About: Spironolactone Attenuates Bleomycin-Induced Pulmonary Injury Partially via Modulating Mononuclear Phagocyte Phenotype Switching in Circulating and Alveolar Compartments

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About: Spironolactone Attenuates Bleomycin-Induced Pulmonary Injury Partially via Modulating Mononuclear Phagocyte Phenotype Switching in Circulating and Alveolar Compartments Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Spironolactone Attenuates Bleomycin-Induced Pulmonary Injury Partially via Modulating Mononuclear Phagocyte Phenotype Switching in Circulating and Alveolar Compartments
Creator	Zhou, Xin Guo, Zhao-Zeng Hu, Dao-Chuan Ji, Wen-Jie Li, Yu-Ming Lu, Rui-Yi Ma, Yong-Qiang Sun, Hai-Ying Wei, Lu-Qing Yang, Guo-Hong Zhang, Yi-Dan
Source	PMC
abstract	BACKGROUND: Recent experimental studies provide evidence indicating that manipulation of the mononuclear phagocyte phenotype could be a feasible approach to alter the severity and persistence of pulmonary injury and fibrosis. Mineralocorticoid receptor (MR) has been reported as a target to regulate macrophage polarization. The present work was designed to investigate the therapeutic potential of MR antagonism in bleomycin-induced acute lung injury and fibrosis. METHODOLOGY/PRINCIPAL FINDINGS: We first demonstrated the expression of MR in magnetic bead-purified Ly6G-/CD11b+ circulating monocytes and in alveolar macrophages harvested in bronchoalveolar lavage fluid (BALF) from C57BL/6 mice. Then, a pharmacological intervention study using spironolactone (20mg/kg/day by oral gavage) revealed that MR antagonism led to decreased inflammatory cell infiltration, cytokine production (downregulated monocyte chemoattractant protein-1, transforming growth factor β1, and interleukin-1β at mRNA and protein levels) and collagen deposition (decreased lung total hydroxyproline content and collagen positive area by Masson’ trichrome staining) in bleomycin treated (2.5mg/kg, via oropharyngeal instillation) male C57BL/6 mice. Moreover, serial flow cytometry analysis in blood, BALF and enzymatically digested lung tissue, revealed that spironolactone could partially inhibit bleomycin-induced circulating Ly6C(hi) monocyte expansion, and reduce alternative activation (F4/80+CD11c+CD206+) of mononuclear phagocyte in alveoli, whereas the phenotype of interstitial macrophage (F4/80+CD11c-) remained unaffected by spironolactone during investigation. CONCLUSIONS/SIGNIFICANCE: The present work provides the experimental evidence that spironolactone could attenuate bleomycin-induced acute pulmonary injury and fibrosis, partially via inhibition of MR-mediated circulating monocyte and alveolar macrophage phenotype switching.
has issue date	2013-11-19(xsd:dateTime)
bibo:doi	10.1371/journal.pone.0081090
bibo:pmid	24260540
has license	cc-by
sha1sum (hex)	801aad4fa6fab8d6d0973eb4df2178454195e037
schema:url	https://doi.org/10.1371/journal.pone.0081090
resource representing a document's title	Spironolactone Attenuates Bleomycin-Induced Pulmonary Injury Partially via Modulating Mononuclear Phagocyte Phenotype Switching in Circulating and Alveolar Compartments
has PubMed Central identifier	PMC3834272
has PubMed identifier	24260540
schema:publication	PLoS One
resource representing a document's body	covid:801aad4fa6fab8d6d0973eb4df2178454195e037#body_text
is schema:about of	named entity 'evidence' named entity 'SPIRONOLACTONE' named entity 'INDUCED' named entity 'COULD BE' named entity 'EVIDENCE' named entity 'INDICATING' named entity 'FIBROSIS' named entity 'EXPERIMENTAL STUDIES' named entity 'APPROACH' named entity 'TARGET' named entity 'MANIPULATION' named entity 'FEASIBLE' named entity 'THERAPEUTIC' named entity 'PROVIDE' named entity 'ACUTE LUNG INJURY' named entity 'RECENT' named entity 'ALTER' named entity 'MACROPHAGE POLARIZATION' named entity 'SEVERITY' named entity 'INDUCED' named entity 'POTENTIAL' named entity 'SWITCHING' named entity 'PULMONARY INJURY' named entity 'ALVEOLAR' named entity 'PRESENT' named entity 'COMPARTMENTS' named entity 'MODULATING' named entity 'CIRCULATING' named entity 'PARTIALLY' named entity 'TO INVESTIGATE' named entity 'ANTAGONISM' named entity 'PERSISTENCE' named entity 'PULMONARY INJURY' named entity 'TO REGULATE' named entity 'BLEOMYCIN' named entity 'REPORTED' named entity 'MONONUCLEAR PHAGOCYTE PHENOTYPE' named entity 'WORK' named entity 'MONONUCLEAR PHAGOCYTE PHENOTYPE' named entity 'MINERALOCORTICOID RECEPTOR' named entity 'BLEOMYCIN' covid:arg/801aad4fa6fab8d6d0973eb4df2178454195e037 named entity 'studies' named entity 'acute lung injury' named entity 'fibrosis' named entity 'mononuclear phagocyte' named entity 'Pulmonary Injury' named entity 'Alveolar' named entity 'Idiopathic pulmonary fibrosis' named entity 'eplerenone' named entity 'steady state' named entity 'fibrosis' named entity 'Isotype' named entity 'DAPI' named entity '1:200' named entity 'lung fibrosis' named entity 'phenotype' named entity 'monocytes' named entity 'clone' named entity 'lung tissue' named entity 'Macrophages' named entity 'alveolar macrophages' named entity 'drug administration' named entity 'myeloid' named entity 'perchloric acid' named entity 'RNA' named entity 'homogenized' named entity 'cell counts' named entity 'binary classification' named entity 'alveolar macrophages' named entity 'RAAS'

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