Response of superoxide anion production by guinea pig eosinophils to various soluble stimuli: Comparison to neutrophils

Yamashita, Tatsuhisa; Someya, Akimasa; Hara, Eriko

doi:10.1016/0003-9861(85)90569-7

Cited by 54 publications

(35 citation statements)

References 22 publications

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“…As expected, airway inflammatory changes were more important in hyperreactive nonallergic and allergic patients, as demonstrated by the correlation between sensitivity to MCh and ECP levels. Eosinophils have been implicated as one of the primary effector cells in tissue damage observed in severe bronchial asthma (7), since they can produce oxygen radicals at two-to threefold the rate of similarly activated neutrophils (26) and various cytotoxic cationic proteins, including ECP ( 3 , 9, 18). In this context, epithelial damage or loss is a well-known characteristic finding in biopsies obtained from patients with asthma (27).…”

Section: Discussionmentioning

confidence: 99%

Airway eosinophilic inflammation, epithelial damage, and bronchial hyperresponsiveness in patients with mild‐moderate, stable asthma

Oddera¹,

Silvestri²,

Balbo

et al. 1996

Allergy

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Allergic asthma is characterized by chronic recruitment of eosinophils in the airways. Once activated, eosinophils release toxic products, including eosinophil cationic protein (ECP), able to damage airway epithelial cells. To test the hypothesis that also in mild‐moderate stable asthma, a significant eosinophil activation could occur, we studied 25 asthmatic patients (34 ± 19 years old), of whom 18 were allergic (27 ± 12 years) and seven nonallergic (42±10 years), with FEV1 values ±70% of predicted, and eight normal volunteers (controls, 33 ±11 years). All subjects underwent methacholine (MCh) challenge on the first visit, and bronchoalveolar lavage (BAL) on the second visit (approximately 3–4 days later). BAL cells were counted and albumin (Alb) (as index of protein dilution in BAL fluid) and ECP levels (as index of eosinophil activation) in BAL fluid were measured. As compared to controls, a significant increase in BAL eosinophil and in BAL epithelial cell numbers was observed in asthmatic patients (P>0.05, each comparison), with no differences between the two asthmatic patient subgroups. Detectable ECP levels (>2 μg/1) were found in BAL of 18 asthmatic patients (14 allergic and four nonallergic asthmatic patients), while Alb levels were measurable in 25 BAL fluids and found to be similar in controls and asthmatic patients, and in the two asthmatic patient subgroups (P>0.05, each comparison). In BAL of asthmatic patients, positive correlations were found between eosinophil numbers and 1) ECP/Alb levels (r= 0.50, P = 0.020); 2) epithelial cell numbers (r = 0.S0, P = 0.014). In asthmatic patients, a significant negative correlation was found between bronchial reactivity to MCh (log Pd15) and ECP/Alb levels in BAL fluid (r=‐0.6, P= 0.005), whereas no correlation was found between log Pd15 MCh and BAL eosinophil or epithelial cell number (P>0.1, each correlation). These data suggest that bronchial eosinophil recruitment and activation may occur also in mild‐moderate stable asthma and that bronchial epithelium damage and airway responsiveness may be partially associated with the eosinophilic inflammatory reaction.

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Section: Discussionmentioning

confidence: 99%

Airway eosinophilic inflammation, epithelial damage, and bronchial hyperresponsiveness in patients with mild‐moderate, stable asthma

Oddera¹,

Silvestri²,

Balbo

et al. 1996

Allergy

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“…[104,105,[108][109][110], and probably 1O 2 as well as OH· [111,112]. With most stimuli, the respiratory burst of eosinophils is greater than that of equivalent numbers of neutrophils [104,105,107,109,113]. A reduced nicotinamide adenine dinucleotide (NADPH) oxidase, similar to that present in neutrophils, appears to be involved [104,106,107].…”

Section: De Novo Synthesized Productsmentioning

confidence: 99%

Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part I)

Kroegel¹,

Virchow²,

Luttmann³

et al. 1994

Eur Respir J

129

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P Pu ul lm mo on na ar ry y i im mm mu un ne e c ce el ll ls s i in n h he ea al lt th h a an nd d d di is se ea as se e: : t th he e e eo os si in no op ph hi il l l le eu uc co oc cy yt te e ( (P Pa ar rt t I I) ) ABSTRACT: Increasing evidence has accumulated to suggest that eosinophils play a key role in the pathogenesis of asthma and other pulmonary diseases by damaging infiltrated bronchial tissue and lung parenchyma. The first part of this review on eosinophils describes the cellular characteristics and properties of the cell, which help in understanding its role in disease. The article focuses on origin, maturation and differentiation of the eosinophil, its morphological and phenotypical properties, as well as its preformed and newly generated mediators of inflammation. The cause and putative significance of eosinophil heterogeneity in respect to function and density will also be discussed. In addition, the naturally occurring mediators through which eosinophils are activated and communicate with other inflammatory cells are outlined.The first part closes with new aspects of eosinophil recruitment from the circulation into perivascular tissue, including nonselective and putative selective adhesion mechanisms and chemotaxis.

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“…The generation of superoxide anion (02-) was meas ured according to the method of Yamashita et al (34). Guinea pig alveolar macrophages were prepared accord ing to the previously described method (35).…”

Section: Measurement Of Superoxide Anion (02-) Productionmentioning

confidence: 99%

Effects of MKS-492 on Antigen-Induced Bronchoconstriction and Allergic Reaction in Guinea Pigs and Rats

Nagai

Sakurai

Iwama

et al. 1993

Japanese Journal of Pharmacology

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ABSTRACT-Effects of R[+]-8-{[1-[3,4-dimethoxyphenyl]-2-hydroxyethyl]amino}-3,7-dihydro-7-[2 methoxyethyl]-1,3-dimethyl-lH-purine-2,6-dione (MKS-492), a reported type III isozyme inhibitor of cyclic nucleotide phosphodiesterase, on antigen or platelet activating factor (PAF)-induced bronchoconstriction and allergic reactions in guinea pigs and rats were investigated. 1) MKS-492 inhibited antigen-induced bron choconstriction in guinea pigs. Aminophylline also inhibited the reaction. 2) MKS-492 inhibited PAF-in duced bronchoconstriction and inhibited the increase in airway responsiveness to histamine in guinea pigs, although aminophylline failed to affect these reactions. 3) MKS-492 relaxed guinea pig tracheal muscle in vitro more potently than aminophylline. 4) MKS-492 inhibited leukotriene B4 (LTB4)-induced airway eosinophilia in guinea pigs. 5) MKS-492 inhibited passive cutaneous anaphylaxis and mediator-induced skin reactions in rats more potently than aminophylline. Both drugs inhibited antigen and phospholipase A2 induced histamine release from guinea pig lung tissue. 6) MKS-492 inhibited PAF-induced 02 generation from guinea pig alveolar macrophages. These results indicate that MKS-492 is a more potent inhibitor of allergic bronchoconstriction and PAF or LTB4-induced inflammatory reactions in guinea pigs and the allergic cutaneous reactions in rats when compared to aminophylline.

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Response of superoxide anion production by guinea pig eosinophils to various soluble stimuli: Comparison to neutrophils

Cited by 54 publications

References 22 publications

Airway eosinophilic inflammation, epithelial damage, and bronchial hyperresponsiveness in patients with mild‐moderate, stable asthma

Airway eosinophilic inflammation, epithelial damage, and bronchial hyperresponsiveness in patients with mild‐moderate, stable asthma

Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part I)

Effects of MKS-492 on Antigen-Induced Bronchoconstriction and Allergic Reaction in Guinea Pigs and Rats

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