Phospholipids and microviscosity study in broncho-alveolar lavage fluids from control subjects and from patients with extrinsic allergic alveolitis

Jouanel, P; Motta, Claude; Brun, J; Molina, C; Dastugue, B.

doi:10.1016/0009-8981(81)90077-2

Cited by 23 publications

(15 citation statements)

References 14 publications

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“…Therefore, changes in the surfactant lipid composition, for instance, more or less PG or other negatively charged lipids, may not only alter the uptake of these lipids but also of DPPC, the most important surface tension-lowering component of surfactant. In various diseases, such as respiratory distress syndrome, extrinsic allergic alveolitis, and respiratory infections, changes in the surfactant lipid composition have been observed (30,31). Whether an altered uptake of surfactant lipids by alveolar cells plays a role in the pathogenesis of respiratory diseases is not yet known.…”

Section: Discussionmentioning

confidence: 99%

A Common Pathway for the Uptake of Surfactant Lipids by Alveolar Cells

Poelma

Ju²,

Bakker³

et al. 2004

Am J Respir Cell Mol Biol

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The uptake of different surfactant lipids-dipalmitoylphosphatidylcholine (DPPC), phosphatidylglycerol (PG), or phosphatidylinositol (PI)-and liposomes with a surfactant-like composition by alveolar type II cells (alveolar type II cells) and macrophages (alveolar macrophages) was studied in vitro. Fluorescent-labeled liposomes containing either 86% of the studied lipid, i.e., DPPC, PG, PI, and 6% labeled phosphatidylethanolamine (PE) and 8% cholesterol or a lipid mixture similar to surfactant (DPPC, PG, PI, phosphatidylcholine, PE, and cholesterol in a weight ratio of 55:8:2:21:8:6) were incubated with alveolar macrophages and alveolar type II cells. The cell-associated fluorescence assessed by flow cytometry demonstrated a higher uptake of PG and PI by both alveolar macrophages and alveolar type II cells, and a lower uptake of DPPC by alveolar macrophages. In addition, fewer alveolar type II cells take up DPPC, whereas there are no differences for the alveolar macrophages in the number of cells involved in the uptake. Competition experiments with Texas Red-labeled liposomes and either DPPC liposomes or PI liposomes labeled with Bodipy indicated that all these liposomes are internalized via the same pathway by alveolar cells. Thus, lipid composition directly influences the (re)uptake of surfactant.

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Section: Discussionmentioning

confidence: 99%

A Common Pathway for the Uptake of Surfactant Lipids by Alveolar Cells

Poelma

Ju²,

Bakker³

et al. 2004

Am J Respir Cell Mol Biol

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“…In HP, surfactant is more viscous because its composition is altered. Increased concentrations of phosphatidylanolamine and phosphatidylinositol are observed in patients (125). Also, the surfactant immunosuppressive function seems to be modified in HP.…”

Section: Surfactantmentioning

confidence: 96%

Hypersensitivity pneumonitis

Girard

and

Cormier

2009

Allergy

115

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The first few cases of hypersensitivity pneumonitis (HP) were described in the early 20th century in farmers exposed to moldy hay or straw. As then, HP has been ascribed to multiple inhaled antigens found in a large variety of environmental settings. Hypersensitivity pneumonitis results from an exaggerated immune response, which gives rise to acute infection‐like symptoms or to progressive, sometimes irreversible lung damage. The diagnosis is based on a combination of clinical characteristics of the disease. Clinical diagnostic criteria have recently been published. The immune mechanisms leading to HP are still incompletely understood. Initially, believed to be a classes III and IV immune response, we now have a clearer understanding of the complex inflammatory events involved. These include the release of pro inflammatory cytokines and a decrease in the immune control mechanisms via surfactant, dendritic and T‐regulatory cells. Despite the improved understanding, the treatment and outcome of HP have not changed. Oral corticosteroids remain the only effective drugs and contact withdrawal constitutes the ideal solution. If unchecked, HP can lead to irreversible lung damage in the form of fibrosis or emphysema, respiratory insufficiency and even death.

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“…The activa tion of macrophages was correlated in both situations with the course of histopathological lung lesions. Furthermore, bronchoalveolar lavage has shown an in crease in phospholipid components of the surfactant in HP patients [26], probably reflecting an increased activity of type II pneumocytes.…”

Section: Discussionmentioning

confidence: 99%

Ultrastructural Features of Alveolar Cells in Experimental Hypersensitivity Pneumonitis

Quezada¹,

Gimpel²,

Miranda³

et al. 1987

Respiration

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An experimental model of hypersensitivity pneumonitis in rats was used to analyze ultrastructural changes in cellular elements of the epithelium and alveolar lumen, in an attempt to correlate the immunological mechanisms responsible for these pulmonary lesions. Semifine and ultrafine sections of pulmonary tissue of immunized and intratracheally challenged rats were analyzed and compared with their respective controls. A thickening of the alveolar walls and an increase in the number of macrophages and type II pneumocytes were observed in the semifine sections. The ultrastructural examination revealed appreciable changes in morphology, size and location of both types of cells. The membranes of the macrophages showed evident alterations and the type II pneumocytes, an increase in size and number of cytoplasmic inclusions corresponding to surfactant. The cellular changes observed are consistent with phenomena of cellular activation, which can be attributed to the release of soluble mediators by T lymphocytes. The important delayed hypersensitivity phenomena based on the morphology of pulmonary lesions in this model contribute data to the pathogenic interpretation of hypersensitivity alveolitis.

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Phospholipids and microviscosity study in broncho-alveolar lavage fluids from control subjects and from patients with extrinsic allergic alveolitis

Cited by 23 publications

References 14 publications

A Common Pathway for the Uptake of Surfactant Lipids by Alveolar Cells

A Common Pathway for the Uptake of Surfactant Lipids by Alveolar Cells

Hypersensitivity pneumonitis

Ultrastructural Features of Alveolar Cells in Experimental Hypersensitivity Pneumonitis

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