐pigs induced by exposure to an aerosol of platelet‐activating factor: effect of anti‐asthma drugs

Antigen induces leucopenia in non‐immunised guinea‐pigs injected with platelets from actively sensitized animals

Inhibition of PAF-induced eosinophil accumulation in pulmonary airways of guinea pigs by anti-asthma drugs.

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