Functional assessment of alveolar macrophages: comparison of cells from asthmatics and normal subjects

Godard, P.; Chaintreuil, J; Damon, Marie; Coupe, Michael; Flandre, O; Paulet, AndréCrastes de; Michel, François

doi:10.1016/0091-6749(82)90234-2

Cited by 166 publications

(36 citation statements)

References 14 publications

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“…In most of these cases, however, the eosinophil inflammation is mild, usually representing < 5% of the total inflammatory cell populations recovered from the lower respiratory tract (38). In addition to these interstitial lung diseases, the individuals with asthma evaluated in the present study had a small percentage of eosinophils recovered by lavage, consistent with that observed in other studies (39).…”

Section: Resultssupporting

confidence: 81%

Acute tropical pulmonary eosinophilia. Characterization of the lower respiratory tract inflammation and its response to therapy.

Pinkston¹,

Vk²,

Nutman³

et al. 1987

J. Clin. Invest.

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Although acute tropical pulmonary eosinophilia (TPE) is well recognized as a manifestation of filarial infection, the processes that mediate the abnormalities of the lung in TPE are unknown. To evaluate the hypothesis that the derangements of the lower respiratory tract in this disorder are mediated by inflammatory cells in the local milieu we utilized bronchoalveolar lavage to evaluate affected individuals before and after therapy. Inflaminatory cells recovered from the lower respiratory tract of individuals with acute, untreated TPE (a = 8) revealed a striking eosinophilic alveolitis, with marked elevations in both the proportion of eosinophils (TPE 54±5%; normal 2±5%; P < 0.001) and the concentration of eosinophils in the recovered epithelial lining fluid (ELF) (TPE 63±20 X 103/Al; normal 03±0.1 X 103/jl; P < 0.01). Importantly, when individuals (a = 5) with acute TPE were treated with diethylcarbamazine (DEC), there was a marked decrease of the lung eosinophils and concomitant increase in lung function. These observations are consistent with the concept that at least some of the abnormalities found in the lung in acute TPE are mediated by an eosinophil-dominated inflammatory process in the lower respiratory tract.

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Section: Resultssupporting

confidence: 81%

Acute tropical pulmonary eosinophilia. Characterization of the lower respiratory tract inflammation and its response to therapy.

Pinkston¹,

Vk²,

Nutman³

et al. 1987

J. Clin. Invest.

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show abstract

“…They appear to be in an activated state and release enzymes (27), eicosanoids (28), PAF, oxygen free radicals (29) and cytokines, including TNF (30) that might be deleterious to the bronchi. They can also synthesize and secrete elastase (31) and a group of metallopreoteinases having the capacity to degrade various extracellular ECM macromolecules including elastin (32).…”

Section: Inflammation and Repair In Asthmamentioning

confidence: 99%

Asthma: a disease remodeling the airways

Bousquet

Chanez

Lacoste

et al. 1992

Allergy

243

151

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“…BAL was performed in all study subjects using five aliquots (50 mL each) of 0.9% saline solution as described previously [16,18]. Briefly, sterile saline solution was introduced into the right fourth or fifth subsegmental bronchus in normal subjects.…”

Section: Preparation Of Lower Respiratory Tract Cellsmentioning

confidence: 99%

Increased exhaled nitric oxide in active pulmonary tuberculosis due to inducible NO synthase upregulation in alveolar macrophages

et al. 1998

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Nitric oxide (NO) plays a major role in the pulmonary host-defence mechanism in response to infections and is implicated in bacteriostatic as well as bactericidal processes [1,2]. NO is generated through the L-arginine pathway and is converted to the related reactive nitrogen intermediates (RNI) . In inflammatory responses, NO is produced by the inducible form of NO synthase (iNOS), which is mostly from inflammatory cells, such as macrophages [3][4][5]. NO production and iNOS expression by alveolar macrophages (AM) is upregulated in response to heat-killed Mycobacterium tuberculosis instilled into the lungs of rats [6] and plays a role in limiting the growth of Mycobacterium avium complex [7,8]. Murine macrophages activated by interferon (IFN)-γ and tumour necrosis factor (TNF)-α are capable of killing M. tuberculosis in vitro via the generation of RNI by iNOS [9]. In addition, pretreatment with NO synthase (NOS) inhibitors profoundly increases bacterial burden, pathological tissue damage and mortality in mice infected with M. tuberculosis [10], thus indicating that NO plays an important role in resistance to M. tuberculosis infection in the mouse. A recent report has shown that iNOS messenger ribonucleic acid (mRNA) is upregulated on AM in patients with active pulmonary tuberculosis (TB) [11], however, it is not known whether the iNOS enzyme activity is also enhanced and leads to increased generation of RNI by AM against M. tuberculosis.NO can be detected in the expired air of animals and humans [12]. Recent reports have shown that the level of exhaled NO is elevated in patients with bronchial asthma and bronchiectasis [13,14], and have suggested that this is due to iNOS upregulation induced by cytokines such as IFN-γ, TNF-α and interleukin (IL)-1β [15] released in chronic airway inflammation. Thus, the measure of exhaled NO concentration may gauge the extent of NOmediated inflammatory responses in the airways. In this study, we measured exhaled NO levels in patients with active pulmonary TB and determined the cellular source of NO by examining the expression of iNOS and the release of RNI from AM. Material and methods Study populationNineteen patients with active pulmonary TB (13 males and 6 females, aged 59.1±4.5 yrs) were studied prior to anti-TB treatment. None of these patients were current smokers. For all patients, at least one recent sputum specimen We conclude that the increase in exhaled nitric oxide observed in patients with active pulmonary tuberculosis is due to an upregulation of inhaled NO synthase expression in alveolar macrophages which have an enhanced capacity for nitric oxide production. Eur Respir J 1998; 11: 809-815.

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Functional assessment of alveolar macrophages: comparison of cells from asthmatics and normal subjects

Cited by 166 publications

References 14 publications

Acute tropical pulmonary eosinophilia. Characterization of the lower respiratory tract inflammation and its response to therapy.

Acute tropical pulmonary eosinophilia. Characterization of the lower respiratory tract inflammation and its response to therapy.

Asthma: a disease remodeling the airways

Increased exhaled nitric oxide in active pulmonary tuberculosis due to inducible NO synthase upregulation in alveolar macrophages

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