Pulmonary phospholipidosis in rats respiring air containing diesel particulates

Eskelson, Cleamond D.; Chvapil, Miloš; Strom, Kenneth A.; Vostal, Jaroslav J.

doi:10.1016/s0013-9351(87)80235-9

Cited by 21 publications

(13 citation statements)

References 13 publications

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“…This result is in agreement with in vivo studies performed with DEPs (17) and another pollutant (silica) (25). Rats chronically exposed to DEPs or given a single intratracheal dose of DEPs showed increased levels of PC (i.e., surfactant) content in the lungs and in pulmonary lavage fluid (17). Silica instillation also induced an alveolar phospholipidosis in rats (25).…”

Section: Discussionsupporting

confidence: 89%

“…Surfactant also maintains alveolar fluid balance and possibly exhibits host defense properties (28,37). It has previously been shown in vivo that exposure to air pollutants including DEPs may alter the composition of the surfactant (17). However, the direct consequences of DEPs exposure on the secretion of surfactant by ATII cells remain unknown, as do the mechanisms mediating these effects.…”

mentioning

confidence: 99%

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Diesel particles increase phosphatidylcholine release through a NO pathway in alveolar type II cells

Juvin

Fournier

Grandsaigne

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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(DEPs) have been shown in vivo as well as in vitro to affect the respiratory function and in particular the immune response to infection and allergens. In the current study, we investigated the effect of DEPs on the production of phosphatidylcholine (PC), a major constituent of surfactant, by rat alveolar type II (ATII) primary cells in vitro. Our results demonstrate that incubation of ATII cells with DEPs lead to a time-and dose-dependent increase in labeled PC release. This effect was mimicked by nitric oxide (NO) donors and cGMP and was abolished by inhibitors of NO synthase (NOS). In addition, a NOS inhibitor inhibits by itself the basal secretion of PC. We next examined the effects of DEPs on NOS gene expression and showed that DEPs increase NO production and upregulate both protein content and mRNA levels of the inducible NOS (NOS II). Together our data demonstrate that DEPs alter the production of surfactant by ATII cells through a NO-dependent signaling pathway. surfactant; nitric oxide MAJOR AIR POLLUTANTS include nitrogen dioxide, ozone sulfur dioxide, and breathable particulate matter of diameter inferior to 10 m (PM10) (12,27). Several studies have particularly implicated diesel exhaust particles (DEPs), a major component of PM10, as contributing to the incidence and severity of respiratory diseases during air pollution episodes. Epidemiological studies have reported that high levels of DEPs are associated with worsening peak flow, inhaler usage, respiratory symptoms, and emergency room visits in asthmatic children and adults (34,38). In a cohort of over half a million adults residing in 151 metropolitan areas in the United States between 1982 and 1989, fine particulate pollution was associated with cardiopulmonary and lung cancer mortality (33). Similarly, a recent work has demonstrated an increased mortality and morbidity rate after DEPs exposure (26).Airway epithelial cells are primary targets for air pollutants. Several studies have investigated the effect of DEPs on nasal, bronchial, and alveolar epithelial cells. In nasal cells, DEPs enhance cytokine expression synergistically with allergens and increase local eosinophil adhesion (15,16,44). In bronchial epithelial cells, DEPs are internalized, inducing airway inflammation (4,8,41) and hyperresponsiveness (43).DEPs also interact with alveolar type II (ATII) cells since their small size (0.1-1 m) allows them to reach the alveolar space (32,46,48). ATII cells regulate the intra-alveolar homeostasis through four main functions. They secrete a large panel of cytokines (5, 13, 31, 39), serve as progenitors to the alveolar type I cells (18), actively transport ions (23), and synthesize and secrete surfactant. We previously demonstrated that one of these functions (i.e., cytokine secretion) was altered by DEPs (24). Synthesis and secretion of surfactant are other very important functions of ATII cells. Surfactant prevents alveolar collapse at end expiration by lowering surface tension at the air/extracellular lining interface in the alveoli and dist...

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Section: Discussionsupporting

confidence: 89%

mentioning

confidence: 99%

Diesel particles increase phosphatidylcholine release through a NO pathway in alveolar type II cells

Juvin

Fournier

Grandsaigne

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Diesel exhausts were shown to induce pulmonary phospholipidosis in rats [37]. In another study, short-term exposure of rats to 6 mg/m 3 diesel exhaust resulted in an increased labeling index in type II cells and enhancement of whole lung D N A synthesis [195].…”

Section: Othersmentioning

confidence: 96%

The surfactant system of the adult lung: physiology and clinical perspectives

1992

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Pulmonary surfactant is synthesized and secreted by alveolar type II cells and constitutes an important component of the alveolar lining fluid. It comprises a unique mixture of phospholipids and surfactant-specific proteins. More than 30 years after its first biochemical characterization, knowledge of the composition and functions of the surfactant complex has grown considerably. Its classically known role is to decrease surface tension in alveolar air spaces to a degree that facilitates adequate ventilation of the peripheral lung. More recently, other important surfactant functions have come into view. Probably most notable among these, surfactant has been demonstrated to enhance local pulmonary defense mechanisms and to modulate immune responses in the alveolar milieu. These findings have prompted interest in the role and the possible alterations of the surfactant system in a variety of lung diseases and in environmental impacts on the lung. However, only a limited number of studies investigating surfactant changes in human lung disease have hitherto been published. Preliminary results suggest that surfactant analyses, e.g., from bronchoalveolar lavage fluids, may reveal quantitative and qualitative abnormalities of the surfactant system in human lung disorders. It is hypothesized that in the future, surfactant studies may become one of our clinical tools to evaluate the activity and severity of peripheral lung diseases. In certain disorders they may also gain diagnostic significance. Further clinical studies will be necessary to investigate the potential therapeutic benefits of surfactant substitution and the usefulness of pharmacologic manipulation of the secretory activity of alveolar type II cells in pulmonary medicine.

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“…Work with animal models has shown effects on surfactant production. Early studies showed that surfactant production is up-regulated in type II alveolar cells exposed to pollutants (98,120,311). Subsequent work has shown that alveolar type II cells, macrophages, and surfactant production and composition are affected by exposure to fungal spores and their mycotoxins, including Cladosporium and Stachybotrys species (181,249,250,255,378; W. G. Sorenson, Proc.…”

Section: Effects Of Stachybotrys In Indoor Air 155mentioning

confidence: 99%

Indoor Mold, Toxigenic Fungi, andStachybotrys chartarum: Infectious Disease Perspective

2003

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Damp buildings often have a moldy smell or obvious mold growth; some molds are human pathogens. This has caused concern regarding health effects of moldy indoor environments and has resulted in many studies of moisture- and mold-damaged buildings. Recently, there have been reports of severe illness as a result of indoor mold exposure, particularly due to Stachybotrys chartarum. While many authors describe a direct relationship between fungal contamination and illness, close examination of the literature reveals a confusing picture. Here, we review the evidence regarding indoor mold exposure and mycotoxicosis, with an emphasis on S. chartarum. We also examine possible end-organ effects, including pulmonary, immunologic, neurologic, and oncologic disorders. We discuss the Cleveland infant idiopathic pulmonary hemorrhage reports in detail, since they provided important impetus for concerns about Stachybotrys. Some valid concerns exist regarding the relationship between indoor mold exposure and human disease. Review of the literature reveals certain fungus-disease associations in humans, including ergotism (Claviceps species), alimentary toxic aleukia (Fusarium), and liver disease (Aspergillys). While many papers suggest a similar relationship between Stachybotrys and human disease, the studies nearly uniformly suffer from significant methodological flaws, making their findings inconclusive. As a result, we have not found well-substantiated supportive evidence of serious illness due to Stachybotrys exposure in the contemporary environment. To address issues of indoor mold-related illness, there is an urgent need for studies using objective markers of illness, relevant animal models, proper epidemiologic techniques, and examination of confounding factors

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Pulmonary phospholipidosis in rats respiring air containing diesel particulates

Cited by 21 publications

References 13 publications

Diesel particles increase phosphatidylcholine release through a NO pathway in alveolar type II cells

Diesel particles increase phosphatidylcholine release through a NO pathway in alveolar type II cells

The surfactant system of the adult lung: physiology and clinical perspectives

Indoor Mold, Toxigenic Fungi, andStachybotrys chartarum: Infectious Disease Perspective

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