{"title":"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。","authors":"Yuanbin Sun, Hongxia Li, Longxian Zhang, Jiahao Zhang","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>This study explored that the possible effects and mechanism of ATG16L1 in pseudomonas aeruginosa lung infection.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":19098,"journal":{"name":"Neuro endocrinology letters","volume":"42 6","pages":"408-416"},"PeriodicalIF":0.6000,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"ATG16L1 regulated IL-22 induced IFN level in Pseudomonas aeruginosa Lung Infection via cGAS signal passage.\",\"authors\":\"Yuanbin Sun, Hongxia Li, Longxian Zhang, Jiahao Zhang\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>This study explored that the possible effects and mechanism of ATG16L1 in pseudomonas aeruginosa lung infection.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>\",\"PeriodicalId\":19098,\"journal\":{\"name\":\"Neuro endocrinology letters\",\"volume\":\"42 6\",\"pages\":\"408-416\"},\"PeriodicalIF\":0.6000,\"publicationDate\":\"2021-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neuro endocrinology letters\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuro endocrinology letters","FirstCategoryId":"3","ListUrlMain":"","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
ATG16L1 regulated IL-22 induced IFN level in Pseudomonas aeruginosa Lung Infection via cGAS signal passage.
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.
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.