Changes of lung surfactant and pressure-volume curve in bleomycin-induced pulmonary fibrosis

Osanai, Kazuhiro; Takahashi, Kumi; Sato, Shigeki; Iwabuchi, Kazunori; Ohtake, Kazuo; Sata, Makoto; Yasui, Shuji

doi:10.1152/jappl.1991.70.3.1300

Cited by 28 publications

(19 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therefore, it is possible that, if the lipids are reduced in quantity or quality, the stimulatory influence of SP-A could be enhanced. 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).…”

Section: Discussionmentioning

confidence: 99%

“…Although most SP-A in the normal alveolar space is thought to be lipid-associated, "lipid-free" SP-A could increase if the balance between SP-A and surfactant lipid were altered under certain conditions (31). 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%

See 1 more Smart Citation

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

View full text Add to dashboard Cite

) 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

show abstract

Section: Discussionmentioning

confidence: 99%

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

View full text Add to dashboard Cite

show abstract

“…Lesions observed in the early stages of lung damage induced by BLM resemble chronic human fibrotic lung disease, both histologically and physiologically. [12][13][14][15][16][17][18][19][20] Interventions designed to limit the consequences of the inflammatory response [such as corticosteroids, anti-tumor necrosis factor (TNF)-a antibody, and anti-transforming growth factor (TGF)-b antibody] and to protect the lung from oxidant damage (such as Ginkgo biloba extract, 8) metalloporphyrin, 9) and N-acetylcysteine 10) ) are effective in suppressing BLM-induced pulmonary fibrosis. These findings suggest that inhibition of lung inflammation and lipid peroxidation may be employed as therapeutic strategies for pulmonary fibrosis in the clinic.…”

mentioning

confidence: 99%

Feitai Attenuates Bleomycin-Induced Pulmonary Fibrosis in Rats

Gong

Wang

et al. 2004

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Pulmonary fibrosis is a common consequence of numerous pulmonary diseases. The current therapeutic approaches for this condition are unsatisfactory. Feitai, a composite formula consisting of several herbs, is used in China as a folk remedy for treating patients with pulmonary tuberculosis. In this study, we extensively investigate the effects and mechanisms of Feitai on bleomycin (BLM)-induced pulmonary fibrosis in rats. One hundred and twenty male Sprague-Dawley rats were randomly divided into four groups, referred to as the saline-water, saline-Feitai, BLM-water, and BLM-Feitai groups. Following a single instillation of BLM (5 mg/kg) or saline, rats were orally administered Feitai at a dose of 3 g/kg body weight or sterilized distilled water once daily. Rats were killed at 7, 14, or 28 d post-BLM. Inflammatory cell count, protein concentration, and lactate dehydrogenase activity in bronchoalveolar lavage fluid were measured, and myeloperoxidase activity and lipid peroxide content in lung homogenates were analyzed. Treatment with Feitai inhibited lung fibrotic progression induced by BLM, as indicated by the decrease in lung hydroproline content and lung fibrosis score at 28 d post-BLM. This was accompanied by significant amelioration of BLM-induced body weight loss, lung edema, and inflammatory response during the development of lung injury in the acute phase. The results strongly indicate the beneficial effects of Feitai in protecting against BLM-induced pulmonary fibrosis. Furthermore, the inflammatory response and lipid peroxidation were inhibited by Feitai, suggesting that the effect of this formula on BLM-induced lung injury and fibrosis is associated with antiinflammatory and antioxidant properties.

show abstract

“…Upregulating their response to adrenergic and cholinergic stimulation may also increase the sensitivity of type II cells to autonomic control during torpor. Understanding how the surfactant system can remain functional over a range of temperatures has important consequences in hypothermic lung transplantation surgery and in the treatment of hypothermia and respiratory distress syndromes (Bernard, 1996;Erasmus et al, 1996;Osanai et al, 1991;Inoue et al, 1981;Meban, 1978).…”

mentioning

confidence: 99%

Thermal acclimation of surfactant secretion and its regulation by adrenergic and cholinergic agonists in type II cells isolated from warm-active and torpid golden-mantled ground squirrels,Spermophilus lateralis

Ormond

Orgeig

Daniels

et al. 2003

Journal of Experimental Biology

View full text Add to dashboard Cite

SUMMARYHomeothermic mammals experience pulmonary surfactant dysfunction with relatively small fluctuations in body temperature. However, ground squirrels survive dramatic changes in body temperature during hibernation, when body temperature drops from 37°C to 0-5°C during prolonged torpor bouts. Using type II cells isolated from both warm-active and torpid squirrels, we determined the effect of assay temperature, autonomic agonists and torpor on surfactant secretion. Basal secretion was significantly higher in type II cells isolated from torpid squirrels compared with warm-active squirrels when assayed at the body temperature of the animal from which they were isolated(4°C and 37°C, respectively). A change in assay temperature significantly decreased surfactant secretion. However, the change in secretory rate between 37°C and 4°C was less than expected if due to temperature alone (Q10 range=0.8-1.2). Therefore, the surfactant secretory pathway in squirrel type II cells demonstrates some temperature insensitivity. When incubated at the body temperature of the animal from which the cells were isolated, the adrenergic agonist, isoproterenol, significantly increased surfactant secretion in both warm-active and torpid squirrel type II cells. However, the cholinergic agonist, carbamylcholine chloride, only increased secretion in torpid squirrel type II cells when incubated at 4°C. Torpor did not affect basal cAMP production from isolated type II cells. However, the production of cAMP appears to be upregulated in response to isoproterenol in torpid squirrel type II cells. Thus, at the cellular level, both the secretory and regulatory pathways involved in surfactant secretion are thermally insensitive. Upregulating basal secretion and increasing the sensitivity of type II cells to cholinergic stimulation may be adaptative characteristics of torpor that enable type II cells to function effectively at 0-5°C.

show abstract

Changes of lung surfactant and pressure-volume curve in bleomycin-induced pulmonary fibrosis

Cited by 28 publications

References 0 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

Feitai Attenuates Bleomycin-Induced Pulmonary Fibrosis in Rats

Thermal acclimation of surfactant secretion and its regulation by adrenergic and cholinergic agonists in type II cells isolated from warm-active and torpid golden-mantled ground squirrels,Spermophilus lateralis

Contact Info

Product

Resources

About