Huan-Zhong Shi

Huazhong University of Science and Technology, Wu-han-shih, Hubei, China

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Publications (56)181.3 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The differential diagnosis of pleural effusions can present a considerable challenge, and the etiology of pleural effusions varies depending on the population studied. This study aimed to assess the efficacy and safety of medical thoracoscopy in the diagnosis of patients with undiagnosed pleural effusions in a Chinese population. Between July 2005 and June 2014, medical thoracoscopy (MT) using the semirigid instrument was performed in 833 patients with pleural effusions of unknown etiology in our Institute, where diagnostic thoracocentesis or/and blind pleural biopsy had failed to yield an answer. Demographic, radiographic, procedural, and histological data were recorded and analyzed. During this 9-year study, satisfactory pleural biopsy samples were obtained in 833 patients, and MT revealed malignant pleural effusion in 342 (41.1%) patients, benign pleural effusion in 429 (51.5%) patients, and 62 (7.4%) patients could not get definite diagnoses. The overall diagnostic efficiency of MT was 92.6% (771/833). After MT, the only severe complication was empyema, seen in 3 patients (0.4%). The most common minor complication was transient chest pain (44.1%) from the indwelling chest tube. MT is an effective and safe procedure for diagnosing pleural effusions of undetermined causes. In areas with high tuberculosis prevalence, MT should be particularly helpful in the differential diagnosis of tuberculous pleural effusion. © 2015 S. Karger AG, Basel.
    Respiration 08/2015; DOI:10.1159/000435962 · 2.92 Impact Factor
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    ABSTRACT: Differentiating tuberculous pleural effusion from other lymphocytic pleural effusions is often challenging. This retrospective study aimed to assess the efficacy and safety of medical thoracoscopy in patients with suspected tuberculous pleural effusion. Between July 2005 and June 2014, patients with pleural effusions of unknown etiologies underwent medical thoracoscopy in our institute after less invasive means of diagnosis had failed. Demographic, radiographic, procedural, and histological data of patients with tuberculous pleural effusion were analyzed. During this 9-year study, 333 of 833 patients with pleural effusion were confirmed to have tuberculous pleurisy. Under thoracoscopy, we observed pleural nodules in 69.4%, pleural adhesion in 66.7%, hyperemia in 60.7%, plaque-like lesions in 6.0%, ulceration in 1.5% of patients with tuberculous pleurisy. Pleural biopsy revealed the presence of Mycobacterium tuberculosis in the pleural tissue or/and demonstration of caseating granulomas in 330 (99.1%) patients. No serious adverse events were recorded, and the most common minor complication was transient chest pain (43.2%) from the indwelling chest tube. Our data showed that medical thoracoscopy is a simple procedure with high diagnostic yield and excellent safety for the diagnosis of tuberculous pleural effusion. Copyright © 2015. Published by Elsevier Ltd.
    Respiratory medicine 07/2015; DOI:10.1016/j.rmed.2015.06.008 · 2.92 Impact Factor
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    ABSTRACT: Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease of unknown cause that typically leads to respiratory failure and death within 3-5 years of diagnosis. TGF-β1 is considered as a major profibrotic factor. However, TGF-β1 is necessary but not sufficient to the pathogenesis of fibrotic lesion of the lungs. Recent observations have revealed that calpain, a calcium dependent protease, plays a pivotal role in tissue remodeling and fibrosis. However, the mechanism of calpain mediating pulmonary fibrosis is not understood. Calpain conditional knockout (ER-Cre(+/-)capns1(flox/flox)) mice and primary human lung fibroblasts (HLFs) were used here to investigate the relationships between calpain and TGF-β1. Calpain knockout mice were protected from fibrotic effects of bleomycin. Bleomycin induced increases in TGF-β1 via calpain activation in HLFs. Moreover, TGF-β1 also activated calpain. This crosstalk between calpain activation and TGF-β1 triggered the downstream signaling pathway including TGF-β1 Smad2/3 and non-Smad (Akt) pathways, as well as collagen-I synthesis. Taken together, our data indicate that the crosstalk between calpain activation and TGF-β1 augments collagen-I synthesis in HLFs and in pulmonary fibrosis. Intervention in the crosstalk between calpain activation and TGF-β1 is a novel potential strategy to prevent pulmonary fibrosis. Copyright © 2015. Published by Elsevier B.V.
    Biochimica et Biophysica Acta 06/2015; 184(9). DOI:10.1016/j.bbadis.2015.06.008 · 4.66 Impact Factor
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    ABSTRACT: The numbers of IL-27-producing CD4(+) T cells and the concentration of soluble IL-27 have been found to be increased in tuberculous pleural effusion (TPE). The objective of the present study was to explore the mechanism by which IL-27(+)CD4(+) T cells are recruited into the pleural space, and to explore the impact of IL-27 on pleural mesothelial cells (PMCs). The expression profiles of chemokine receptor (CCR) were determined by flow cytometry. The chemoattractant activity of chemokines CCL20 and CCL22 for IL-27(+)CD4(+) T cells in vitro was observed. Effects of IL-27 on wound healing, proliferation and apoptosis of PMCs were also investigated. IL-27(+)CD4(+) T cells in TPE expressed high level of CCR6, medium level of CCR4, and low levels of CCR2, CCR3, CCR5, CCR7, CCR10, and CXCR3. Recruitment of IL-27(+)CD4(+) T cells into TPE could be induced by pleural CCL20 and CCL22. By activating STAT3 signaling, IL-27 significantly improved wound healing and promoted proliferation of PMCs, and completely prevented apoptosis of PMCs induced by IFN-γ. After being recruited into pleural space by CCL20 or/and CCL22, these pleural IL-27-producing CD4(+) T cells may play important roles in tuberculosis immunity by affecting PMC functions.
    Beiträge zur Klinik der Tuberkulose 05/2015; DOI:10.1007/s00408-015-9738-2 · 2.17 Impact Factor
  • Chinese medical journal 01/2015; 128(8):1032. DOI:10.4103/0366-6999.155073 · 1.02 Impact Factor
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    Kan Zhai · Jie Ding · Huan-Zhong Shi
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    ABSTRACT: Corresponding author at: Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China. Tel.: +86 10 85231624.
    Journal of clinical virology: the official publication of the Pan American Society for Clinical Virology 12/2014; 63. DOI:10.1016/j.jcv.2014.12.002 · 3.47 Impact Factor
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    Kan Zhai · Jie Ding · Huan-Zhong Shi
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    ABSTRACT: The potential causal association between human papillomavirus (HPV) and lung cancer (LC) remains controversial. We performed this meta-analysis to evaluate whether HPV infection in lung tissue is associated with LC compared with non-cancer controls. We also quantified this association in different LC subtypes. MEDLINE, EMBASE and Web of Science were searched through March 2014, using the search terms "lung cancer", "human papillomavirus", "HPV" and their combinations. Association was tested using odds ratio (OR) with 95% confidence intervals (95% CI). Heterogeneity was assessed using Q and I(2) statistic. Finally, nine studies, for a total of 1094 LCs and 484 non-cancer controls, were identified as eligible publications. The pooled results showed that HPV infection was associated with LC (OR=5.67, 95% CI: 3.09-10.40, P<0.001). Similar results were also observed in HPV16 and/or HPV18 (HPV16/18) infection analyses (OR=6.02, 95% CI: 3.22-11.28, P<0.001). HPV16/18 was significantly associated with lung squamous cell carcinoma (SCC) (OR=9.78, 95% CI: 6.28-15.22, P<0.001), while the pooled OR was 3.69 in lung adenocarcinoma (95% CI: 0.99-13.71, P=0.052). Our results suggest that lung tissue with HPV infection has a strong association with LC, and especially, HPV16/18 infection significantly increases SCC risk, which indicates a potential pathogenesis link between HPV and LC.
    Journal of clinical virology: the official publication of the Pan American Society for Clinical Virology 10/2014; 63. DOI:10.1016/j.jcv.2014.09.014 · 3.47 Impact Factor
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    ABSTRACT: The objective of the present study was to figure out whether human IL-27-producing CD4+ T cells represent a distinct T cell subset in tuberculosis pleural effusion (TPE). Distribution, phenotypic features of IL-27-producing CD4+ T cells in TPE were determined. The required transcription factors and signal transductions for IL-27-producing CD4+ T cell differentiation were explored. The immune regulation of IL-27 on pleural mesothelial cells was observed. We have determined the presence of a subset of human Th cells that infiltrated into tuberculous pleural effusion, which was characterized by the secretion of IL-27, and somehow IFN-γ, but not of IL-4, IL-9, IL-17, or IL-22. These IL-27-producing CD4+ T cells were effector memory cells and exhibited a transcription profile clearly separated from those of Th2, Th17, Th9, and Th22 cells. The in vitro experiments showed that IL-1β, IL-2 and IL-12, or their various combinations could promote IL-27+CD4+ T cell differentiation from naive CD4+ T cells by means of phosphorylation of STAT3, STAT4, or/and STAT5. Transcription factors c-Fos and T-bet were required for IL-27+CD4+ T cell differentiation. By activating STAT3 signaling, IL-27 not only restored a clear epithelial phenotype of pleural mesothelial cells, but also further reversed IFN-γ-induced epithelial–mesenchymal transition of pleural mesothelial cells. These data suggested that human IL-27+CD4+ T cells might represent a distinct human T cell subset with unique expression profiles of transcription factors and proinflammatory cytokines, and these IL-27+CD4+ T cells may play important roles in tuberculosis immunity by affecting pleural mesothelial cells.
    Tuberculosis 07/2014; 94(6). DOI:10.1016/j.tube.2014.07.003 · 3.50 Impact Factor
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    Ai Cui · Xiao-Guang Jin · Kan Zhai · Zhao-Hui Tong · Huan-Zhong Shi
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    ABSTRACT: Although the values of soluble mesothelin-related peptides (SMRPs), including mesothelin and megakaryocyte potentiating factor, in serum and/or pleural fluid for diagnosing malignant pleural mesothelioma (MPM) have been extensively studied, the exact diagnostic accuracy of these SMRPs remains controversial. The purpose of the present meta-analysis is to update the overall diagnostic accuracy of SMRPs in serum and, furthermore, to establish diagnostic accuracy of SMRPs in pleural fluid for MPM. Systematic review and meta-analysis. A total of 30 articles of diagnostic studies were included in the current meta-analysis. Sensitivity, specificity and other measures of accuracy of SMRPs in serum and pleural fluid for the diagnosis of MPM were pooled using random effects models. Summary receiver operating characteristic curves were used to summarise overall test performance. The summary estimates of sensitivity, specificity, positive likelihood ratio, negative likelihood ratio and diagnostic OR were 0.61, 0.87, 5.71, 0.43 and 14.43, respectively, for serum and 0.79, 0.85, 4.78, 0.30 and 19.50, respectively, for pleural fluid. It was also found that megakaryocyte potentiating factor in serum had a superior diagnostic accuracy compared with mesothelin for MPM. SMRPs in both serum and pleural fluid are helpful markers for diagnosing MPM with similar diagnostic accuracy. The negative results of SMRP determinations are not sufficient to exclude non-MPM, and the positive test results indicate that further invasive diagnostic steps might be necessary for the diagnosis of MPM.
    BMJ Open 01/2014; 4(2):e004145. DOI:10.1136/bmjopen-2013-004145 · 2.06 Impact Factor
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    Huan Xia · Xiao-Juan Wang · Qiong Zhou · Huan-Zhong Shi · Zhao-Hui Tong
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    ABSTRACT: Talc pleurodesis has been widely used to control malignant pleural effusion; however, it is still not clear whether talc pleurodesis is more effective than other local therapies. We performed a meta-analysis to evaluate the efficacy and safety of talc pleurodesis in the management of malignant pleural effusion. PubMed, Embase, and Web of Science were searched for English-language studies of clinical controlled trials comparing talc pleurodesis with control therapies until August 8, 2013. Success rate and incidence of adverse events were evaluated. Relative risks were estimated using random- or fixed- effects model and statistical heterogeneity was assessed using I(2) test. Twenty trials involving 1,525 patients with malignant pleural effusion were included. The success rate of talc pleurodesis was significantly higher than that of control therapies (relative risk, 1.21; 95% confidence interval, 1.01-1.45; p = 0.035) with similar adverse events. In addition, thoracoscopic talc poudrage was more effective than bedside talc slurry (relative risk, 1.12; 95% confidence interval, 1.01-1.23; p = 0.026). The current evidences suggested the benefit for talc pleurodesis in the treatment of malignant pleural effusion. Talc pleurodesis, especially thoracoscopic talc poudrage pleurodesis, should be performed in patients with malignant pleural effusion, especially those with life-expectancy longer than one month.
    PLoS ONE 01/2014; 9(1):e87060. DOI:10.1371/journal.pone.0087060 · 3.23 Impact Factor
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    ABSTRACT: Rationale: IFN-γ-producing CD4+ T (Th1) cells and IL-17-producing CD4+ T (Th17) cells have been found to be involved in multiple malignancies; however, the reciprocal relationship between Th1 and Th17 cells in malignant pleural effusion (MPE) remain to be elucidated. Objectives: To explore the differentiation and immune regulation of Th1 and Th17 cells in the development of MPE in murine models. Methods: The distribution and differentiation of Th1 and Th17 cells in MPE were investigated in IFN-γ-/-, IL-17-/-, and wild type mice. The effects of Th1 and Th17 cells on the development of MPE and the survival of mice bearing MPE were also investigated. Measurements and Main Results: We have demonstrated that increased Th1 and Th17 cells could be found in MPE as compared with blood and spleen. Compared with wild type mice, Th17 cells were markedly augmented in MPE from IFN-γ-/- mice, and improved survival could be seen in IFN-γ-/- mice. Th1 cell numbers were elevated in MPE from IL-17-/- mice, and decreased survival could be seen in IL-17-/- mice. The in vitro experiments showed that IFN-γ deficiency promoted Th17 cell differentiation via suppressing STAT3 pathway, and that IL-17 deficiency promoted Th1 cell differentiation via suppressing STAT1 pathway. Conclusions: IFN-γ inhibited Th17 cell differentiation while IL-17 inhibited Th1 cell differentiation in mouse models of MPE. IL-17 inhibited the formation of MPE and improved the survival of mice bearing MPE; in contrast, IFN-γ promoted MPE formation and mouse death.
    American Journal of Respiratory and Critical Care Medicine 01/2014; 189(6). DOI:10.1164/rccm.201310-1776OC · 11.99 Impact Factor
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    ABSTRACT: Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) have been demonstrated to be expressed on pleural mesothelial cells (PMCs), and to mediate leukocyte adhesion and migration; however, little is known about whether adhesion molecule-dependent mechanisms are involved in the regulation of CD4(+) T cells by PMCs in tuberculous pleural effusion (TPE). Expressions of ICAM-1 and VCAM-1 on PMCs, as well as expressions of CD11a and CD29, the counter-receptors for ICAM-1 and VCAM-1, respectively, expressed on CD4(+) T cells in TPE were determined using flow cytometry. The immune regulations on adhesion, proliferation, activation, selective expansion of CD4(+) helper T cell subgroups exerted by PMCs via adhesion molecule-dependent mechanisms were explored. Percentages of ICAM-1-positive and VCAM-1‒positive PMCs in TPE were increased compared with PMC line. Interferon-γ enhanced fluorescence intensity of ICAM-1, while IL-4 promoted VCAM-1 expression on PMCs. Percentages of CD11a(high)CD4(+) and CD29(high)CD4(+) T cells in TPE significantly increased as compared with peripheral blood. Prestimulation of PMCs with anti‒ICAM-1 or ‒VCAM-1 mAb significantly inhibited adhesion, activation, as well as effector regulatory T cell expansion induced by PMCs. Our current data showed that adhesion molecule pathways on PMCs regulated adhesion and activation of CD4(+) T cells, and selectively promoted the expansion of effector regulatory T cells.
    PLoS ONE 09/2013; 8(9):e74624. DOI:10.1371/journal.pone.0074624 · 3.23 Impact Factor
  • Yan-Bin Wu · Zhi-Jian Ye · Sou-Ming Qin · Cong Wu · Yi-Qiang Chen · Huan-Zhong Shi
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    ABSTRACT: Previous studies reported interleukin-27 (IL-27), interferon-γ (IFN-γ), or adenosine deaminase (ADA) alone plays a helpful role in diagnosing tuberculous pleural effusion (TPE). The present study aims at comparing the diagnostic accuracy of pleural IL-27, IFN-γ, and ADA, and investigate the diagnostic accuracy of the combination of IL-27, IFN-γ, or/and ADA for differentiating TPE from pleural effusions with the other etiologies. The concentrations of IL-27, IFN-γ and ADA were simultaneously determined in pleural fluids and sera from 40 patients with TPE; 26 with malignant pleural effusion, seven with infectious pleural effusion, and eight with transudative pleural effusion by enzyme linked immunosorbent assay and colorimetric method. The corresponding biochemical indexs were also simultaneously determined. The concentrations of pleural IL-27 and IFN-γ in the tuberculous group were significantly higher than those in the malignant, infectious, and transudative groups. The concentrations of ADA in TPE were significantly higher than those in MPE or transudative effusions, while much lower than those in infectious effusions. Among these three biomarkers, IL-27 was the most effective for TPE diagnosis, with the cut off value of 900.8 ng/L. IL-27 had a high sensitivity of 95% and specificity of 97.6% for differential diagnosis of TPE from non-TPEs. Combinations of IL-27, IFN-γ and ADA measurements further increased the sensitivity or specificity up to 100%. Compared to non-TPEs, IL-27, IFN-γ and ADA all simultaneously increased in TPE; and among these three rapid detection methods, IL-27 appeared to be the best for distinguishing tuberculous from non-TPEs, especially from MPE. Combinations of the three markers (IL-27, IFN-γ and ADA) yielded the highest sensitivity and specificity. These findings suggest that the applications of a new biomarker, IL-27, alone or with IFN-γ and ADA, may contribute to more efficient diagnosis strategies in the management of tuberculous pleurisy.
    Chinese medical journal 09/2013; 126(17):3215-21. DOI:10.3760/cma.j.issn.0366-6999.20130020 · 1.02 Impact Factor
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    ABSTRACT: BACKGROUND: Our previous data have demonstrated that the number of IL-9-producing CD4(+) T cells (Th9 cells) in malignant pleural effusion (MPE) was significantly increased when compared with that in blood. The aim of the present study was to investigate the mechanism by which Th9 cells were recruited into MPE and the phenotypic characteristics of pleural Th9 cells. METHODS: The expression patterns of chemokine receptors (CCRs) on Th9 cells and the chemoattractant activity of chemokine CCL20 for Th9 cells in vitro were observed. The phenotypic features of Th9 cells in MPE were determined by flow cytometry. RESULTS: We found that Th9 cells in both MPE and blood expressed a high level of CCR6 on their surface. An in vitro migration assay confirmed that both MPE and supernatants of cultured pleural mesothelial cells could induce the migration of Th9 cells, and anti-CCL20 mAb significantly inhibited the ability of MPE or supernatants to stimulate Th9 cell chemotaxis. We also noted that pleural Th9 cells expressed high levels of CD45RO and very low levels of CD45RA and CD62L, displaying the phenotype of effector memory cells. CONCLUSIONS: Our data revealed that recruitment of Th9 cells into MPE could be induced by pleural CCL20 and that the majority of Th9 cells in MPE displayed the phenotype of effector memory cells.
    Beiträge zur Klinik der Tuberkulose 05/2013; 191(4). DOI:10.1007/s00408-013-9474-4 · 2.17 Impact Factor
  • Zhao-Hui Tong · Huan-Zhong Shi
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    ABSTRACT: Although it is curable, tuberculosis continues to be is a major global public health problem, especially in developing countries. Tuberculous pleural effusion (TPE) is one of the most common forms of extrapulmonary tuberculosis. It has been well documented that CD4+ T lymphocytes are dominant leukocytes present in TPE. Traditionally, CD4+ T cells have been classified into two functionally distinct subsets, helper T-cell type 1 (Th1) and Th2 cells, based on their cytokine production profiles. Recently, regulatory T cells, Th17 cells, Th9 cells, and Th22 cells have been added to the 'portfolio' of Th cells. In this review, we summarize recent findings regarding the phenotypic characteristics of the above Th cells, the mechanisms of differentiation and recruitment of Th cells into pleural space, and the immune regulation of Th cells in TPE environment. We also describe the interplay between different Th cells, as well as between Th cells and other type of cells, such as pleural mesothelial cells in TPE. Further studies should be directed at identifying the mediators and mechanisms involved in the immunoregulatory properties of pleural Th cells in tuberculosis infection.
    Tuberculosis (Edinburgh, Scotland) 03/2013; 93(3). DOI:10.1016/j.tube.2013.02.014 · 3.50 Impact Factor
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    ABSTRACT: Programmed death 1 (PD-1), PD-ligand 1 (PD-L1), and PD-L2 have been demonstrated to be involved in tuberculosis immunity, however, the expression and regulation of PD-1/PD-Ls pathways in pleural mesothelial cells (PMCs) and CD4+ T cells in tuberculous pleural effusion (TPE) have not been investigated. Expression of PD-1 on CD4+ T cells and expressions of PD-L1 and PD-L2 on PMCs in TPE were determined. The impacts of PD-1/PD-Ls pathways on proliferation, apoptosis, adhesion, and migration of CD4+ T cells were explored. Concentrations of soluble PD-l, but not of soluble PD-Ls, were much higher in TPE than in serum. Expressions of PD-1 on CD4+ T cells in TPE were significantly higher than those in blood. Expressions of PD-Ls were much higher on PMCs from TPE when compared with those from transudative effusion. Interferon-γ not only upregulated the expression of PD-1 on CD4+ T cells, but also upregulated the expressions of PD-Ls on PMCs. Blockage PD-1/PD-Ls pathways abolished the inhibitory effects on proliferation and adhesion activity of CD4+ T cells induced by PMCs. PD-1/PD-Ls pathways on PMCs inhibited proliferation and adhesion activity of CD4+ T cells, suggesting that Mycobacterium tuberculosis might exploit PD-1/PD-Ls pathways to evade host cell immune response in human.
    Tuberculosis (Edinburgh, Scotland) 01/2013; 94(2). DOI:10.1016/j.tube.2013.10.007 · 3.50 Impact Factor
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    ABSTRACT: RATIONALE: IL-9-producing CD4+ T cells (Th9 cells) have been reported to be involved in inflammation and immune diseases. However, the involvement of Th9 cells in malignancy has not been investigated. OBJECTIVES: To elucidate the mechanism by which Th9 cells differentiate in malignant pleural effusion (MPE), and to explore the immune regulation of Th9 cells on lung cancer cells. METHODS: Distribution of Th9 cells in relation to Th17 and Th1 cells in both MPE and blood were determined. The effects and mechanisms of proinflammatory cytokines and regulatory T cells on differentiation of Th9 cells in vitro were explored. The impacts and signal transductions of IL-9, IL-17 and IFN-γ on lung cancer cell lines were also investigated. MEASUREMENTS AND MAIN RESULTS: The numbers of Th9, Th17 and Th1 cells were all increased in MPE when compared with blood. The increase in Th9 cells in MPE was due to the promotion by cytokines and regulatory T cells. By activating STAT3 signaling, both IL-9 and IL-17 substantially promoted the proliferation and migratory activity of lung cancer cells, whereas IFN-γ which activated STAT1 signaling was noted to suppress lung cancer cell proliferation and migration; whereas IFN-γ could induce lung cancer cell apoptosis. Moreover, IL-9 and IFN-γ, but not by IL-17, could strongly facilitate intercellular adhesion of lung cancer cells to pleural mesothelial cell monolayers. CONCLUSIONS: Our data revealed that Th9 cells were increased in MPE, and that Th9 cells exerted an important immune regulation on lung cancer cells in human tumor environment.
    American Journal of Respiratory and Critical Care Medicine 10/2012; DOI:10.1164/rccm.201207-1307OC · 11.99 Impact Factor
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    ABSTRACT: Th22 cells have been reported to be involved in human cancers. However, differentiation and immune regulation of Th22 cells in malignant pleural effusion (MPE) remain unknown. We noted that Th22 cell numbers were increased in MPE, and that IL-22 substantially promoted the proliferation and migratory activity of A549 cells. Moreover, IL-22 could strongly facilitate intercellular adhesion of A549 cells to pleural mesothelial cell monolayers. Our data revealed that the increase in Th22 cells in MPE was due to pleural cytokines and chemokines, and that Th22 exerted an important immune regulation on cancer cells in human pleural malignant environment.
    Cancer letters 07/2012; 326(1):23-32. DOI:10.1016/j.canlet.2012.07.013 · 5.62 Impact Factor
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    ABSTRACT: The objective of the present study was to investigate the presence of interleukin (IL)-27 in pleural effusions and to evaluate the diagnostic significance of pleural IL-27. The concentrations of IL-27 were determined in pleural fluids and sera from 68 patients with tuberculous pleural effusion, 63 malignant pleural effusion, 22 infectious pleural effusion, and 21 transudative pleural effusion. Flow cytometry was used to identify which pleural cell types expressed IL-27. It was found that the concentrations of pleural IL-27 in tuberculous group were significantly higher than those in malignant, infectious, and transudative groups, respectively. Pleural CD4(+) T cells, CD8(+) T cells, NK cells, NKT cells, B cells, monocytes, macrophages, and mesothelial cells might be the cell sources for IL-27. IL-27 levels could be used for diagnostic purpose for tuberculous pleural effusion, with the cut off value of 1,007 ng/L, IL-27 had a sensitivity of 92.7% and specificity of 99.1% for differential diagnosing tuberculous pleural effusion from non-tuberculous pleural effusions. Therefore, compared to non-tuberculous pleural effusions, IL-27 appeared to be increased in tuberculous pleural effusion. IL-27 in pleural fluid is a sensitive and specific biomarker for the differential diagnosing tuberculous pleural effusion from pleural effusions with the other causes.
    PLoS ONE 07/2012; 7(7):e40450. DOI:10.1371/journal.pone.0040450 · 3.23 Impact Factor
  • Qiong Zhou · Huan-zhong Shi
    Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases 07/2012; 35(7):483-4.

Publication Stats

771 Citations
181.30 Total Impact Points

Institutions

  • 2009–2015
    • Huazhong University of Science and Technology
      • Department of Respiratory Medicine
      Wu-han-shih, Hubei, China
  • 2014
    • Beijing Zoo
      Peping, Beijing, China
  • 2013–2014
    • Capital Medical University
      Peping, Beijing, China
  • 2004–2009
    • Guangxi Medical University
      • First Affiliated Hospital
      Yung-ning, Guangxi Zhuangzu Zizhiqu, China