Pulmonary Expression of Leukemia Inhibitory Factor Induces B Cell Hyperplasia and Confers Protection in Hyperoxia

Wang, Jingming; Chen, Qingsheng; Corne, Jonathan; Zhu, Zhou; Lee, Chang-Min; Bhandari, Vineet; Homer, Robert J.; Elias, Jack A.

doi:10.1074/jbc.m301820200

Cited by 25 publications

(28 citation statements)

References 36 publications

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“…In accord with studies from our laboratory and others, WT mice died after 3-6 days of exposure to 100% O 2 (11)(12)(13)(14)16). In this setting, 50% of WT mice were dead after 4.5 days and 100% had died by day 5.5 ( Fig.…”

Section: Role Of Il-13 In Halisupporting

confidence: 62%

“…In the normal and injured lung, the severity and consequences of oxidant injury are modulated by generalized and tissue-specific protective mechanisms. Previous studies from our laboratory and others demonstrated that exogenously administered cytokines, including IL-13, confer tissue cytoprotection in HALI (11)(12)(13)(14). Surprisingly, the role(s) that endogenous IL-13 plays in the control of these oxidant-induced responses has not been adequately defined.…”

mentioning

confidence: 93%

“…Four-to 6-wk-old mice were placed in cages in an airtight Plexiglas chamber (55 ϫ 40 ϫ 50 cm), as described previously (11)(12)(13). Throughout the experiment, they were given free access to food and water.…”

Section: Oxygen Exposurementioning

confidence: 99%

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Increased Hyperoxia-Induced Mortality and Acute Lung Injury in IL-13 Null Mice

Bhandari

Choo-Wing

Homer

et al. 2007

The Journal of Immunology

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IL-13 is a critical effector at sites of Th2 inflammation and remodeling. As a result, anti-IL-13-based therapies are being actively developed to treat a variety of diseases and disorders. However, the beneficial effects of endogenous IL-13 in the normal and diseased lung have not been adequately defined. We hypothesized that endogenous IL-13 is an important regulator of oxidant-induced lung injury and inflammation. To test this hypothesis, we compared the effects of 100% O2 in mice with wild-type and null IL-13 loci. In this study, we demonstrate that hyperoxia significantly augments the expression of the components of the IL-13R, IL-13Rα1, and IL-4Rα. We also demonstrate that, in the absence of IL-13, hyperoxia-induced tissue inflammation is decreased. In contrast, in the IL-13 null mice, DNA injury, cell death, caspase expression, and activation and mortality are augmented. Interestingly, the levels of the cytoprotective cytokines vascular endothelial cell growth factor, IL-6, and IL-11 were decreased in the bronchoalveolar lavage fluid. These studies demonstrate that the expression of the IL-13R is augmented and that the endogenous IL-13-IL-13R pathway contributes to the induction of inflammation and the inhibition of injury in hyperoxic acute lung injury.

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Section: Role Of Il-13 In Halisupporting

confidence: 62%

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confidence: 93%

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Increased Hyperoxia-Induced Mortality and Acute Lung Injury in IL-13 Null Mice

Bhandari

Choo-Wing

Homer

et al. 2007

The Journal of Immunology

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“…IGF-I, and to a lesser extent LIF, are factors known as general inductors of cell proliferation in a variety of tissues, including the lung. Thus, transgenic mice overexpressing either IGF-I or LIF in the adult lung depict hyperplasia of certain cell types (Wang et al, 2003;Frankel et al, 2005). Paradoxically, the progressive lung hypoplasia observed in E18.5 Igf-I nulls and Lif/Igf-I double-nulls is accompanied by a progressive increase in lung proliferation.…”

Section: Discussionmentioning

confidence: 99%

Alterations in alveolar epithelium differentiation and vasculogenesis in lungs of LIF/IGF‐I double deficient embryos

Moreno-Barriuso¹,

López-Malpartida²,

Pablo³

et al. 2006

Developmental Dynamics

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Previous studies on double deficient mice for leukemia inhibitory factor (LIF) and insulin-like growth factor I (IGF-I) reported that they died of respiratory failure, with abnormal lung histology and altered expression of pulmonary markers. Here we analyzed prenatal Lif/Igf-I double mutant mouse embryos to characterize LIF and IGF-I cooperative roles in distal lung epithelium and vascular maturation. Lungs of IGF-I-deficient embryos displayed a higher proportion of type II pneumocytes, less differentiated type I pneumocytes, and failure in alveolar capillary remodeling compared to wild type and LIF-deficient mice. Lif/Igf-I double knockout lungs showed aggravated pulmonary hypoplasia, lower airway volume, increased proliferation, and elevated levels of ERK1/2 activation. In addition, their alveoli were collapsed and lined by type II cells. The differentiation of type I cells barely occurred and capillaries remained in the abundant mesenchyme. These results indicate that LIF collaborates with IGF-I in lung alveolar epithelium and vascular maturation.

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“…Mice (4-6 wk old) were placed in cages in an airtight Plexiglas chamber (55 3 40 3 50 cm), as described previously (6,10,32). Throughout the experiment, they were given free access to food and water.…”

Section: Oxygen Exposurementioning

confidence: 99%

The Chitinase-like Proteins Breast Regression Protein-39 and YKL-40 Regulate Hyperoxia-induced Acute Lung Injury

Sohn

Kang²,

Mizunuma³

et al. 2010

Am J Respir Crit Care Med

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101

118

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Rationale: Prolonged exposure to 100% O 2 causes hyperoxic acute lung injury (HALI), characterized by alveolar epithelial cell injury and death. We previously demonstrated that the murine chitinase-like protein, breast regression protein (BRP)-39 and its human homolog, YKL-40, inhibit cellular apoptosis. However, the regulation and roles of these molecules in hyperoxia have not been addressed. Objectives: We hypothesized that BRP-39 and YKL-40 (also called chitinase-3-like 1) play important roles in the pathogenesis of HALI. Methods: We characterized the regulation of BRP-39 during HALI and the responses induced by hyperoxia in wild-type mice, BRP-39-null (2/2) mice, and BRP-39 2/2 mice in which YKL-40 was overexpressed in respiratory epithelium. We also compared the levels of tracheal aspirate YKL-40 in premature newborns with respiratory failure. Measurements and MainResults: These studies demonstrate that hyperoxia inhibits BRP-39 in vivo in the murine lung and in vitro in epithelial cells. They also demonstrate that BRP-39 2/2 mice have exaggerated permeability, protein leak, oxidation, inflammatory, chemokine, and epithelial apoptosis responses, and experience premature death in 100% O 2 . Lastly, they demonstrate that YKL-40 ameliorates HALI, prolongs survival in 100% O 2 , and rescues the exaggerated injury response in BRP-39 2/2 animals. In accord with these findings, the levels of tracheal aspirate YKL-40 were lower in premature infants treated with hyperoxia for respiratory failure who subsequently experienced bronchopulmonary dysplasia or death compared with those that did not experience these complications.Conclusions: These studies demonstrate that hyperoxia inhibits BRP-39/YKL-40, and that BRP-39 and YKL-40 are critical regulators of oxidant injury, inflammation, and epithelial apoptosis in the murine and human lung.

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Pulmonary Expression of Leukemia Inhibitory Factor Induces B Cell Hyperplasia and Confers Protection in Hyperoxia

Cited by 25 publications

References 36 publications

Increased Hyperoxia-Induced Mortality and Acute Lung Injury in IL-13 Null Mice

Increased Hyperoxia-Induced Mortality and Acute Lung Injury in IL-13 Null Mice

Alterations in alveolar epithelium differentiation and vasculogenesis in lungs of LIF/IGF‐I double deficient embryos

The Chitinase-like Proteins Breast Regression Protein-39 and YKL-40 Regulate Hyperoxia-induced Acute Lung Injury

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