The role of IFN-γ/CXCL10 axis in Mycoplasma pneumonia infection
Abstract Mycoplasma pneumoniae caused lower respiratory tract infection in children and can exacerbate these infections through the production of various inflammatory factors, with chemokines playing a key role. However, the pathogenesis of this infection is complicated and thus has not been thoroug...
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| Format: | Article |
| Language: | English |
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Nature Portfolio
2025-01-01
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| Series: | Scientific Reports |
| Online Access: | https://doi.org/10.1038/s41598-024-84969-x |
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| author | Yanxia Zou Feng Huang Jiying Sun Yidan Zheng Ge Dai Ting Wang Canhong Zhu Yongdong Yan Renzheng Wang Zhengrong Chen |
| author_facet | Yanxia Zou Feng Huang Jiying Sun Yidan Zheng Ge Dai Ting Wang Canhong Zhu Yongdong Yan Renzheng Wang Zhengrong Chen |
| author_sort | Yanxia Zou |
| collection | DOAJ |
| description | Abstract Mycoplasma pneumoniae caused lower respiratory tract infection in children and can exacerbate these infections through the production of various inflammatory factors, with chemokines playing a key role. However, the pathogenesis of this infection is complicated and thus has not been thoroughly studied. We clarified that cytokine expression levels were analyzed in both peripheral blood and bronchoalveolar lavage fluid (BALF), and in vitro assays were conducted using THP-1 macrophages. We discovered that, compared to control children, M. pneumoniae pneumonia (MPP) patients expressed significantly higher levels of CXCL10 both in the peripheral blood and BALF. Moreover, numbers of macrophages, predominantly with a M1 phenotype, were significantly increased in BALFs of children of MPP. In vitro, coculture with IFN-γ or activated CD4+ Th1 cells significantly promoted CXCL10 expressions in THP-1 derived macrophages, which was largely reversed by siRNA-mediated down regulation of STAT1. In addition, IFN-γ-stimulated macrophages greatly promoted the trans-migration of Th1 cells. our data show that Th1 cells-derived IFN-γ augments CXCL10 production in macrophages via the JAK-STAT1 pathway, which subsequently recruits more immune cells like Th1 cells into the infection sites, thereby constituting a positive feedback loop and aggravating the type I inflammatory responses in MPP patients. |
| format | Article |
| id | doaj-art-dbd8d63904e94f63884616b2f2c9f8fd |
| institution | Kabale University |
| issn | 2045-2322 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Scientific Reports |
| spelling | doaj-art-dbd8d63904e94f63884616b2f2c9f8fd2025-01-26T12:25:00ZengNature PortfolioScientific Reports2045-23222025-01-011511910.1038/s41598-024-84969-xThe role of IFN-γ/CXCL10 axis in Mycoplasma pneumonia infectionYanxia Zou0Feng Huang1Jiying Sun2Yidan Zheng3Ge Dai4Ting Wang5Canhong Zhu6Yongdong Yan7Renzheng Wang8Zhengrong Chen9Department of Respiratory Medicine, Children’s Hospital of Soochow UniversityDepartment of Respiratory Medicine, Children’s Hospital of Soochow UniversityDepartment of Respiratory Medicine, Children’s Hospital of Soochow UniversityDepartment of Respiratory Medicine, Children’s Hospital of Soochow UniversityDepartment of Respiratory Medicine, Children’s Hospital of Soochow UniversityDepartment of Respiratory Medicine, Children’s Hospital of Soochow UniversityDepartment of Respiratory Medicine, Children’s Hospital of Soochow UniversityDepartment of Respiratory Medicine, Children’s Hospital of Soochow UniversityDepartment of Pediatrics, Xiangcheng District People’s HospitalDepartment of Respiratory Medicine, Children’s Hospital of Soochow UniversityAbstract Mycoplasma pneumoniae caused lower respiratory tract infection in children and can exacerbate these infections through the production of various inflammatory factors, with chemokines playing a key role. However, the pathogenesis of this infection is complicated and thus has not been thoroughly studied. We clarified that cytokine expression levels were analyzed in both peripheral blood and bronchoalveolar lavage fluid (BALF), and in vitro assays were conducted using THP-1 macrophages. We discovered that, compared to control children, M. pneumoniae pneumonia (MPP) patients expressed significantly higher levels of CXCL10 both in the peripheral blood and BALF. Moreover, numbers of macrophages, predominantly with a M1 phenotype, were significantly increased in BALFs of children of MPP. In vitro, coculture with IFN-γ or activated CD4+ Th1 cells significantly promoted CXCL10 expressions in THP-1 derived macrophages, which was largely reversed by siRNA-mediated down regulation of STAT1. In addition, IFN-γ-stimulated macrophages greatly promoted the trans-migration of Th1 cells. our data show that Th1 cells-derived IFN-γ augments CXCL10 production in macrophages via the JAK-STAT1 pathway, which subsequently recruits more immune cells like Th1 cells into the infection sites, thereby constituting a positive feedback loop and aggravating the type I inflammatory responses in MPP patients.https://doi.org/10.1038/s41598-024-84969-x |
| spellingShingle | Yanxia Zou Feng Huang Jiying Sun Yidan Zheng Ge Dai Ting Wang Canhong Zhu Yongdong Yan Renzheng Wang Zhengrong Chen The role of IFN-γ/CXCL10 axis in Mycoplasma pneumonia infection Scientific Reports |
| title | The role of IFN-γ/CXCL10 axis in Mycoplasma pneumonia infection |
| title_full | The role of IFN-γ/CXCL10 axis in Mycoplasma pneumonia infection |
| title_fullStr | The role of IFN-γ/CXCL10 axis in Mycoplasma pneumonia infection |
| title_full_unstemmed | The role of IFN-γ/CXCL10 axis in Mycoplasma pneumonia infection |
| title_short | The role of IFN-γ/CXCL10 axis in Mycoplasma pneumonia infection |
| title_sort | role of ifn γ cxcl10 axis in mycoplasma pneumonia infection |
| url | https://doi.org/10.1038/s41598-024-84969-x |
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