Accumulation of Eosinophils in Response to Intracutaneous Paf-Acether and Allergens in Man

Hénocq, E; Vargäftig, B. Boris

doi:10.1016/s0140-6736(86)91683-1

Cited by 149 publications

(53 citation statements)

References 6 publications

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“…PAF and lyso-PAF, the precursor and metabolite of PAF, are released into the airway lumen of lungs from sensitized guinea-pigs after exposure to antigen (Fitzgerald et al, 1986) and increased levels of lyso-PAF have been detected in serum of asthma patients in whom there was a late-onset reaction to allergen (Nakamura et al, 1987). PAF is released during allergic reactions, is chemoattractant for both neutrophils and eosinophils in vitro (Wardlaw et al, 1986) and induces accumulation of such cells in vivo (Dewar et al, 1984;Henocq & Vargaftig, 1986); hence, it is reasonable to anticipate that PAF formation will contribute to the accumulation of such inflammatory cells in the lungs of asthma patients.…”

Section: Discussionmentioning

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

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: Discussionmentioning

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

101

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“…PAF is known to be a potent chemotactic agent, and previous studies (Archer et al, 1985a;Henocq & Vargaftig, 1986) clear evidence of cellular infiltration as a result of intradermal PAF injection. The cell type involved appears to be neutrophilic in non-atopic subjects, while in atopic subjects the predominant cell type appears to be eosinophilic.…”

Section: Tolerancementioning

confidence: 92%

Inflammatory responses to intradermal injection of platelet activating factor, histamine and prostaglandin E2 in healthy volunteers: a double blind investigation.

Sciberras¹,

Mm²,

Bolognese³

et al. 1987

Brit J Clinical Pharma

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“…Indeed, PAF is found in association with inflammatory skin diseases (24,25), intradermal injections of PAF induce inflammation (24,26), and human keratinocytes both synthesize PAF and 1-acyl PAF species as well as express functional PAF-Rs (27)(28)(29). Activation of the epidermal PAF-R leads to the production of PAF, prostaglandins, IL-6, IL-8, and the inducible form of cyclooxygenase (COX-2) (30).…”

mentioning

confidence: 99%

Augmentation of Ultraviolet B Radiation-induced Tumor Necrosis Factor Production by the Epidermal Platelet-activating Factor Receptor

Dy¹,

Pei²,

Travers³

1999

Journal of Biological Chemistry

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Ultraviolet B radiation (UVB) has been shown to damage human keratinocytes in part by inducing oxidative stress and cytokine production. Indeed, UVB-induced production of the pro-inflammatory and cytotoxic cytokine tumor necrosis factor ␣ (TNF-␣) has been implicated in the epidermal damage seen in response to acute solar radiation. Though the lipid mediator platelet-activating factor (PAF) is synthesized in response to oxidative stress, and keratinocytes express PAF receptors linked to cytokine biosynthesis, it is not known whether PAF is involved in UVB-induced epidermal cell cytokine production. These studies examined the role of the PAF system in UVB-induced epidermal cell TNF-␣ biosynthesis using a novel model system created by retroviralmediated transduction of the PAF receptor-negative human epidermal cell line KB with the human PAF receptor (PAF-R). Treatment of PAF-R-expressing KB cells with the metabolically stable PAF-R agonist carbamoyl-PAF resulted in increased TNF-␣ mRNA and protein, indicating that activation of the epidermal PAF-R was linked to TNF-␣ production. UVB irradiation of PAF-R-expressing KB cells resulted in significant increases in both TNF-␣ mRNA and protein in comparison to UVB-treated control KB cells. However, UVB treatment up-regulated cyclooxygenase-2 mRNA levels to the same extent in both PAF-R-expressing and control KB cells. Pretreatment with the antioxidant vitamin E or the PAF-R antagonists WEB 2086 and A-85783 inhibited UVB-induced TNF-␣ production in the PAF-R-positive but not control KB cells. These studies suggest that the epidermal PAF-R may be a pharmacological target for UVB in skin.

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Accumulation of Eosinophils in Response to Intracutaneous Paf-Acether and Allergens in Man

Cited by 149 publications

References 6 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

Inflammatory responses to intradermal injection of platelet activating factor, histamine and prostaglandin E2 in healthy volunteers: a double blind investigation.

Augmentation of Ultraviolet B Radiation-induced Tumor Necrosis Factor Production by the Epidermal Platelet-activating Factor Receptor

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