Nippostrongylus brasiliensis: Lung mast cell populations in repeatedly inoculated rats

Wells, Phyllis D.

doi:10.1016/0014-4894(77)90037-6

Cited by 9 publications

(2 citation statements)

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“…In a group of mild asthmatic patients whose non-specific airways reactivity was close to the normal range, allergen provocation sufficient to pro duce an early reaction was associated with significant increases in circulating concentrations of plasma his tamine and serum high-molecular-weight neutrophil chemotactic factor which preceded the onset of maxi mum bronchoconstriction [10]. The demonstration that both the airways and circulating mediator re sponses with allergen challenge could be inhibited by pretreatment with sodium cromoglycate (20 mg) and the beta-2-adrenoceptor agonist, salbutamol (200 ug), provided evidence that the increased circulating me diators were derived from activated mast cells within the lung rather than from basophils, the latter cells be ing unresponsive or insensitive to these pharmacolog ical agents [11,12].…”

Section: The Early Asthmatic Reactionmentioning

confidence: 99%

“…Mast cells ob tained by BAL from allergic asthmatic patients exhib it increased spontaneous release of histamine and are hyperresponsive both to IgE-dependent stimulation and inhibition of mediator secretion by sodium crom oglycate [17], Since mast cell hyperplasia at mucosal surfaces in rodents may occur in response to the re lease of growth factors, e.g., interleukin-3, from al lergen-stimulated T lymphocytes [18][19][20], it is tempt ing to speculate that mast cell hyperplasia occurring in the bronchial mucosa in asthma is induced by simi lar immunological mechanisms. In support of this view we have recently demonstrated that the number of bronchial epithelial mast cells increases greatly in guinea-pigs following a 3-week sensitisation of their respiratory tract with aerosolised ovalbumin.…”

Section: The Early Asthmatic Reactionmentioning

confidence: 99%

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Primary and Secondary Effector Cells in the Pathogenesis of Bronchial Asthma

Holgate¹,

Twentyman²,

Rafferty³

et al. 1987

Int Arch Allergy Immunol

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The immediate and late asthmatic reactions provoked by inhaled allergens have provided useful models enabling the dissection of individual inflammatory cells and their mediators that may contribute to the pathogenesis of asthma. The immediate reaction is considered to be mast cell-mediated on the basis that about 50% of the response is inhibitable by potent and selective H₁-receptor antagonists such as terfenadine and astemizole. Additional inhibition (∼30%) by the potent cyclooxygenase inhibitor flurbiprofen implies an important role for prostanoids in the immediate response, the most likely mast cell-derived product being prostaglandin (PG) D₂. In man, PGD2 is selectively metabolised to 9α1 1β-PGF₂, a unique prostaglandin which shares with PGD₂ contractile properties on guinea-pig and human airways smooth muscle. The inability of piriprost, a potent leukotriene synthesis inhibitor, to influence the allergen-provoked immediate reaction raises the possibility that sulphidopeptide leukotrienes play a minor role in this response. The late asthmatic reaction is considered to resemble clinical asthma since it is accompanied by increased responsiveness of the airways to a wide range of stimuli. The late reaction in man is inhibited by nedocromil sodium (4 mg) but only marginally attenuated by salbutamol (200 μg) if both drugs are administered prior to allergen challenge. Since salbutamol, in the dose administered, is a potent mast cell-stabilising agent, these findings must question the obligatory role of mast cell mediator release in the pathogenesis of the late response. A model of the late reaction in conscious guinea-pigs demonstrates a selective influx of neutrophils followed by eosinophils 6–12 h after challenge in relation to the late reaction, suggesting a role for these secondary effector cells in mediating this response and possibly the acquisition of increased bronchial responsiveness. These human and animal studies demonstrate a complex interaction of primary and secondary effector cells in the pathogenesis of bronchoconstrictor responses to allergen and should help to clarify the contribution of ‘inflammation’ to clinical asthma.

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Section: The Early Asthmatic Reactionmentioning

confidence: 99%