Altered regulation of surfactant phospholipid and protein A during acute pulmonary inflammation

Viviano, Charles J.; Bakewell, William E.; Dixon, Darlene; Dethloff, Lloyd A.; Hook, Gary E. R.

doi:10.1016/0005-2760(95)00167-0

Cited by 33 publications

(32 citation statements)

References 37 publications

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“…In fact, in bleomycininduced pulmonary fibrosis, changes in surfactant composition and function have been revealed in animal models (30,38). Studies in rat indicate that there is a significant increase of SP-A but not of surfactant phospholipids in response to bleomycin treatment (32,44). We showed that, although surfactant lipids by themselves had no effect on cytokine production, Infasurf completely inhibited SP-A proinflammatory function observed in both ELISA and RPA assays of cytokine protein and mRNA, respectively.…”

Section: Discussionmentioning

confidence: 68%

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Combined SP-A-bleomycin effect on cytokines by THP-1 cells: impact of surfactant lipids on this effect

Huang

Wang

Phelps

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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) plays a role in host defense and inflammation in the lung. In the present study, we investigated the hypothesis that SP-A is involved in bleomycin-induced pulmonary fibrosis. We studied the effects of human SP-A on bleomycin-induced cytokine production and mRNA expression in THP-1 macrophage-like cells and obtained the following results. 1) Bleomycin-treated THP-1 cells increased tumor necrosis factor (TNF)-␣, interleukin (IL)-8, and IL-1␤ production in dose-and time-dependent patterns, as we have observed with SP-A. TNF-␣ levels were unaffected by treatment with cytosine arabinoside.2) The combined bleomycin-SP-A effect on cytokine production is additive by RNase protection assay and synergistic by enzyme-linked immunosorbent assay. 3) Although the bleomycin effect on cytokine production was not significantly affected by the presence of surfactant lipid, the additive and synergistic effect of SP-A-bleomycin on cytokine production was significantly reduced. We speculate that the elevated cytokine levels resulting from the bleomycin-SP-A synergism are responsible for bleomycin-induced pulmonary fibrosis and that surfactant lipids can help ameliorate pulmonary complications observed during bleomycin chemotherapy. chemotherapeutic agent; enzyme-linked immunosorbent assay; synergistic effect; ribonuclease protection assay; surfactant protein A

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Section: Discussionmentioning

confidence: 68%

“…There is evidence that bleomycin-induced lung injury in animal models is accompanied by qualitative and quantitative changes of surfactant lipids (30,38). Increased SP-A contents in rats has been reported after intratracheal treatment of bleomycin (32,44).…”

mentioning

confidence: 99%

Combined SP-A-bleomycin effect on cytokines by THP-1 cells: impact of surfactant lipids on this effect

Huang

Wang

Phelps

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…The present study demonstrates an elevated total volume of lamellar bodies per lung due to an increase in the number of type II cells and in the number of lamellar bodies per cell. This accumulation of intracellular surfactant, together with the progressive accumulation of intraalveolar surfactant that was demonstrated previously (Hawgood et al, 2002), reflects metabolic disturbances either directly due to A Ϫ D Ϫ deficiency or connected with lung inflammation (Lesur et al, 1995;Viviano et al, 1995;Ikegami et al, 2000b). At present, it is not clear if the lung collectins directly influence type II cell proliferation and metabolism or rather indirectly by modulating lung inflammation in vivo.…”

Section: Discussionmentioning

confidence: 97%

Design‐based stereological analysis of the lung parenchymal architecture and alveolar type II cells in surfactant protein A and D double deficient mice

et al. 2005

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Alveolar epithelial type II cells synthesize and secrete surfactant. The surfactant-associated proteins A and D (SP-A and SP-D), members of the collectin protein family, participate in pulmonary immune defense, modulation of inflammation, and surfactant metabolism. Both proteins are known to have overlapping as well as distinct functions. The present study provides a design-based stereological analysis of adult mice deficient in both SP-A and SP-D (A Ϫ D Ϫ ) with special emphasis on parameters characterizing alveolar architecture and surfactant-producing type II cells. Compared to wild-type, A Ϫ D Ϫ mice have fewer and larger alveoli, an increase in the number and size of type II cells, as well as more numerous and larger alveolar macrophages. More surfactant-storing lamellar bodies are seen in type II cells, leading to a threefold increase in the total volume of lamellar bodies per lung, but the mean volume of a single lamellar body remains constant. These results demonstrate that chronic deficiency of SP-A and SP-D in mice leads to parenchymal remodeling, type II cell hyperplasia and hypertrophy, and disturbed intracellular surfactant metabolism. The design-based stereological approach presented here provides a framework for the quantitative lung structure analysis in gene-manipulated mice as well as in human lung disease.

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“…One study found 3-7 fold increases in PL and SP, respectively, occurring in a rat model with acid-washed silica, but not with unwashed silica [15]. Another study found sustained elevations (in weeks) in PL and SP-A in response to silica [16]. Several other studies found silica-induced increases in PL and SP [17,18] including specific increases in SP-A [19,20], SP-D [19,21], Vitamin E [22], and phosphotidyl inositol [23].…”

Section: Effect Of Silica Exposure On Lung Surfactantmentioning

confidence: 99%

Silica binding and toxicity in alveolar macrophages

Hamilton

Thakur

Holian

2008

Free Radical Biology and Medicine

342

242

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Inhalation of the crystalline form of silica is associated with a variety of pathologies from acute lung inflammation to silicosis, in addition to autoimmune disorders and cancer. Basic science researchers looking at the mechanisms involved with the earliest initiators of disease are focused on how the alveolar macrophage (AM) interacts with the inhaled silica particle and the consequences of silicainduced toxicity on the cellular level. Based on experimental results, several rationales have been developed on exactly how crystalline silica particles are toxic to the macrophage cell that is functionally responsible for clearance of the foreign particle. For example, silica is capable of producing reactive oxygen species (ROS) either directly (on the particle surface) or indirectly (produced by the cell as a response to silica) triggering cell-signaling pathways initiating cytokine release and apoptosis. With murine macrophages, reactive nitrogen species (RNS) are produced in the initial respiratory burst in addition to ROS. An alternative explanation for silica toxicity includes lysosomal permeability, where silica disrupts the normal internalization process leading to cytokine release and cell death. Still other research has focused on the cell surface receptors (collectively known as scavenger receptors) involved in silica binding and internalization. The silica-induced cytokine release and apoptosis is described as the function of receptor-mediated signaling rather than free radical damage. Current research ideas on silica toxicity and binding in the alveolar macrophage are reviewed and discussed.

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Altered regulation of surfactant phospholipid and protein A during acute pulmonary inflammation

Cited by 33 publications

References 37 publications

Combined SP-A-bleomycin effect on cytokines by THP-1 cells: impact of surfactant lipids on this effect

Combined SP-A-bleomycin effect on cytokines by THP-1 cells: impact of surfactant lipids on this effect

Design‐based stereological analysis of the lung parenchymal architecture and alveolar type II cells in surfactant protein A and D double deficient mice

Silica binding and toxicity in alveolar macrophages

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