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Journal ArticleDOI

Eosinophil cationic protein stimulates and major basic protein inhibits airway mucus secretion

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TLDR
Possible roles of eosinophil products in modulating the release of mucus from airway explants were investigated and three proteins derived from EO granules, EO-derived neurotoxin, Eo cationic protein (ECP), and major basic protein (MBP) were separated.
Abstract
Possible roles of eosinophil (EO) products in modulating the release of mucus from airway explants were investigated. Cell- and membrane-free lysates from purified human EOs (1 to 20 x 10(5)) caused a dose-dependent release of respiratory glycoconjugates (RGC) from cultured feline tracheal explants. Crude extracts from isolated EO granules also stimulated RGC release, suggesting that a granular protein might be responsible. Three proteins derived from EO granules, EO-derived neurotoxin, EO cationic protein (ECP), and major basic protein (MBP) were separated by sequential sizing and affinity chromatography. ECP (0.025 to 25 micrograms/ml) caused a dose-dependent increase in RGC release from both feline and human airway explants and also stimulated the release of the serous cell-marker, lactoferrin, from human bronchial explants. EO-derived neurotoxin (0.025 to 50 micrograms/ml) failed to affect RGC release, whereas MBP (50 micrograms/ml) significantly inhibited RGC release from feline explants. Thus, ECP stimulates RGC and lactoferrin release from airway explants, whereas MBP inhibits RGC release.

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Prominent neutrophilic inflammation in sputum from subjects with asthma exacerbation

TL;DR: Neutrophils predominate more frequently than eosinophils as the major inflammatory cell in sputum from patients with asthma in acute exacerbation, which suggests that IL-8 may mediate airway neutrophilia in acute asthma and that neutrophil elastase may mediated mucin glycoprotein hypersecretion in acute allergy.
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Induction of Airway Mucus Production By T Helper 2 (Th2) Cells: A Critical Role For Interleukin 4 In Cell Recruitment But Not Mucus Production

TL;DR: It is suggested that IL-4 is crucial for Th2 cell recruitment to the lung and for induction of inflammation, but has no direct role in mucus production.
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A novel role for murine IL-4 in vivo: induction of MUC5AC gene expression and mucin hypersecretion.

TL;DR: The overexpression of IL-4 locally within the lung enhances mucus glycoprotein synthesis by altering gene expression, results in the accumulation of mucus Glycoprotein in nonciliated epithelial cells, and induces the release of mucin into the airway lumen.
Journal ArticleDOI

Analysing the eosinophil cationic protein - a clue to the function of the eosinophil granulocyte

TL;DR: The levels of ECP measured in disease in combination with the catalogue of known functions of the protein and its polymorphisms presented here will build a foundation for further speculations of the role of E CP, and ultimately the role in homeostasis and in disease of the eosinophil.
Journal ArticleDOI

Remodeling of the Airway Epithelium in Asthma

TL;DR: Improved understanding of epithelial goblet cell abnormalities in asthma will hopefully lead to novel therapies for mucin hypersecretion, which is an important cause of morbidity and mortality.
References
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Journal ArticleDOI

Damage of the airway epithelium and bronchial reactivity in patients with asthma.

TL;DR: In this paper, the authors measured bronchial reactivity to inhaled histamine and prepared electron micrographs from 8 asthmatic patients who never smoked (2 females, 6 males, 18 to 62 yr of age).
Journal Article

1. Damage of the Airway Epithelium and Bronchial : Reactivity in Patients with Asthma

TL;DR: Fresh biopsies showed that asthma patients can have epithelial destruction at all levels of the airways, and Epithelial destruction in the respiratory tract of the asthma patients with mild to severe bronchial hyperresponsiveness was prominent enough to expose the epithelial nerves for specific or nonspecific stimuli.
Journal ArticleDOI

Bronchoalveolar eosinophilia during allergen-induced late asthmatic reactions.

TL;DR: Bronchoalveolar lavage was performed in 19 asthmatic patients and in 5 control subjects to suggest that eosinophils and their mediators might be involved in the development of LAR after allergen inhalation.
Book ChapterDOI

The Eosinophilic Leukocyte: Structure and Function

TL;DR: The evidence reviewed here indicates that the eosinophil has the ability to kill many species of helminths and likely does so during worm infection and also participate in inflammation in human disease especially asthma, skin diseases, and heart disease.
Journal ArticleDOI

Asthma as an axon reflex

Peter J. Barnes
- 01 Feb 1986 - 
TL;DR: In asthma, damage to airway epithelium, possibly caused by eosinophil products, exposes C-fibre afferent nerve endings and Stimulation of these endings by inflammatory mediators may result in an axon (local) reflex, which could account for at least some of the pathophysiology of asthma and this concept might lead to new strategies for treatment.
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