Pleural Mesothelial Cells-Induced Monocytes to the Pleural Cavity through the Effect of C3 Lytic Products in Tuberculous Pleural Effusion
Background. The activation of complement is involved in monocyte recruitment in tuberculous pleural effusion (TPE), while the role of the cleavage product of complement C3 in this process needs further research. Methods. The expression of complement components in pleural biopsy specimens of TPE pati...
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| Format: | Article |
| Language: | English |
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Wiley
2024-01-01
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| Series: | International Journal of Clinical Practice |
| Online Access: | http://dx.doi.org/10.1155/2024/5544085 |
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| author | Lisha Luo Juntao Feng Shuanglinzi Deng Xinyue Hu Bingrong Zhao Wei Tang Xiaozhao Li |
| author_facet | Lisha Luo Juntao Feng Shuanglinzi Deng Xinyue Hu Bingrong Zhao Wei Tang Xiaozhao Li |
| author_sort | Lisha Luo |
| collection | DOAJ |
| description | Background. The activation of complement is involved in monocyte recruitment in tuberculous pleural effusion (TPE), while the role of the cleavage product of complement C3 in this process needs further research. Methods. The expression of complement components in pleural biopsy specimens of TPE patients was measured. The concentration of cleavage products of complement was tested in TPE by ELISA. Moreover, the colocalizations of C3b and CR1, C3d and CR3, and CXCL12 and CXCR4 in monocytes and pleural mesothelial cells (PMCs) isolated from TPE were determined by an immunofluorescent assay. Monocyte chemotaxis assay was analyzed via transwell chambers. Results. Three pathways of the complement system were activated in tuberculous pleurisy. In patients with TPE, C3 lysis was more active than peripheral blood in pleural cavity. Tuberculous protein Mpt64 and anaphylatoxin C3a could significantly promote CXCL12 production in human PMCs isolated from TPE. C3b-CR1, C3d-CR3, and CXCL12-CXCR4 were colocalized in PMCs and monocytes from TPE. The recruitment of monocytes into TPE mediated by PMCs could be inhibited by anti-CR1, anti-CR3, and anti-CXCL12 monoclonal antibodies (mAbs). Conclusions. Complement activates strongly in TPE, and PMCs induced monocytes to the pleural cavity through C3a, C3b, and C3d. |
| format | Article |
| id | doaj-art-fbce490cc9c7420cb8dbd69a9ac64c12 |
| institution | Kabale University |
| issn | 1742-1241 |
| language | English |
| publishDate | 2024-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Clinical Practice |
| spelling | doaj-art-fbce490cc9c7420cb8dbd69a9ac64c122025-02-03T01:29:35ZengWileyInternational Journal of Clinical Practice1742-12412024-01-01202410.1155/2024/5544085Pleural Mesothelial Cells-Induced Monocytes to the Pleural Cavity through the Effect of C3 Lytic Products in Tuberculous Pleural EffusionLisha Luo0Juntao Feng1Shuanglinzi Deng2Xinyue Hu3Bingrong Zhao4Wei Tang5Xiaozhao Li6Department of Respiratory MedicineDepartment of Respiratory MedicineDepartment of Respiratory MedicineDepartment of Respiratory MedicineDepartment of Respiratory MedicineDepartment of Function ExaminationDepartment of NephrologyBackground. The activation of complement is involved in monocyte recruitment in tuberculous pleural effusion (TPE), while the role of the cleavage product of complement C3 in this process needs further research. Methods. The expression of complement components in pleural biopsy specimens of TPE patients was measured. The concentration of cleavage products of complement was tested in TPE by ELISA. Moreover, the colocalizations of C3b and CR1, C3d and CR3, and CXCL12 and CXCR4 in monocytes and pleural mesothelial cells (PMCs) isolated from TPE were determined by an immunofluorescent assay. Monocyte chemotaxis assay was analyzed via transwell chambers. Results. Three pathways of the complement system were activated in tuberculous pleurisy. In patients with TPE, C3 lysis was more active than peripheral blood in pleural cavity. Tuberculous protein Mpt64 and anaphylatoxin C3a could significantly promote CXCL12 production in human PMCs isolated from TPE. C3b-CR1, C3d-CR3, and CXCL12-CXCR4 were colocalized in PMCs and monocytes from TPE. The recruitment of monocytes into TPE mediated by PMCs could be inhibited by anti-CR1, anti-CR3, and anti-CXCL12 monoclonal antibodies (mAbs). Conclusions. Complement activates strongly in TPE, and PMCs induced monocytes to the pleural cavity through C3a, C3b, and C3d.http://dx.doi.org/10.1155/2024/5544085 |
| spellingShingle | Lisha Luo Juntao Feng Shuanglinzi Deng Xinyue Hu Bingrong Zhao Wei Tang Xiaozhao Li Pleural Mesothelial Cells-Induced Monocytes to the Pleural Cavity through the Effect of C3 Lytic Products in Tuberculous Pleural Effusion International Journal of Clinical Practice |
| title | Pleural Mesothelial Cells-Induced Monocytes to the Pleural Cavity through the Effect of C3 Lytic Products in Tuberculous Pleural Effusion |
| title_full | Pleural Mesothelial Cells-Induced Monocytes to the Pleural Cavity through the Effect of C3 Lytic Products in Tuberculous Pleural Effusion |
| title_fullStr | Pleural Mesothelial Cells-Induced Monocytes to the Pleural Cavity through the Effect of C3 Lytic Products in Tuberculous Pleural Effusion |
| title_full_unstemmed | Pleural Mesothelial Cells-Induced Monocytes to the Pleural Cavity through the Effect of C3 Lytic Products in Tuberculous Pleural Effusion |
| title_short | Pleural Mesothelial Cells-Induced Monocytes to the Pleural Cavity through the Effect of C3 Lytic Products in Tuberculous Pleural Effusion |
| title_sort | pleural mesothelial cells induced monocytes to the pleural cavity through the effect of c3 lytic products in tuberculous pleural effusion |
| url | http://dx.doi.org/10.1155/2024/5544085 |
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