Airway epithelial damage and inflammation in children with recurrent bronchitis.

Gaillard, Dominique; Jouet, Jacques; Egreteau, Laurent; Plotkowski, L; Zahm, J.M.; Benali, Rachid; Pierrot, D.; Puchelle, Édith

doi:10.1164/ajrccm.150.3.8087356

Cited by 20 publications

(11 citation statements)

References 16 publications

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“…Our hypothesis that early respiratory insults (whether medical or infectious) can cause chronic self-perpetuating respiratory inflammation is supported by two recent bronchoscopic studies. HEINO et al [26] studied seven children referred because of a productive cough lasting more than 3 months, and GAILLARD et al [27] studied 31 children referred with a loosely defined history of recurrent bronchitis. In both cases, bronchoscopy revealed chronic airway inflammation.…”

Section: Discussionmentioning

confidence: 99%

Chronic cough and wheeze in children: do they all have asthma?

Seear¹,

Wensley²

1997

Eur Respir J

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In the experience of both authors, children referred for investigation of a chronic productive cough often do not fit conventional diagnostic categories. The aim of this study was to answer two questions: 1) do such diagnostic orphans exist? and, 2) if so, can they be classified in a clinically useful manner?Eighty one previously undiagnosed children referred with a history of more than 3 months productive or rattly cough were studied prospectively. Investigations consisted of a detailed history, physical examination, and an extensive set of clinical investigations. Sixty randomly selected asthmatic children served as demographic controls.Children fell into three groups: 23 had newly diagnosed conditions, such as cystic fibrosis, or were indistinguishable from asthma; 24 had a history of major medical interventions (cardiac surgery, chemotherapy, tracheo-oesophageal fistula repair); 34 had a history of significant early respiratory tract infections, usually combined with poor social conditions. The latter group differed significantly from asthmatic controls in a wide range of demographic and clinical comparisons. Native American children were overrepresentedThe results of this study suggest that early respiratory insults (whether viral or medical) can induce self-perpetuating inflammation, manifesting as a chronic productive cough and intermittent wheeze. The associations between poverty and infant chest infections or early invasive medical treatment with subsequent chronic respiratory disease are clearly definable and probably justify diagnostic terms distinct from asthma, particularly for use in epidemiological studies.

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Section: Discussionmentioning

confidence: 99%

Chronic cough and wheeze in children: do they all have asthma?

Seear¹,

Wensley²

1997

Eur Respir J

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“…In addition, airway epithelial cells have also been identified as a source of extracellular ATP. Although the active release mechanisms of ATP from epithelial cells are not understood (5,7,11,36,37), epithelial trauma associated with asthma (12,18) can result in damaged cells that passively release ATP.…”

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confidence: 99%

ATP stimulates Ca²⁺oscillations and contraction in airway smooth muscle cells of mouse lung slices

Bergner

Sanderson

2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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2ϩ oscillations that were accompanied by airway contraction. After ϳ1 min, the Ca 2ϩ oscillations subsided and the airway relaxed. By contrast, Ն0.5 M adenosine 5Ј-O-(3-thiotriphosphate) (nonhydrolyzable) induced Ca 2ϩ oscillations in the SMCs and an associated airway contraction that persisted for Ͼ2 min. Adenosine 5Ј-O-(3-thiotriphosphate)-induced Ca 2ϩ oscillations occurred in the absence of external Ca 2ϩ but were abolished by the phospholipase C inhibitor U-73122 and the inositol 1,4,5-trisphosphate receptor inhibitor xestospongin. Adenosine, AMP, and ␣,␤-methylene ATP had no effect on airway caliber, and the magnitude of the contractile response induced by a variety of nucleotides could be ranked in the following order: ATP ϭ UTP Ͼ ADP. These results suggest that the SMC response to ATP is impaired by ATP hydrolysis and mediated via P2Y 2 or P2Y 4 receptors, activating phospholipase C to release Ca 2ϩ via the inositol 1,4,5-trisphosphate receptor. We conclude that ATP can serve as a spasmogen of airway SMCs and that Ca 2ϩ oscillations in SMCs are required to sustain airway contraction. calcium signaling; confocal microscopy; ATP hydrolysis ASTHMA IS AN AIRWAY DISEASE characterized by a hyperreactive response of airway smooth muscle cells (SMCs) to spasmogens such as histamine, leukotrienes, and perhaps serotonin (2, 6, 25). A major source of histamine and other agonists is an exocytotic release from inflammatory cells (i.e., mast cells and basophils) within the submucosal tissue, in close proximity to the SMCs. However, mast cell degranulation can simultaneously release another potential spasmogen, ATP, which is packaged in the same exocytotic vesicles (23). In addition, airway epithelial cells have also been identified as a source of extracellular ATP. Although the active release mechanisms of ATP from epithelial cells are not understood (5,7,11,36,37), epithelial trauma associated with asthma (12, 18) can result in damaged cells that passively release ATP.In many other tissues, ATP has been found to stimulate P2X and P2Y receptors, both of which have been identified in lung tissue (19,29,34,35 ] i ) of SMCs usually result in the phosphorylation of myosin light chain and the stimulation of contraction (15, 16), ATP is likely to be a potent spasmogen of airway SMCs.Surprisingly, the effects of ATP on the [Ca 2ϩ ] i of airway SMCs or on airway contraction have not been extensively studied, and the few reports that exist are inconsistent. For example, ATP was found to increase in vivo airway resistance in rats (9) or induce contraction in isolated guinea pig tracheae (8). On the other hand, ATP was reported to relax rabbit tracheal smooth muscle strips (1) and isolated mouse trachea (10, 17) that had been previously contracted with acetylcholine (ACh). These tissue preparations were derived from the large airways and consisted of tracheal rings or strips. As a result, these studies were not able to focus on the responses of individual SMCs. In addition, it is not clear whether results obtained from large air...

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“…Data from other reports on bronchial gland inflammation also give relatively limited pathological data. One of two reports is that of Gaillard et al [20], who examined biopsy tissues from 30 children with recurrent bronchitis and noted dense lymphocytic infiltrates in the submucosa but "rarely around the deepest glands." The second report, by Soutar et al [46,47], deals with the examination of entire rings of main stem bronchial tissue and describes "large and numerous" IgA-containing cells in glands of "incidental" bronchitics.…”

Section: Discussionmentioning

confidence: 99%

Chronic glandular bronchitis in young individuals residing in a metropolitan area

Sherwin¹,

Richters²,

Everson

et al. 1998

Virchows Archiv

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A study of 161 Los Angeles County residents aged 12-28 years old who had died sudden violent deaths showed frequent and severe chronic glandular bronchitis (CGB), that is to say grade > or =5 (0-10) chronic inflammation involving at least one, half or more, and all submucosal glands in 53.4%, 21%, and 4.4% of the main stem bronchi, respectively. The mean plasma cell/gland/bronchus was high (> or =5) for 22 subjects (13.7%), while only 2 bronchi (1.2%) had a correspondingly high lymphocyte mean (P<0.001). Of the bronchi, 75.2% were affected by glandular atrophy (> or =5 in 8.1%), 10.6% had neutrophil infiltration of glands, and 3.1% had acute sialadenitis. Of the total of 1040 glands, CGB was found in 83.8% (> or =5 in 26.5%). Of 25 non-smokers identified, 14 (56%) had some degree of CGB in > or =50% of the glands, severe in 7 (26%). Severe CGB in many young individuals raises concern that a subpopulation of living cohorts may have an increased susceptibility to disease and a rising incidence of chronic lung disease. Demographic analysis is pending, but respiratory infection, smoking, adverse socioeconomic factors, and air pollution are all potential causative factors. Since pollution in Los Angeles frequently exceeds air quality standards, an ongoing multicity study is attempting to distinguish between the suspected effects of air pollution and confounding variables.

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Airway epithelial damage and inflammation in children with recurrent bronchitis.

Cited by 20 publications

References 16 publications

Chronic cough and wheeze in children: do they all have asthma?

Chronic cough and wheeze in children: do they all have asthma?

ATP stimulates Ca²⁺oscillations and contraction in airway smooth muscle cells of mouse lung slices

Chronic glandular bronchitis in young individuals residing in a metropolitan area

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Airway epithelial damage and inflammation in children with recurrent bronchitis.

Cited by 20 publications

References 16 publications

Chronic cough and wheeze in children: do they all have asthma?

Chronic cough and wheeze in children: do they all have asthma?

ATP stimulates Ca2+oscillations and contraction in airway smooth muscle cells of mouse lung slices

Chronic glandular bronchitis in young individuals residing in a metropolitan area

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ATP stimulates Ca²⁺oscillations and contraction in airway smooth muscle cells of mouse lung slices