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KMID : 1035620210090020076
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Allergy Asthma & Respiratory Disease
2021 Volume.9 No. 2 p.76 ~ p.83
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Therapeutic effect of atorvastatin on interleukin-13-induced lung pathology
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Mo Yo-Sep
Bae Bo-Ram
Kim Jung-Hyun
Kim Ruth Lee
Son Kyung-Hee
Kang Min-Jong
Lee Chun-Gen
Cho Sang-Heon
Kang Hye-Ryun
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Abstract
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Purpose: Asthma is a common chronic lung disease, in which interleukin (IL)-13 is implicated as a central regulator of IgE synthesis, mucus hypersecretion, airway hyperresponsiveness (AHR), and fibrosis. This study was designed to determine the anti-inflammatory effect of atorvastatin, a widely used lipid-lowering agent, on the IL-13-induced lung pathology through the modulation of macrophages.
Methods: Atorvastatin (40 mg/kg) was given to transgenic mice overexpressing IL-13 (IL-13 TG mice) and their wild type littermates by oral gavage for 2 weeks. AHR, numbers of inflammatory cells in the airway, and cytokine levels in IL-13 TG mice were measured. Using the alveolar macrophage cell line CRL-2456, the direct effect of atorvastatin on macrophages activated by recombinant IL-13 was assessed.
Results: Significant reduction in total leukocytes and alleviation of AHR were observed with administration of atorvastatin in IL-13 TG mice compared to those without atorvastatin treatment (P<0.05). Atorvastatin administration resulted in upregulation of IL-10 in the lungs of IL-13 TG mice (P<0.05). In addition, mRNA expression of connective tissue growth factor, fibronectin, and type III collagen as well as chord length enhanced by IL-13 overexpression were reduced by atorvastatin administration (P<0.05). M2 macrophage markers, such as Ym-1 and CD206, were decreased, while M1 macrophage marker, inducible nitric oxide synthase, was increased upon atorvastatin treatment (P<0.05). Administration of atorvastatin resulted in improved removal of apoptotic cells (P<0.05).
Conclusion: The results of this study reveal a potential of atorvastatin as an effective antiasthmatic agent by reducing IL-13-induced lung inflammation via the modulation of macrophage polarization.
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KEYWORD
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Asthma, interleukin-13, Atorvastatin, Antiasthmatic agents, Macrophage
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