Myeloid-derived suppressor cells (MDSCs) and mechanistic target of rapamycin (mTOR) signaling pathway interact through inducible nitric oxide synthase (iNOS) and nitric oxide (NO) in asthma.

作者: Bin Luan , Xiaorong Xiong , Yanli Zhang , Yan Zhang , Hongke Shi

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摘要: Background Down-regulation of mechanistic target rapamycin (mTOR) activity in myeloid-derived suppressor cells (MDSCs) has been shown to promote inducible nitric oxide (NO) synthase (iNOS) expression and NO production. Importantly, pharmacological inhibition iNOS blocks MDSCs recruitment immunological hepatic injury. As bronchial asthma is also an immune disease, whether mTOR could interact with via or not unclear. Objective The aim this study was determine asthma. Methods Ovalbumin-induced mouse model established perform our investigation, asthmatic markers were evaluated by hematoxylin eosin (H&E), immunohistochemistry (IHC), periodic acid-Schiff (PAS) staining. levels serum determined enzyme linked immunosorbent assay (ELISA). Mice lung tissues stained antibodies against phosphorylated (p)-mTOR, p-p70S6K, yellow/brown staining considered as giving a positive signal, meanwhile, the protein p-mTOR, p-p70S6K detected using western blot assay. radioimmunoassay. Results Tumor-derived mice regulated iNOS. pathway activation tumor-derived MDSCs. production tumor-extracted Positive correlation observed. Conclusion data indicated that rapamycin, inhibitor mTOR, blocked during onset. Thus, results revealed potential novel targets for therapy.

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