Decreased Asbestos-Induced Lung Inflammation and Fibrosis after Radiation and Bone Marrow Transplant

Levis, Jamie E.; Loi, Roberto; Butnor, Kelly J.; Vacek, Pamela M.; Steele, Chad; Mossman, Brooke T.; Weiss, Daniel J.

doi:10.1165/rcmb.2007-0249oc

Cited by 21 publications

(15 citation statements)

References 43 publications

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“…However, BMDC therapy minimized the levels of IL-1β and IL-1R1 mRNA (Fig. 5A,B) in concordance with Ortiz et al [9] and Levis et al [20], who observed a downregulation of both after infusion of BMDCs in experimental lung fibrosis. The high levels of IL-1RN induced after BMDC therapy (Fig.…”

Section: Discussionsupporting

confidence: 89%

Repeated Administration of Bone Marrow-Derived Cells Prevents Disease Progression in Experimental Silicosis

Lopes‐Pacheco

Xisto

Ornellas

et al. 2013

Cell Physiol Biochem

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Background/Aims: Bone marrow-derived cells (BMDCs) reduced mechanical and histologic changes in the lung in a murine model of silicosis, but these beneficial effects did not persist in the course of lung injury. We hypothesized that repeated administration of BMDCs may decrease lung inflammation and remodeling thus preventing disease progression. Methods: One hundred and two C57BL/6 mice were randomly divided into SIL (silica, 20 mg intratracheally [IT]) and control (C) groups (saline, IT). C and SIL groups were further randomized to receive BMDCs (2×10⁶ cells) or saline IT 15 and 30 days after the start of the protocol. Results: By day 60, BMDCs had decreased the fractional area of granuloma and the number of polymorphonuclear cells, macrophages (total and M1 phenotype), apoptotic cells, the level of transforming growth factor (TGF)-β‚ and types I and III collagen fiber content in the granuloma. In the alveolar septa, BMDCs reduced the amount of collagen and elastic fibers, TGF-β, and the number of M1 and apoptotic cells. Furthermore, interleukin (IL)-1β, IL-1R1, caspase-3 mRNA levels decreased and the level of IL-1RN mRNA increased. Lung mechanics improved after BMDC therapy. The presence of male donor cells in lung tissue was not observed using detection of Y chromosome DNA. Conclusion: repeated administration of BMDCs reduced inflammation, fibrogenesis, and elastogenesis, thus improving lung mechanics through the release of paracrine factors.

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Section: Discussionsupporting

confidence: 89%

Repeated Administration of Bone Marrow-Derived Cells Prevents Disease Progression in Experimental Silicosis

Lopes‐Pacheco

Xisto

Ornellas

et al. 2013

Cell Physiol Biochem

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“…Because we know so much about the fundamental details of this model (17,18), it offers an outstanding opportunity to learn a great deal about what stem cells can do as the lesions develop. In a similar study (19), investigators in Vermont suggested that a bone marrow transplant could ameliorate the fibrogenic effects of asbestos exposure.…”

Section: Experimental Modelsmentioning

confidence: 97%

“…The bulk of the evidence suggests that MSCs migrating to lesions produce favorable results, such as in ameliorating fibrogenesis caused by bleomycin (4), radiation and inhaled asbestos (19), and reducing inflammation and mortality in a model of acute lung injury as discussed above (10). In an elegant study from Ortiz's laboratory (4), it was shown that MSCs block production of TNF-a and IL-1 that apparently mediate bleomycin-induced lung injury.…”

Section: Experimental Modelsmentioning

confidence: 99%

Mesenchymal Stem Cells Modulate Lung Injury

Brody¹,

Salazar²,

Lankford³

2010

Proceedings of the American Thoracic Society

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Mesenchymal stem cells (MSCs) have been shown to differentiate into a variety of mesenchymal cell types, including fibroblasts, myofibroblasts, osteoblasts, chondroblasts, adipocytes, and myoblasts, as well as epithelial cells. It has been shown that these cells can be recovered from bone marrow as well as umbilical cord blood, and they can be propagated, stored, and administered to animals and patients in clinical trials. It is clear that the cells engraft in the lung, and several laboratories have demonstrated an ameliorating effect in models of acute injury caused by LPS and in chronic lung injury induced by bleomycin and asbestos. However, it is not at all clear under what conditions these cells must be applied to provide an advantage and when using these cells might cause exacerbation of the lung injury. This brief review focuses on the biology of MSCs in vitro, how the cells have been used in some animal models, and the potential for their use in therapeutic strategies for diseases as diverse as lung cancer and interstitial fibrosis.

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“…Using transgenic (Tg) mice expressing an inhibitory κ B (I κ B) mutant resistant to phosphorylation-induced degradation and targeted to the bronchiolar epithelium via the CC10 promoter in a murine model of asbestosis, Tg(+) mice exposed to asbestos had less BALF inflammatory cytokine levels (eg, KC, IL-6, and IL-1 β ) and reduced levels of bronchiolar and distal epithelial proliferation as compared with Tg(−) mice 96. Two groups have recently shown that bone marrow progenitor cells contribute to the inflammatory and fibrogenic effects of asbestos 97,98. These studies underscore the importance of TNF- α , the NF- κ B–dependent pathway, and bone marrow progenitor cells in the pathogenesis of asbestos-induced lung disease that may lead to novel therapeutic strategies.…”

Section: Pathophysiology—what’s New?mentioning

confidence: 99%

Asbestos-induced lung diseases: an update

Kamp¹

2009

Translational Research

219

151

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Asbestos causes asbestosis (pulmonary fibrosis caused by asbestos inhalation) and malignancies (bronchogenic carcinoma and mesothelioma) by mechanisms that are not fully elucidated. Despite a dramatic reduction in asbestos use worldwide, asbestos-induced lung diseases remain a substantial health concern primarily because of the vast amounts of fibers that have been mined, processed, and used during the 20th century combined with the long latency period of up to 40 years between exposure and disease presentation. This review summarizes the important new epidemiologic and pathogenic information that has emerged over the past several years. Whereas the development of asbestosis is directly associated with the magnitude and duration of asbestos exposure, the development of a malignant clone of cells can occur in the setting of low-level asbestos exposure. Emphasis is placed on the recent epidemiologic investigations that explore the malignancy risk that occurs from nonoccupational, environmental asbestos exposure. Accumulating studies are shedding light on novel mechanistic pathways by which asbestos damages the lung. Attention is focused on the importance of alveolar epithelial cell (AEC) injury and repair, the role of iron-derived reactive oxygen species (ROS), and apoptosis by the p53- and mitochondria-regulated death pathways. Furthermore, recent evidence underscores crucial roles for specific cellular signaling pathways that regulate the production of cytokines and growth factors. An evolving role for epithelial-mesenchymal transition (EMT) is also reviewed. The translational significance of these studies is evident in providing the molecular basis for developing novel therapeutic strategies for asbestos-related lung diseases and, importantly, other pulmonary diseases, such as interstitial pulmonary fibrosis and lung cancer.

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Decreased Asbestos-Induced Lung Inflammation and Fibrosis after Radiation and Bone Marrow Transplant

Cited by 21 publications

References 43 publications

Repeated Administration of Bone Marrow-Derived Cells Prevents Disease Progression in Experimental Silicosis

Repeated Administration of Bone Marrow-Derived Cells Prevents Disease Progression in Experimental Silicosis

Mesenchymal Stem Cells Modulate Lung Injury

Asbestos-induced lung diseases: an update

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