Constituents of Sputum: A Simple Method

Epstein, Ralph L.

doi:10.7326/0003-4819-77-2-259

Cited by 30 publications

(10 citation statements)

References 11 publications

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“…Bronchial asthma is commonly characterised by increased airway reactivity to spasmogens (Cockcroft, 1983) and eosinophilia of sputum (Epstein, 1972), peripheral blood (Horn et al, 1975) or bronchial tissue (Huber & Koessler, 1922;Dunnill, 1960;Filley et al, 1982). Clinical studies strongly suggest a close link between airway eosinophilia and increased airway reactivity.…”

Section: Discussionmentioning

confidence: 99%

“…Increased eosinophil numbers in peripheral blood, sputum or lung tissue are now widely acknowledged to be characteristic of asthma (Dunnill, 1960;Epstein, 1972;Horn et al, 1975;Frigas & Gleich, 1986). In addition, toxic eosinophil products, such as major basic protein (MBP) (Frigas et al, 1981) and eosinophil cationic protein (ECP) (Dahl et al, 1978) have been demonstrated in the sputum and blood of asthma patients.…”

Section: Introductionmentioning

confidence: 99%

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Antigen challenge induces pulmonary airway eosinophil accumulation and airway hyperreactivity in sensitized guinea‐pigs: the effect of anti‐asthma drugs

Sanjar

Kristersson

et al. 1990

British J Pharmacology

188

114

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Guinea‐pigs were sensitized with 3 injections of ovalbumin (OA) (1 or 10 μg per animal) using Al(OH)3 and pertussis vaccine as adjuvants at two week intervals. Sensitized guinea‐pigs were challenged with an aerosol of OA (0.1%) over a one hour period and both airway reactivity and cellular content of bronchoalveolar lavage (BAL) fluid were assessed at intervals for up to 7 days. Guinea‐pigs sensitized with 1 μg of ovalbumin responded to an aerosol of OA with increased pulmonary airway eosinophilia, which was evident 1 day after challenge and was present for up to 7 days. Airway hyperreactivity was not detectable in these animals. Guinea‐pigs sensitized with 10 μg of ovalbumin responded to an aerosol of OA with increased pulmonary airway neutrophilia and eosinophilia and with increased airway reactivity which was maximal between 8 and 24 h after exposure to OA. Depletion of circulating platelets or neutrophils, by use of selective antisera, did not alter either the magnitude of eosinophilia or the intensity of airway reactivity in sensitized guinea‐pigs (10 μg) exposed to an aerosol of OA. Pretreatment of sensitized guinea‐pigs (10 μg) for 6 days with AH 21–132, aminophylline, dexamethasone or ketotifen inhibited pulmonary airway eosinophilia, but did not diminish airway hyperreactivity. Neither eosinophil accumulation nor development of airway hyperreactivity was influenced by treatment with mepyramine or salbutamol over a 6 day period before OA inhalation. Although eosinophilia may occur in association with increased airway reactivity in this animal model, there is no evidence of a causal relationship.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Antigen challenge induces pulmonary airway eosinophil accumulation and airway hyperreactivity in sensitized guinea‐pigs: the effect of anti‐asthma drugs

Sanjar

Kristersson

et al. 1990

British J Pharmacology

188

114

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“…The number of ciliated epithelial cells tends to be higher in asthmatics with more severe bronchial hyperresponsiveness to methacholine [137]. Furthermore, the appearance of Curschmann spirals, which consist of exudated fluid, proteins, migratory inflammatory cells, and sloughed epithelium, has been reported as pathognomonic of asthma [36, 46,112]. An increase in sloughed epithelial cells and degenerated epithelial cells has also been reported in BAL following inhalational challenge in occupationally induced red cedar asthma [84].…”

Section: Epithelial Cellsmentioning

confidence: 98%

“…Unfortunately, although cellular analysis of sputum in chronic obstructive airway disease is simple and inexpensive [97], and has the capacity to yield diagnostically relevant information in the evaluation of all patients with pulmonary diseases [46], it is often not routinely employed in clinical practice.…”

Section: Charcot-leyden Crystals Lysophospholipasementioning

confidence: 99%

Cellular and immunological markers of allergic and intrinsic bronchial asthma

Virchow

Kroegel

Walker

et al. 1994

Lung

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Based on a growing body of evidence, allergic as well as intrinsic bronchial asthma have recently been defined as chronic persistent inflammatory disorders. Agreement has been reached that asthma can no longer be equated with bronchospasm only, and that the absence of reversibility of airflow obstruction does not exclude bronchial asthma. Bronchial hyperreactivity, on the other hand, although common to the vast majority of asthmatics, is not specific for bronchial asthma and provocation tests to measure bronchial hyperreactivity are not suited for routine monitoring of bronchial asthma. The clinical features of asthma are related to cellular as well as to soluble parameters of bronchial inflammation. Therefore, means of assessing and monitoring asthmatic inflammation have been investigated. Since eosinophils, T lymphocytes, mast cells, macrophages, neutrophils, epithelial cells, and structural cells, as well as various proinflammatory mediators and proteins, have been implicated in the pathogenesis of bronchial asthma, it has been anticipated that several of these cells or mediators might be either diagnostic of bronchial asthma or could serve as markers to monitor the underlying bronchial inflammation. Currently there is no diagnostic marker of bronchial asthma, which, on its own, either confirms or excludes bronchial asthma with appropriate sensitivity and specificity. Clinically the most reliable feature of bronchial asthma that seems to be related closely to the symptomatology still is the presence of eosinophils in peripheral blood, and especially in sputum. Eosinophil-derived products, particularly eosinophil granule proteins, have been investigated as markers of eosinophil participation in the pathogenesis of asthma and, comparable to eosinophil numbers themselves, are possible predictors of impending exacerbations of allergic, as well as intrinsic bronchial asthma. However, clinically their precise value in diagnosing and monitoring of bronchial asthma has not been documented convincingly and requires further investigation. Increasing data suggest that the regulation of eosinophilia is largely conveyed by interleukin-5 (IL-5) released from activated T-helper lymphocytes and possibly other cells. Therefore, T-lymphocyte activation, and especially assessment of systemic and local IL-5 levels, might be of diagnostic value and possibly useful in monitoring of inflammation in bronchial asthma in the future. A possible role and future applications for other markers of inflammation not related to eosinophils in monitoring or diagnosing bronchial asthma need to be established.

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“…B. beim Differentialblutbild, existiert bisher nicht. Ebenso bestehen unterschiedliche Auffassungen über den diagnostischen '$ü'ert der TBS-Zytologie (Kirstaedter, 1971,;Epstein, 1972; lVbituell und Greet, 7984;Larson und Busch, 1985;Derksen et al, t989;lVinder et al, 1939). Neben grundlegenden Arbeiten, die die zelligen und nichtzelligen Inhalte des TBS beschreiben, werden TBS-Untersuchungen vor allem im Zusammenhang mit chronisch obstruktiven Lungenkrankheiten durchgeführt (Manslnann und Knight, L972;Beech, 1975;Hajer, 1979;Nuytten et al, 1983;lf,/bituell und Greet, 1984;Deconto und Deegen, L983;Mair, 1987).…”

Section: Introductionunclassified

Clinical aspect of tracheobronchial aspirates cytology

Dieckmann¹,

Deegen²

1990

PHK

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Constituents of Sputum: A Simple Method

Cited by 30 publications

References 11 publications

Antigen challenge induces pulmonary airway eosinophil accumulation and airway hyperreactivity in sensitized guinea‐pigs: the effect of anti‐asthma drugs

Antigen challenge induces pulmonary airway eosinophil accumulation and airway hyperreactivity in sensitized guinea‐pigs: the effect of anti‐asthma drugs

Cellular and immunological markers of allergic and intrinsic bronchial asthma

Clinical aspect of tracheobronchial aspirates cytology

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