The Experts below are selected from a list of 942 Experts worldwide ranked by ideXlab platform
Veena B Antony - One of the best experts on this subject based on the ideXlab platform.
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mycobacterium mediated chemokine expression in pleural mesothelial cells role of c c chemokines in Tuberculous Pleurisy
The Journal of Infectious Diseases, 1998Co-Authors: Kamal A Mohammed, Najmunnisa Nasreen, Melissa J Ward, Kamal K Mubarak, Francisco Rodriguezpanadero, Veena B AntonyAbstract:Pulmonary tuberculosis is characterized by granulomatous inflammation with an extensive infiltration of mononuclear phagocytes, but the mechanisms of phagocyte recruitment to the pleural space is unknown. In this study, pleural fluid from patients with tuberculosis contained significantly (P<.001) more biologically active MIP-1alpha and MCP-1 (C-C cytokines) than did effusions from patients with congestive heart failure. Antigenic MIP-1alpha and MCP-1 was detected by immunocytochemistry in pleural biopsy sections of patients with Tuberculous Pleurisy. In vitro, pleural mesothelial cells stimulated with bacille Calmette-Guerin (BCG) or interferon (IFN)-gamma produced MIP-1alpha and MCP-1. Reverse transcription-polymerase chain reaction studies confirmed that both BCG and IFN-gamma induced MIP-1alpha and MCP-1 expression in mesothelial cells, demonstrating that mesothelial cell-derived C-C chemokines play a biologically important role in the recruitment of mononuclear cells to the pleural space.
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mycobacterium mediated chemokine expression in pleural mesothelial cells role of c c chemokines in Tuberculous Pleurisy
The Journal of Infectious Diseases, 1998Co-Authors: Kamal A Mohammed, Najmunnisa Nasreen, Melissa J Ward, Kamal K Mubarak, Francisco Rodriguezpanadero, Veena B AntonyAbstract:Pulmonary tuberculosis is characterized by granulomatous inflammation with an extensive infiltration of mononuclear phagocytes, but the mechanisms of phagocyte recruitment to the pleural space is unknown. In this study, pleural fluid from patients with tuberculosis contained significantly ( ) more biologically active MIP-1a and MCP-1 (C-C cytokines) than did P ! .001 effusions from patients with congestive heart failure. Antigenic MIP-1a and MCP-1 was detected by immunocytochemistry in pleural biopsy sections of patients with Tuberculous Pleurisy. In vitro, pleural mesothelial cells stimulated with bacille Calmette-Guerin (BCG) or interferon (IFN)-g produced MIP-1a and MCP-1. Reverse transcription-polymerase chain reaction studies confirmed that both BCG and IFN-g induced MIP-1a and MCP-1 expression in mesothelial cells, demonstrating that mesothelial cell-derived C-C chemokines play a bi- ologically important role in the recruitment of mononuclear cells to the pleural space. Tuberculosis (TB), a chronic mycobacterial infection caused by Mycobacterium tuberculosis (MTB), is the leading infectious cause of mortality in the world, and approximately one-third of the world's population is infected with the organism (1). In many areas, TB remains the most common cause of pleural effusions. MTB infection results in chronic granulomatous in- flammation that is characterized by the presence of lymphocytes (2, 3) and mononuclear phagocytes at the site of infection (4, 5). MIP-1a and MCP-1 (C-C chemokines) are chemotactic for mononuclear phagocytic cells (6, 7). MIP-1a is a low-molecular- mass heparin-binding protein known to exert chemotactic and activating effects on phagocytic mononuclear cells (8, 9). In addition, MIP-1a is expressed in both acute and chronic in- flammatory disease states (10, 11). MCP-1 is an 8.7-kDa protein and has specific chemoattractant and activating activity for monocytes in acute inflammatory conditions (12). Chemokine synthesis is induced in various cells by inflammatory stimuli. Mesothelial cells have been observed to produce C-C chemo- kine upon stimulation by inflammatory mediators (13); how- ever, their role in MTB-mediated Pleurisy is undefined. Mesothelial cells are metabolically active and continuously
Fumitaka Ogushi - One of the best experts on this subject based on the ideXlab platform.
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asymptomatic primary Tuberculous Pleurisy with intense 18 fluorodeoxyglucose uptake mimicking malignant mesothelioma
BMC Infectious Diseases, 2013Co-Authors: Tsutomu Shinohara, Naoki Shiota, Motohiko Kume, Norihiko Hamada, Keishi Naruse, Fumitaka OgushiAbstract:Background The pathogenesis of primary Tuberculous Pleurisy is a delayed-type hypersensitivity immunogenic reaction to a few mycobacterial antigens entering the pleural space rather than direct tissue destruction by mycobacterial proliferation. Although it has been shown that pulmonary tuberculosis induces 18-fluorodeoxyglucose (FDG) uptake in active lesions, little is known about the application of FDG positron emission/computed tomography (FDG PET/CT) to the management of primary Tuberculous Pleurisy.
Changyou Wu - One of the best experts on this subject based on the ideXlab platform.
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identification of m tuberculosis specific th1 cells expressing cd69 generated in vivo in pleural fluid cells from patients with Tuberculous Pleurisy
PLOS ONE, 2011Co-Authors: Li Li, Xianlan Zhang, Xiaoying Fu, Dan Qiao, Changyou WuAbstract:Th1 cell-mediated immune responses at the site of active infection are important to restrict the growth of M.tuberculosis (MTB) and for the spontaneous resolution of patients with Tuberculous Pleurisy (TBP). In the present study, we found that without any stimulation, CD4+ T cells in pleural fluid cells (PFCs) from patients with TBP expressed significantly higher levels of CD69 than PBMCs from patients with tuberculosis (TB) or healthy donors. CD4+CD69+ T cells expressed T-bet and IL-12Rβ2. After stimulation with MTB-specific antigens, CD4+CD69+ T cells expressed significantly higher levels of IFN-γ, IL-2 and TNF-α than CD4+CD69− T cells, demonstrating that CD4+CD69+ T cells were MTB-specific Th1 cells. In addition, CD4+CD69+ T cells were mostly polyfunctional Th1 cells that simultaneously produced IFN-γ, IL-2, TNF-α and displayed an effector or effector memory phenotype (CD45RA−CCR7−CD62L−CD27−). Moreover, the percentages of CD4+CD69+ T cells were significantly and positively correlated with polyfunctional T cells. Interestingly, sorted CD4+CD69+ but not CD4+CD69− fractions by flow cytometry produced IFN-γ, IL-2 and TNF-α that were significantly regulated by CD4+CD25+ Treg cells. Taken together, based on the expression of CD69, we found a direct quantitative and qualitative method to detect and evaluate the in vivo generated MTB-specific polyfunctional CD4+ T cells in PFCs from patients with TBP. This method can be used for the potential diagnosis and enrichment or isolation of MTB-specific Th1 cells in the investigations.
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esat 6 and cfp 10 specific th1 th22 and th17 cells in Tuberculous Pleurisy may contribute to the local immune response against mycobacterium tuberculosis infection
Scandinavian Journal of Immunology, 2011Co-Authors: Dan Qiao, Li Li, Binyan Yang, X L Zhang, Changyou WuAbstract:Th1 cell-mediated adaptive immune response is very important but may not be sufficient to control Mycobacterium tuberculosis (M. tuberculosis) infection. The roles of the various T cell subsets and cytokines in the inflammatory processes are not clearly elucidated. We investigated whether Th1, Th22 and Th17 cells mediated cellular immunity at the local site of M. tuberculosis infection in patients with Tuberculous Pleurisy (TBP). The results showed that the cytokines IFN-γ and IL-22 but not IL-17 were elevated in tubercular pleural fluid. Following stimulation with immune-dominant peptides of early secreted antigenic target-6 (ESAT-6), culture filtrate protein-10 (CFP-10) or Bacille Calmette–Guerin, pleural fluid mononuclear cells expressed high levels of cytokines IFN-γ, IL-22 and IL-17 as revealed by mRNA and protein measurements. In addition, we showed that cytokines IFN-γ, IL-22 and IL-17 were produced in M. tuberculosis-specific immune response by distinct subsets of CD4+ T cells with the phenotype of CD45RA−CD62L−CCR7+CD27+. Our results demonstrated for the first time that ESAT-6- and CFP-10-specific Th1, Th22 and Th17 cells existed in the patients with TBP and might play an essential role against M. tuberculosis infection. The findings of this study raised the possibility of unravelling the critical targets for therapeutic intervention in chronic inflammatory diseases such as TBP.
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Identification of mycobacterium tuberculosis-specific Th1, Th17 and Th22 cells using the expression of CD40L in Tuberculous Pleurisy
PLoS ONE, 2011Co-Authors: Li Li, Suihua Lao, Xianlan Zhang, Xiaoying Fu, Dan Qiao, Changyou WuAbstract:Important advances have been made in the immunodiagnosis of tuberculosis (TB) based on the detection of Mycobacterium tuberculosis (MTB)-specific T cells. However, the sensitivity and specificity of the immunological approach are relatively low because there are no specific markers for antigen-specific Th cells, and some of the Th cells that do not produce cytokines can be overlooked using this approach. In this study, we found that MTB-specific peptides of ESAT-6/CFP-10 can stimulate the expression of CD40L specifically in CD4(+) T cells but not other cells from pleural fluid cells (PFCs) in patients with Tuberculous Pleurisy (TBP). CD4(+)CD40L(+) but not CD4(+)CD40L(-) T cells express IFN-gamma, IL-2, TNF-alpha, IL-17 or IL-22 after stimulation with MTB-specific peptides. In addition, CD4(+)CD40L(+) T cells were found to be mostly polyfunctional T cells that simultaneously produce IFN-gamma, IL-2 and TNF-alpha and display an effector or effector memory phenotype (CD45RA(-)CD45RO(+)CCR7(-)CD62L(-)ICOS(-)). To determine the specificity of CD4(+)CD40L(+) T cells, we incubated PFCs with ESTA-6/CFP-10 peptides and sorted live CD4(+)CD40L(+) and CD4(+)CD40L(-) T cells by flow cytometry. We further demonstrated that sorted CD4(+)CD40L(+), but not CD4(+)CD40L(-) fractions, principally produced IFN-gamma, IL-2, TNF-alpha, IL-17 and IL-22 following restimulation with ESTA-6/CFP-10 peptides. Taken together, our data indicate that the expression of CD40L on MTB-specific CD4(+) T cells could be a good marker for the evaluation and isolation of MTB-specific Th cells and might also be useful in the diagnosis of TB.
Kamal A Mohammed - One of the best experts on this subject based on the ideXlab platform.
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mycobacterium mediated chemokine expression in pleural mesothelial cells role of c c chemokines in Tuberculous Pleurisy
The Journal of Infectious Diseases, 1998Co-Authors: Kamal A Mohammed, Najmunnisa Nasreen, Melissa J Ward, Kamal K Mubarak, Francisco Rodriguezpanadero, Veena B AntonyAbstract:Pulmonary tuberculosis is characterized by granulomatous inflammation with an extensive infiltration of mononuclear phagocytes, but the mechanisms of phagocyte recruitment to the pleural space is unknown. In this study, pleural fluid from patients with tuberculosis contained significantly (P<.001) more biologically active MIP-1alpha and MCP-1 (C-C cytokines) than did effusions from patients with congestive heart failure. Antigenic MIP-1alpha and MCP-1 was detected by immunocytochemistry in pleural biopsy sections of patients with Tuberculous Pleurisy. In vitro, pleural mesothelial cells stimulated with bacille Calmette-Guerin (BCG) or interferon (IFN)-gamma produced MIP-1alpha and MCP-1. Reverse transcription-polymerase chain reaction studies confirmed that both BCG and IFN-gamma induced MIP-1alpha and MCP-1 expression in mesothelial cells, demonstrating that mesothelial cell-derived C-C chemokines play a biologically important role in the recruitment of mononuclear cells to the pleural space.
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mycobacterium mediated chemokine expression in pleural mesothelial cells role of c c chemokines in Tuberculous Pleurisy
The Journal of Infectious Diseases, 1998Co-Authors: Kamal A Mohammed, Najmunnisa Nasreen, Melissa J Ward, Kamal K Mubarak, Francisco Rodriguezpanadero, Veena B AntonyAbstract:Pulmonary tuberculosis is characterized by granulomatous inflammation with an extensive infiltration of mononuclear phagocytes, but the mechanisms of phagocyte recruitment to the pleural space is unknown. In this study, pleural fluid from patients with tuberculosis contained significantly ( ) more biologically active MIP-1a and MCP-1 (C-C cytokines) than did P ! .001 effusions from patients with congestive heart failure. Antigenic MIP-1a and MCP-1 was detected by immunocytochemistry in pleural biopsy sections of patients with Tuberculous Pleurisy. In vitro, pleural mesothelial cells stimulated with bacille Calmette-Guerin (BCG) or interferon (IFN)-g produced MIP-1a and MCP-1. Reverse transcription-polymerase chain reaction studies confirmed that both BCG and IFN-g induced MIP-1a and MCP-1 expression in mesothelial cells, demonstrating that mesothelial cell-derived C-C chemokines play a bi- ologically important role in the recruitment of mononuclear cells to the pleural space. Tuberculosis (TB), a chronic mycobacterial infection caused by Mycobacterium tuberculosis (MTB), is the leading infectious cause of mortality in the world, and approximately one-third of the world's population is infected with the organism (1). In many areas, TB remains the most common cause of pleural effusions. MTB infection results in chronic granulomatous in- flammation that is characterized by the presence of lymphocytes (2, 3) and mononuclear phagocytes at the site of infection (4, 5). MIP-1a and MCP-1 (C-C chemokines) are chemotactic for mononuclear phagocytic cells (6, 7). MIP-1a is a low-molecular- mass heparin-binding protein known to exert chemotactic and activating effects on phagocytic mononuclear cells (8, 9). In addition, MIP-1a is expressed in both acute and chronic in- flammatory disease states (10, 11). MCP-1 is an 8.7-kDa protein and has specific chemoattractant and activating activity for monocytes in acute inflammatory conditions (12). Chemokine synthesis is induced in various cells by inflammatory stimuli. Mesothelial cells have been observed to produce C-C chemo- kine upon stimulation by inflammatory mediators (13); how- ever, their role in MTB-mediated Pleurisy is undefined. Mesothelial cells are metabolically active and continuously
Li Peng - One of the best experts on this subject based on the ideXlab platform.
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is xpert mtb rif appropriate for diagnosing Tuberculous Pleurisy with pleural fluid samples a systematic review
BMC Infectious Diseases, 2018Co-Authors: Zhenyu Huo, Li PengAbstract:Tuberculous Pleurisy (TP) presents a diagnostic problem due to the limitations of traditional diagnostic methods. Different studies with the Xpert MTB/RIF assay have drawn variable conclusions about its values in TP diagnosis. We conducted a meta-analysis to assess whether the Xpert MTB/RIF assay is appropriate for the diagnosis of TP using pleural fluid samples. A systematic search of four literature databases in English and Chinese language was performed to identify studies involving the use of Xpert MTB/RIF in patients with TP confirmed by plural biopsy and/or mycobacterial culture. Pooled sensitivity, specificity and accordance proportion were calculated, and the forest plots were generated to assess the accuracy of Xpert MTB/RIF for TP diagnosis. We identified 23 studies meeting our inclusion criteria. The pooled sensitivity and specificity of Xpert MTB/RIF were 30% (95% CI: 21–42%, I2 = 87.93%) and 99% (95% CI: 97–100%, I2 = 96.20%), respectively, and the area under the SROC curve (AUC) of Xpert MTB/RIF was 0.86 (95% CI: 0.83–0.89). Compared with drug susceptibility testing (DST), the pooled accordance rate of Xpert MTB/RIF in detecting rifampicin-susceptible cases and rifampicin-resistant cases was 99% (95% CI: 95–104%, I2 = 8.7%) and 94% (95% CI: 86–102%), respectively. Our analysis suggests that the Xpert MTB/RIF assay is of limited value as a screening test for TP but has a high potential for confirming TP diagnosis and differentiating TP from non-TB diseases using pleural fluid samples.
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Is Xpert MTB/RIF appropriate for diagnosing Tuberculous Pleurisy with pleural fluid samples? A systematic review
'Springer Science and Business Media LLC', 2018Co-Authors: Zhenyu Huo, Li PengAbstract:Abstract Background Tuberculous Pleurisy (TP) presents a diagnostic problem due to the limitations of traditional diagnostic methods. Different studies with the Xpert MTB/RIF assay have drawn variable conclusions about its values in TP diagnosis. We conducted a meta-analysis to assess whether the Xpert MTB/RIF assay is appropriate for the diagnosis of TP using pleural fluid samples. Methods A systematic search of four literature databases in English and Chinese language was performed to identify studies involving the use of Xpert MTB/RIF in patients with TP confirmed by plural biopsy and/or mycobacterial culture. Pooled sensitivity, specificity and accordance proportion were calculated, and the forest plots were generated to assess the accuracy of Xpert MTB/RIF for TP diagnosis. Results We identified 23 studies meeting our inclusion criteria. The pooled sensitivity and specificity of Xpert MTB/RIF were 30% (95% CI: 21–42%, I2 = 87.93%) and 99% (95% CI: 97–100%, I2 = 96.20%), respectively, and the area under the SROC curve (AUC) of Xpert MTB/RIF was 0.86 (95% CI: 0.83–0.89). Compared with drug susceptibility testing (DST), the pooled accordance rate of Xpert MTB/RIF in detecting rifampicin-susceptible cases and rifampicin-resistant cases was 99% (95% CI: 95–104%, I2 = 8.7%) and 94% (95% CI: 86–102%), respectively. Conclusions Our analysis suggests that the Xpert MTB/RIF assay is of limited value as a screening test for TP but has a high potential for confirming TP diagnosis and differentiating TP from non-TB diseases using pleural fluid samples
