21 results on '"Shi, Xin-Yu"'
Search Results
2. New spectral-induced polarization measurement with low cost and high efficiency
- Author
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Deng, Ming, Ge, Shuang-chao, Li, Bin, Chen, Kai, and Shi, Xin-yu
- Published
- 2018
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- View/download PDF
3. Diagnostic value of (1 → 3)-β-D-glucan in bronchoalveolar lavage fluid for invasive fungal disease: A meta-analysis
- Author
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Shi, Xin-yu, Liu, Yao, Gu, Xian-min, Hao, Sheng-yu, Wang, Yu-hong, Yan, Di, and Jiang, Shu-juang
- Published
- 2016
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- View/download PDF
4. The relationship of plasma fibrinogen with clinicopathological stages and tumor markers in patients with non-small cell lung cancer
- Author
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Bian, Nan-Nan, Shi, Xin-Yu, Qi, Hong-Yu, Hu, Xin, Ge, Yang, An, Guang-Yu, and Feng, Guo-Sheng
- Published
- 2019
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- View/download PDF
5. S100A9 Regulated M1/M2 Macrophage Polarization in Interleukin-10-Induced Promotion of Malignant Pleural Effusion.
- Author
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Pei, Xue-Bin, Yi, Feng-Shuang, Dong, Shu-Feng, Chen, Qing-Yu, and Shi, Xin-Yu
- Subjects
SMALL interfering RNA ,PLEURAL effusions ,MESSENGER RNA ,MACROPHAGES ,RNA sequencing ,T cells - Abstract
Interleukin-10 (IL-10) promotes the formation and development of malignant pleural effusion (MPE). Previous studies have elucidated the pathogenesis from the view of the immune-regulation function of CD4
+ T-cells. However, the underlying mechanism is still not fully understood. In this study, our results showed that IL-10 deficiency reduced the percentage of macrophages in mouse MPE and regulated M1/M2 polarization in vivo and in vitro. The migration capacity of tumor cells was suppressed, and apoptosis was promoted when tumor cells were cocultured with MPE macrophages in the absence of IL-10. Messenger RNA sequencing of MPE macrophages showed that S100A9 was downregulated in IL-10−/− mice. Bone marrow-derived macrophages obtained from wild-type mice transfected with S100A9-specific small interfering RNAs (siRNAs) also showed less M2 and more M1 polarization than those from the siRNA control group. Furthermore, downregulation of S100A9 using S100A9-specific siRNA suppressed MPE development, decreased macrophages, and modulated macrophage polarization in MPE in vivo. In conclusion, S100A9 plays a vital role in the process of IL-10 deficiency-mediated MPE suppression by regulating M1/M2 polarization, thus influencing the tumor-migration capacity and apoptosis. This could result in clinically applicable strategies to inhibit the formation of MPE by regulating the polarization of MPE macrophages. [ABSTRACT FROM AUTHOR]- Published
- 2023
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- View/download PDF
6. Impact of pulmonary rehabilitation on patients with different chronic respiratory diseases during hospitalization.
- Author
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Shi, Xin-Yu, Ren, Yi, Gu, Xiao-Meng, Jia, Yan-Rui, and Wang, Xue
- Published
- 2024
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- View/download PDF
7. Total Protein–Chloride Ratio in Pleural Fluid Independently Predicts Overall Survival in Malignant Pleural Effusion at the First Diagnosis.
- Author
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Qiao, Xin, Zhang, Zhi-Rong, Shi, Xin-Yu, and Yi, Feng-Shuang
- Subjects
PLEURAL effusions ,OVERALL survival ,LEUCOCYTES ,PROPORTIONAL hazards models ,MULTIVARIATE analysis ,ALKALINE phosphatase - Abstract
Objective: Pre-treatment biomarkers to estimate overall survival (OS) for malignant pleural effusion (MPE) are unidentified, especially those in pleural fluid. We evaluated the relationship between OS and total protein–chloride ratio in malignant pleural effusion (PE TPClR). Materials and Methods: A retrospective study was undertaken to identify patients from 2006 to 2018 who had pathologically or cytologically confirmed MPE and received no tumor-targeted therapy. We recorded the pre-treatment clinicopathologic characteristics and follow-up status. OS was estimated by the Kaplan–Meier method, and the association between variables and OS was evaluated by Cox proportional hazards models. Results: We screened 214 patients who met the eligibility criteria. The optimal cutoff value for the PE TPClR was set at 0.53. The univariate analysis showed that there was a significant correlation between PE TPClR and OS (P < 0.001). The multivariate analysis between OS and the variables selected from the univariate analysis showed that the levels of neutrophil, alkaline phosphatase, neuron-specific enolase, platelets, albumin in peripheral blood, and white blood cells in pleural effusion were also independent predictors of OS. Conclusion: In patients with MPE, pre-treatment PE TPClR independently predicts OS. Although further research is necessary to generalize our results, this information will help clinicians and patients to determine the most appropriate treatment for MPE patients. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
8. Diagnostic accuracy of interleukin-33 for tuberculous pleural effusion: A systematic review and meta-analysis.
- Author
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Xin-Yu Shi, Feng-Shuang Yi, Xin Qiao, Xue-Bin Pei, Shu-Feng Dong, Shi, Xin-Yu, Yi, Feng-Shuang, Qiao, Xin, Pei, Xue-Bin, and Dong, Shu-Feng
- Published
- 2021
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9. Metal organic framework Cu/MIL-53(Ce)-mediated synthesis of highly active and stable CO oxidation catalysts
- Author
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Tan, Hai-Yan, Zhou, Yin, Yan, Yun-Fan, Wu, De-Yong, Hu, Wei-Bing, and Shi, Xin-Yu
- Published
- 2017
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10. IL‐10 promotes malignant pleural effusion by regulating TH1 response via an miR‐7116‐5p/GPR55/ERK pathway in mice.
- Author
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Zhai, Kan, Shi, Xin‐Yu, Yi, Feng‐Shuang, Huang, Zhong‐Yin, Wu, Xiu‐Zhi, Dong, Shu‐Feng, Wang, Wen, Wu, Min‐Ting, and Shi, Huan‐Zhong
- Subjects
PLEURAL effusions ,TH1 cells ,G protein coupled receptors ,CELL physiology ,TUMOR growth - Abstract
IL‐10, produced by a wide variety of cells, is a highly pleiotropic cytokine that plays a critical role in the control of immune responses. However, its regulatory activity in tumor immunity remains poorly understood. In this study, we report that IL‐10 deficiency robustly suppressed the formation of malignant pleural effusion (MPE) and significantly enhanced miR‐7116‐5p expression in pleural CD4+ T cells. We demonstrated that miR‐7116‐5p suppressed IL‐10‐mediated MPE formation by inhibiting pleural vascular permeability as well as tumor angiogenesis and tumor growth. IL‐10 promoted MPE formation by suppressing miR‐7116‐5p that enhances TH1 response. We identified G protein‐coupled receptor 55 (GPR55) as a potential target of miR‐7116‐5p, and miR‐7116‐5p promoted TH1 cell function by downregulating GPR55. Moreover, GPR55 promoted MPE formation by inhibiting TH1 cell expansion through the ERK phosphorylation pathway. These results uncover an IL‐10‐mediated pathway controlling TH1 cells and demonstrate a central role for miR‐7116‐5p/GPR55/ERK signaling in the physiological regulation of IL‐10‐driven pro‐malignant responses. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
11. Prognostic value of a new score using serum alkaline phosphatase and pleural effusion lactate dehydrogenase for patients with malignant pleural effusion.
- Author
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Shi, Xin‐Yu, Yi, Feng‐Shuang, Wang, Zheng, Qiao, Xin, and Zhai, Kan
- Subjects
- *
ALKALINE phosphatase , *BIOMARKERS , *BLOOD sedimentation , *BLOOD platelets , *C-reactive protein , *COMPARATIVE studies , *CONFIDENCE intervals , *LACTATE dehydrogenase , *LYMPHOCYTES , *RESEARCH methodology , *MONOCYTES , *NEUTROPHILS , *SCIENTIFIC observation , *PLEURA cancer , *PLEURAL effusions , *SERUM albumin , *SURVIVAL , *MULTIPLE regression analysis , *PREDICTIVE tests , *RETROSPECTIVE studies , *DESCRIPTIVE statistics - Abstract
Background: The objective of our study was to analyze the prognostic value of the combination of serum ALP and pleural effusion LDH (AL score) for malignant pleural effusion (MPE) patients. Methods: This study includes retrospective, descriptive and observational research from 1 June 2006 to 1 December 2017, which aimed to identify prognostic factors related to MPE patients. We analyzed the association of various clinical features, routinely tested markers from peripheral blood and MPE at diagnosis and overall survival (OS). All MPE patients were assigned to three groups according to their AL score. The impact of the AL score and other prognostic factors were evaluated with multivariable regression. Results: According to their AL score, 193 patients were assigned to three groups with 25 in group 0 (sALP < 65 U/L and pLDH < 155 U/L), 121 in group 1 (sALP > 65 U/L or pLDH > 155 U/L) and 47 (sALP > 65 U/L and pLDH > 155 U/L) in group 2. For groups 0, 1 and 2, median survival times (MST) were 23, 15 and 7 months, respectively. Among the three groups, MST, serum albumin level, C reactive protein, erythrocyte sedimentation rate, the ratios of platelet‐to‐lymphocyte, neutrophil‐to‐lymphocyte showed significant differences. The counts of neutrophils, monocytes, platelets and AL score (0 vs. 1, P = 0.038, hazard ratio [HR]: 1.858, 95% confidence interval [CI]: [1.034, 3.339]; 0 vs. 2, P = 0.001, HR: 2.993, 95% CI: [1.556, 5.531]) were independent prognostic indicators for OS of MPE patients. Conclusion: AL score is a promising indicator which can be used to predict the prognosis of MPE patients. It can assist physicians in the selection of patients for appropriate palliative treatment. Key points: To our knowledge, this paper is the first study that combined two enzymes (sALP and pLDH) from serum and pleural effusion and studied the prognostic value for MPE patients. It has been proved to be a promising indicator to assist physicians select patients for appropriate palliative treatment. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
12. Metal–organic framework MIL-53(Al)-supported copper catalyst for CO catalytic oxidation reaction
- Author
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Tan, Zhi-Dou, Tan, Hai-Yan, Shi, Xin-Yu, Zhuan-Ji, Yan, Yun-Fan, and Yin-Zhou
- Published
- 2015
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13. IL‐10 promotes malignant pleural effusion in mice by regulating TH1‐ and TH17‐cell differentiation and migration.
- Author
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Wu, Xiu‐Zhi, Zhai, Kan, Yi, Feng‐Shuang, Wang, Zhen, Wang, Wen, Wang, Yao, Pei, Xue‐Bin, Shi, Xin‐Yu, Xu, Li‐Li, and Shi, Huan‐Zhong
- Abstract
The role of IL‐10 in malignant pleural effusion (MPE) remains unknown. By using murine MPE models, we observed that an increase in pleural IL‐10 was a significant predictor of increased risk of death. We noted that TH1‐ and TH17‐cell content in MPE was higher in IL‐10–/– mice than in WT mice, and IL‐10 deficiency promoted differentiation into TH1 but not into TH17 cells. A higher fraction of TH1 and TH17 cells in the MPE of IL‐10–/– mice expressed CXCR3 compared with WT mice. We also demonstrated that Lewis lung cancer and colon adenocarcinoma cells secreted large amounts of CXCL10, a ligand of CXCR3, which induced the migration of TH1 and TH17 cells into the MPE, and IFN‐γ could promote this signaling cascade. Furthermore, intrapleural injection of mice with CXCL10‐deficient tumor cells led to decreased TH1‐ and TH17‐cell content in MPE, increased MPE volume, and reduced survival of MPE‐bearing mice. Taken together, we demonstrated that IL‐10 deficiency promoted T‐cell differentiation into TH1 cells and upregulated the CXCR3‐CXCL10 signaling pathway that recruits TH1 and TH17 cells into MPE, ultimately resulting in decreased MPE formation and longer survival time of mice‐bearing MPE. IL‐10 promoted the development of malignant pleural effusion by suppressing the differentiation of naïve CD4+ T cells into TH1 cells and by suppressing the CXCR3‐CXCL10 signal that traffics TH1 and TH17 cells into the pleural space. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
14. Simultaneous enhancement of initial Coulombic efficiency and cycling performance of silicon-based anode materials for lithium-ion batteries.
- Author
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Li, Shi, Shi, Xin-Yu, Tang, Zheng-Peng, Li, De-Xin, Zhang, Yu-Chao, Xiao, Yao, Song, Yang, Zheng, Zhuo, Zhong, Yan-Jun, Wu, Zhen-Guo, Zhong, Ben-He, and Guo, Xiao-Dong
- Subjects
- *
LITHIUM-ion batteries , *ELECTROCHEMICAL electrodes , *ANODES , *CARBON composites , *GRAPHITE , *BIOPOLYMERS - Abstract
A series of natural-biogum-deprived carbon composites Si@GAC, Si@GGC and Si@XGC anode materials have been constructed, among which Si@GAC shows the best initial Coulombic efficiency (ICE) resulting from conformal carbon layer containing heteroatoms and covalent interactions with Si core. Based on this result, artificial graphite (AGr) and natural graphite (NGr) are added during the preparation process of Si@GAC to further elevate ICE and cycling stability. This strategy successfully realizes simultaneous and effective improvement of ICE and cycling performance, which could ultimately provide inspiration for high-performance silicon-based anodes. [Display omitted] • Si@C@Graphite materials with enhanced ICE and cycling stability are synthesized. • N, O render dominant capacitive Li+ storage mechanism and faster Li+ transfer. • Artificial graphite better enhances overall electrochemical performance. • Covalently-attached C layer with heteroatoms is conducive to cycling stability. Regarded as one of the most prospective anode materials for lithium-ion batteries (LIBs), silicon (Si) exhibits the highest theoretical capacity (4200 mAh g−1) among various anode materials while generally suffers from huge volume change, resultant rapid capacity fading and low initial Coulombic efficiency (ICE). Here, the ICE and cycling performance of Si-based anode have been simultaneously improved through preparing Si@C@Graphite materials where the conformal carbon modifiers derived from natural biopolymer binders covalently attached to Si particles could enhance the cycling stability, among which GA-derived carbon layer with N, O heteroatoms could best ameliorate the Li+ transport kinetics and thereby rendering superior electrochemical properties, while artificial graphite (AGr) could significantly promote the overall ICE and more effectively elevate the reversible capacity. An excellent ICE (86.4%), a prominent rate performance (1240.6 mAh g−1 at 2000 mA g−1) and a promoted cycling stability (1320.5 mAh g−1 at 800 mA g−1 after 100 cycles) could be presented by Si@GAC@AGr anode. This research provides an effective strategy of simultaneously improving ICE and cycling performance of Si-based anodes and inspires rational design of high-energy–density LIB anodes. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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15. Spectroscopic Analysis of the Binding Interaction Between Tinidazole and Bovine Serum Albumin (BSA).
- Author
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Shi, Xin Yu, Cao, Hui, Ren, Feng Lian, and Xu, Ming
- Published
- 2007
- Full Text
- View/download PDF
16. Diagnostic accuracy of interleukin-33 for tuberculous pleural effusion: A systematic review and meta-analysis.
- Author
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Shi XY, Yi FS, Qiao X, Pei XB, and Dong SF
- Subjects
- Biomarkers analysis, Humans, Pleural Effusion physiopathology, Sensitivity and Specificity, Tuberculosis complications, Diagnostic Techniques and Procedures standards, Interleukin-33 analysis, Pleural Effusion etiology, Tuberculosis diagnosis
- Abstract
Background: The detection of interleukin 33 (IL-33) in pleural effusion may be more sensitive in diagnosing tuberculous pleural effusion (TPE). The present study aimed to assess the accuracy of pleural IL-33 for the diagnosis of TPE by means of meta-analysis and systematic review of relevant studies., Method: After retrieving the published studies, the sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, diagnostic odds ratio, and a summary receiver operating characteristic curve were assessed to estimate the usefulness of pleural IL-33 in diagnosing TPE using meta-analysis with a random-effects model. We also performed meta-regression and subgroup analysis., Results: A total of 639 patients from 6 studies were analyzed. The pooled sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, and diagnostic odds ratio were 0.87 (95% confidence interval [CI], 0.82-0.91), 0.76 (95% CI, 0.72-0.80), 6.54 (95% CI, 2.65-16.15), 0.17 (95% CI, 0.10-1.27), and 45.40 (95% CI, 12.83-160.70) respectively. The area under the curve was 0.94. The composition of the included population was the main cause of heterogeneity and subgroup analysis showed that pleural IL-33 had a higher specificity (0.93, 95% CI 0.87-0.96) when used for differential diagnosis between TPE and malignant pleural effusion., Conclusion: The detection of IL-33 alone in pleural effusion seems to not be an efficient diagnostic marker for TPE but may serve as a novel biomarker to differentiate between TPE and malignant pleural effusion., Competing Interests: No potential conflicts of interest relevant to this article were reported. The authors have no conflicts of interest to disclose., (Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc.)
- Published
- 2021
- Full Text
- View/download PDF
17. Genome variation in colorectal cancer patient with liver metastasis measured by whole-exome sequencing.
- Author
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Yi H, Liao ZW, Chen JJ, Shi XY, Chen GL, Wu GT, Zhou DY, Zhou GQ, Huang JY, Lian L, Yu ZY, and He SB
- Abstract
Background: Liver metastasis of colorectal cancer (CRC) is an important cause of death from CRC, but its molecular mechanism is still unclear. In recent years, whole-exome sequencing has played an increasingly important role in the study of the occurrence and development of diseases, especially malignant tumors. Its high throughput and low cost advantages enable researchers to explore the pathogenic genes of diseases, and screen potential molecular markers and therapeutic targets from the level of genomics., Methods: This study collected the primary tumor tissues, matched paracancerous, normal tissues, and liver metastases of 4 CRC patients admitted to the Department of General Surgery of the First Affiliated Hospital of Soochow University, and performed high-depth whole-exome sequencing, with the sequencing depth of each sample reaching 123× on average, then filtered the sequencing data, compared them, and analyzed the bioinformatics data., Results: we found 8,565 single nucleotide variants (SNV) and 429 insertions/deletions (InDel) in the primary and hepatic lesion tissues, and the genes with the highest mutation frequency were titin (TTN), obscurin (OBSCN), and homeodomain-interacting protein kinase 2 (HIPK2). The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of the mutant genes was conducted, and it was found that the mutant genes were mainly concentrated in the cells, cell parts, and cellular process of GO. The results of KEGG pathway analysis showed that mutations were mainly distributed in circadian entrainment, insulin secretion, and glutamatergic synapse. Further, we identified 723 SNV and Indel genes with high frequency mutations including TTN, OBSCN, and hydrocephalus-inducing protein homolog (HYDIN) across all tissues of liver metastases. The GO analysis showed that the mutated genes in liver metastatic tissues were mainly concentrated in cell, cell part, and cellular process. The KEGG pathway analysis showed that high frequency mutation genes were focused on gastric acid secretion, bile secretion, and melanogenesis., Conclusions: This study found some candidate genes related to the occurrence of CRC and liver metastasis through whole-exome sequencing of relevant tissues in CRC patients with liver metastasis, which is expected to provide new markers and therapeutic targets for such patients., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/jgo-21-9). The authors have no conflicts of interest to declare., (2021 Journal of Gastrointestinal Oncology. All rights reserved.)
- Published
- 2021
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18. TSAd Plays a Major Role in Myo9b-Mediated Suppression of Malignant Pleural Effusion by Regulating T H 1/T H 17 Cell Response.
- Author
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Yi FS, Zhang X, Zhai K, Huang ZY, Wu XZ, Wu MT, Shi XY, Pei XB, Dong SF, Wang W, Yang Y, Du J, Luo ZT, and Shi HZ
- Subjects
- Adaptor Proteins, Signal Transducing genetics, Animals, Biopsy, Cell Line, Tumor transplantation, Disease Models, Animal, Female, Gene Knockdown Techniques, Gene Knockout Techniques, Humans, Lung pathology, Lung Neoplasms blood, Lung Neoplasms immunology, Male, Mice, Mice, Knockout, Middle Aged, Myosins genetics, Pleura pathology, Pleural Effusion, Malignant blood, Pleural Effusion, Malignant pathology, Signal Transduction immunology, Th1 Cells immunology, Th17 Cells immunology, Adaptor Proteins, Signal Transducing metabolism, Lung Neoplasms pathology, Myosins metabolism, Pleural Effusion, Malignant immunology
- Abstract
Emerging evidence indicates that Myo9b is a cancer metastasis-related protein and functions in a variety of immune-related diseases. However, it is not clear whether and how Myo9b functions in malignant pleural effusion (MPE). In this study, our data showed that Myo9b expression levels correlated with lung cancer pleural metastasis, and nucleated cells in MPE from either patients or mice expressed a lower level of Myo9b than those in the corresponding blood. Myo9b deficiency in cancer cells suppressed MPE development via inhibition of migration. Myo9b deficiency in mice suppressed MPE development by decreasing T
H 1 cells and increasing TH 17 cells. CD4+ naive T cells isolated from Myo9b-/- mouse spleens exhibited less TH 1 cell differentiation and more TH 17 cell differentiation in vitro. mRNA sequencing of nucleated cells showed that T cell-specific adaptor protein (TSAd) was downregulated in Myo9b-/- mouse MPE, and enrichment of the H3K27me3 mark in the TSAd promoter region was found in the Myo9b-/- group. Naive T cells purified from wild type mouse spleens transfected with TSAd-specific small interfering RNAs (siRNAs) also showed less TH 1 cell differentiation and more TH 17 cell differentiation than those from the siRNA control group. Furthermore, downregulation of TSAd in mice using cholesterol-conjugated TSAd-specific siRNA suppressed MPE development, decreased TH 1 cells, and increased TH 17 cells in MPE in vivo. Taken together, Myo9b deficiency suppresses MPE development not only by suppressing pleural cancer metastasis but also by regulating TH 1/TH 17 cell response via a TSAd-dependent pathway. This work suggests Myo9b and TSAd as novel candidates for future basic and clinical investigations of cancer., (Copyright © 2020 by The American Association of Immunologists, Inc.)- Published
- 2020
- Full Text
- View/download PDF
19. IL-10 promotes malignant pleural effusion by regulating T H 1 response via an miR-7116-5p/GPR55/ERK pathway in mice.
- Author
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Zhai K, Shi XY, Yi FS, Huang ZY, Wu XZ, Dong SF, Wang W, Wu MT, and Shi HZ
- Subjects
- Animals, CD4-Positive T-Lymphocytes immunology, Cell Line, Cell Line, Tumor, Down-Regulation immunology, HEK293 Cells, Humans, Mice, Interleukin-10 immunology, MAP Kinase Signaling System immunology, MicroRNAs immunology, Pleural Effusion, Malignant immunology, Receptors, Cannabinoid immunology, Signal Transduction immunology, Th1 Cells immunology
- Abstract
IL-10, produced by a wide variety of cells, is a highly pleiotropic cytokine that plays a critical role in the control of immune responses. However, its regulatory activity in tumor immunity remains poorly understood. In this study, we report that IL-10 deficiency robustly suppressed the formation of malignant pleural effusion (MPE) and significantly enhanced miR-7116-5p expression in pleural CD4
+ T cells. We demonstrated that miR-7116-5p suppressed IL-10-mediated MPE formation by inhibiting pleural vascular permeability as well as tumor angiogenesis and tumor growth. IL-10 promoted MPE formation by suppressing miR-7116-5p that enhances TH 1 response. We identified G protein-coupled receptor 55 (GPR55) as a potential target of miR-7116-5p, and miR-7116-5p promoted TH 1 cell function by downregulating GPR55. Moreover, GPR55 promoted MPE formation by inhibiting TH 1 cell expansion through the ERK phosphorylation pathway. These results uncover an IL-10-mediated pathway controlling TH 1 cells and demonstrate a central role for miR-7116-5p/GPR55/ERK signaling in the physiological regulation of IL-10-driven pro-malignant responses., (© 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)- Published
- 2020
- Full Text
- View/download PDF
20. IL-10 promotes malignant pleural effusion in mice by regulating T H 1- and T H 17-cell differentiation and migration.
- Author
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Wu XZ, Zhai K, Yi FS, Wang Z, Wang W, Wang Y, Pei XB, Shi XY, Xu LL, and Shi HZ
- Subjects
- Animals, Biomarkers, Disease Models, Animal, Interleukin-10 genetics, Mice, Mice, Knockout, Pleural Effusion, Malignant diagnosis, Pleural Effusion, Malignant etiology, Pleural Effusion, Malignant mortality, Positron Emission Tomography Computed Tomography, Signal Transduction, Th1 Cells cytology, Th1 Cells immunology, Th17 Cells cytology, Th17 Cells immunology, Cell Differentiation immunology, Cell Movement immunology, Interleukin-10 metabolism, Pleural Effusion, Malignant metabolism, Th1 Cells metabolism, Th17 Cells metabolism
- Abstract
The role of IL-10 in malignant pleural effusion (MPE) remains unknown. By using murine MPE models, we observed that an increase in pleural IL-10 was a significant predictor of increased risk of death. We noted that T
H 1- and TH 17-cell content in MPE was higher in IL-10-/- mice than in WT mice, and IL-10 deficiency promoted differentiation into TH 1 but not into TH 17 cells. A higher fraction of TH 1 and TH 17 cells in the MPE of IL-10-/- mice expressed CXCR3 compared with WT mice. We also demonstrated that Lewis lung cancer and colon adenocarcinoma cells secreted large amounts of CXCL10, a ligand of CXCR3, which induced the migration of TH 1 and TH 17 cells into the MPE, and IFN-γ could promote this signaling cascade. Furthermore, intrapleural injection of mice with CXCL10-deficient tumor cells led to decreased TH 1- and TH 17-cell content in MPE, increased MPE volume, and reduced survival of MPE-bearing mice. Taken together, we demonstrated that IL-10 deficiency promoted T-cell differentiation into TH 1 cells and upregulated the CXCR3-CXCL10 signaling pathway that recruits TH 1 and TH 17 cells into MPE, ultimately resulting in decreased MPE formation and longer survival time of mice-bearing MPE., (© 2019 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)- Published
- 2019
- Full Text
- View/download PDF
21. Activated naïve B cells promote development of malignant pleural effusion by differential regulation of T H 1 and T H 17 response.
- Author
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Wu XZ, Shi XY, Zhai K, Yi FS, Wang Z, Wang W, Pei XB, Xu LL, Wang Z, and Shi HZ
- Subjects
- Animals, B-Lymphocytes pathology, Mice, Mice, Knockout, Neoplasm Proteins genetics, Neoplasm Proteins immunology, Pleural Effusion, Malignant genetics, Pleural Effusion, Malignant pathology, Signal Transduction genetics, Th1 Cells pathology, Th17 Cells pathology, B-Lymphocytes immunology, Pleural Effusion, Malignant immunology, Signal Transduction immunology, Th1 Cells immunology, Th17 Cells immunology
- Abstract
Inflammatory signaling networks between tumor cells and immune cells contribute to the development of malignant pleural effusion (MPE). B cells have been found in MPE; however, little is known about their roles there. In the present study, by using mouse MPE models, we noted that although the total B cells in MPE were decreased as compared with the corresponding blood and spleen, the percentage of activated naïve B cells expressing higher levels of CD80, CD86, myosin heavy chain-II, CD44, CD69, and programmed cell death-ligand 1 (PD-L1) molecules were increased in wild-type mouse MPE. Compared with wild-type mice, decreased T helper (T
H )1 cells and increased TH 17 cells were present in B cell-deficient mouse MPE, which paralleled to the reduced MPE volume and longer survival time. Adoptive transfer of activated naïve B cells into B cell-deficient mice was able to increase TH 1 cells and decrease TH 17 cells in MPE and shorten the survival of mice bearing MPE. Furthermore, we demonstrated that activated naïve B cells inhibited TH 17-cell expansion via the PD-1/PD-L1 pathway and promoted naïve CD4+ T-cell differentiation into TH 1/TH 17 cells through secreting IL-27/IL-6 independent of the PD-1/PD-L1 pathway. Collectively, our data uncovered a mechanism by which naïve B cells promote MPE formation by regulating TH 1/TH 17 cell responses, making these B cells an attractive target for therapeutic intervention in the fight against cancer.- Published
- 2018
- Full Text
- View/download PDF
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