ATG16L1 regulated IL-22 induced IFN level in Pseudomonas aeruginosa Lung Infection via cGAS signal passage.

IF 0.6 4区医学 Q4 ENDOCRINOLOGY & METABOLISM

Neuro endocrinology letters Pub Date : 2021-10-01

Yuanbin Sun, Hongxia Li, Longxian Zhang, Jiahao Zhang

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引用次数: 0

Abstract

Objective: This study explored that the possible effects and mechanism of ATG16L1 in pseudomonas aeruginosa lung infection.

Methods: C57BL/6J mice were anesthetized with isoflurane and intratracheally (I.T.) inoculated with 5 × 106 CFU of Pseudomonas aeruginosa strain PA14. RAW264.7 macrophages were stimulated with 0.1 mg/ml of lipopolysaccharide (LPS). RAW264.7 macrophages were stimulated with 0.1 mg/ml LPS. Hematoxylin-Eosin (H&E), Immunofluorescence, sample acquisition, qPCR validation, Enzyme linked immunosorbent assay (ELISA) and immunofluorescence analysis were used this experiment.

Results: ATG16L1 mRNA and protein expressions in mice with pseudomonas aeruginosa lung infection were also suppressed. ATG16L1 gene reduced inflammation and INF-γ levels in vitro model. On the other hand, ATG16L1 protein presented lung injury and inflammation levels in mice of pseudomonas aeruginosa lung infection. ATG16L1 regulated cGAS/IL-22 signal passage in model of pseudomonas aeruginosa lung onfection.

Conclusion: These findings indicate that ATG16L1 reduced IL-22 induced IFN level in pseudomonas aeruginosa lung infection via cGAS signal passage, which may provide a new therapeutic scheme for viral diseases or inflammatory diseases and its associated complications.

本刊更多论文

ATG16L1 通过 cGAS 信号通道调节 IL-22 在铜绿假单胞菌肺部感染中诱导的 IFN 水平。

研究目的本研究探讨了ATG16L1在铜绿假单胞菌肺部感染中的可能作用和机制：用异氟烷麻醉 C57BL/6J 小鼠，气管内接种 5 × 106 CFU 铜绿假单胞菌 PA14 株。用 0.1 毫克/毫升的脂多糖（LPS）刺激 RAW264.7 巨噬细胞。用 0.1 毫克/毫升 LPS 刺激 RAW264.7 巨噬细胞。本实验采用了血色素-伊红（H&E）、免疫荧光、样品采集、qPCR 验证、酶联免疫吸附试验（ELISA）和免疫荧光分析等方法：结果：铜绿假单胞菌肺部感染小鼠的 ATG16L1 mRNA 和蛋白表达均受到抑制。在体外模型中，ATG16L1 基因降低了炎症和 INF-γ 水平。另一方面，ATG16L1 蛋白在铜绿假单胞菌肺部感染小鼠中呈现肺损伤和炎症水平。在铜绿假单胞菌肺部感染模型中，ATG16L1调节cGAS/IL-22信号通过：这些研究结果表明，ATG16L1通过cGAS信号通道降低了IL-22在铜绿假单胞菌肺部感染中诱导的IFN水平，这可能为病毒性疾病或炎症性疾病及其相关并发症提供了一种新的治疗方案。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Neuro endocrinology letters 医学-内分泌学与代谢

CiteScore

1.00

自引率

14.30%

发文量

审稿时长

6 months

期刊介绍： Neuroendocrinology Letters is an international, peer-reviewed interdisciplinary journal covering the fields of Neuroendocrinology, Neuroscience, Neurophysiology, Neuropsychopharmacology, Psychoneuroimmunology, Reproductive Medicine, Chronobiology, Human Ethology and related fields for RAPID publication of Original Papers, Review Articles, State-of-the-art, Clinical Reports and other contributions from all the fields covered by Neuroendocrinology Letters. Papers from both basic research (methodology, molecular and cellular biology, anatomy, histology, biology, embryology, teratology, normal and pathological physiology, biophysics, pharmacology, pathology and experimental pathology, biochemistry, neurochemistry, enzymology, chronobiology, receptor studies, endocrinology, immunology and neuroimmunology, animal physiology, animal breeding and ethology, human ethology, psychology and others) and from clinical research (neurology, psychiatry and child psychiatry, obstetrics and gynecology, pediatrics, endocrinology, immunology, cardiovascular studies, internal medicine, oncology and others) will be considered. The Journal publishes Original papers and Review Articles. Brief reports, Special Communications, proved they are based on adequate experimental evidence, Clinical Studies, Case Reports, Commentaries, Discussions, Letters to the Editor (correspondence column), Book Reviews, Congress Reports and other categories of articles (philosophy, art, social issues, medical and health policies, biomedical history, etc.) will be taken under consideration.