Role of interleukin-17 in alveolar fluid clearance in mice with acute lung injury / 南方医科大学学报
Journal of Southern Medical University
; (12): 494-498, 2016.
Article
em Zh
| WPRIM
| ID: wpr-273736
Biblioteca responsável:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the role of interleukin-17 (IL-17) in alveolar fluid clearance in mice with acute lung injury (ALI) and explore the possible mechanism.</p><p><b>METHODS</b>Sixteen IL-17-knockout mice and 16 wild-type mice were both randomized for intratracheal instillation of PBS (control) on lipopolysaccharide (LPS) to induce ALI. Forty-eight hours after the treatments, the wet-dry ratio (W/D) of the lungs, IL-8 in the bronchoalveolar lavage fluid (BALF) and histopathological changes of the lung tissues were examined. The expressions of epithelial sodium channel α subunit (α-ENaC) was detected with Western blotting and liver kinase B1 (LKB1) was detected with immunohistochemistry.</p><p><b>RESULTS</b>Compared with wild-type mice treated with LPS, IL-17 knockout mice showed significantly decreased W/D of the lungs (9.739∓3.3 vs 5.351∓0.56) and IL-8 level in the BALF (67.50∓7.33 vs 41.00∓3.16 pg/mL) following LPS challenge. Pathological examination revealed reduced alveolar edema fluid aggregations and lower lung injury score in IL-17 knockout mice with also higher expression levels of ENaC and LKB1 compared with the wild-type mice.</p><p><b>CONCLUSION</b>Knocking out IL-17 in mice not only alleviates inflammation of the lung tissue following ALI but also reduces the loss of ENaC protein and promotes alveolar fluid clearance, mechanism of which is probably associated with LKB1.</p>
Texto completo:
1
Base de dados:
WPRIM
Assunto principal:
Patologia
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Líquido da Lavagem Broncoalveolar
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Química
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Lipopolissacarídeos
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Interleucina-8
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Proteínas Serina-Treonina Quinases
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Interleucina-17
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Canais Epiteliais de Sódio
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Lesão Pulmonar Aguda
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Técnicas de Inativação de Genes
Limite:
Animals
Idioma:
Zh
Revista:
Journal of Southern Medical University
Ano de publicação:
2016
Tipo de documento:
Article
País de publicação:
CHINA
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CN
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REPUBLIC OF CHINA