Prokineticin 2 promotes macrophages-mediated antibacterial host defense against bacterial pneumonia
ABSTRACT: Objectives: Bacterial pneumonia is a common serious infectious disease with high morbidity and mortality. Prokineticin 2 (PK2) has recently been identified as a novel immunomodulator in a variety of diseases; however, its role in bacterial pneumonia remains unclear. Methods: The levels of...
| Main Authors: | , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2022-12-01
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| Series: | International Journal of Infectious Diseases |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S1201971222005410 |
| _version_ | 1811198690265661440 |
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| author | Qianqian Tu Xiaoyan Yu Wei Xie Yetao Luo Hong Tang Kai Chen Yanting Ruan Yue Li Jie Zhou Yibing Yin Dapeng Chen Zhixin Song |
| author_facet | Qianqian Tu Xiaoyan Yu Wei Xie Yetao Luo Hong Tang Kai Chen Yanting Ruan Yue Li Jie Zhou Yibing Yin Dapeng Chen Zhixin Song |
| author_sort | Qianqian Tu |
| collection | DOAJ |
| description | ABSTRACT: Objectives: Bacterial pneumonia is a common serious infectious disease with high morbidity and mortality. Prokineticin 2 (PK2) has recently been identified as a novel immunomodulator in a variety of diseases; however, its role in bacterial pneumonia remains unclear. Methods: The levels of PK2 were measured and analyzed in patients with pneumonia and healthy controls. The effects of PK2 on the host response to pneumonia were evaluated by in vivo animal experiments and in vitro cell experiments. Results: PK2 levels dramatically decreased in patients with pneumonia compared with healthy controls, and PK2 levels were lower in patients with severe pneumonia than in pneumonia. In a mouse model of bacterial pneumonia, transtracheal administration of recombinant PK2 significantly alleviated lung injury and improved the survival, which was associated with increased host's bacterial clearance capacity, as manifested by decreased pulmonary bacterial loads. PK2 enhanced the chemotaxis, phagocytosis, and killing ability of macrophages, whereas the protective efficacy of PK2 was abolished after macrophage depletion. Conclusion: Impaired alveolar macrophage function caused by decreased PK2 is a new endogenous cause of the occurrence and development of bacterial pneumonia. The administration of recombinant PK2 may be a potential adjuvant therapy for bacterial pneumonia. |
| first_indexed | 2024-04-12T01:35:35Z |
| format | Article |
| id | doaj.art-bf88f6eaaef440328efdd98757159f79 |
| institution | Directory Open Access Journal |
| issn | 1201-9712 |
| language | English |
| last_indexed | 2024-04-12T01:35:35Z |
| publishDate | 2022-12-01 |
| publisher | Elsevier |
| record_format | Article |
| series | International Journal of Infectious Diseases |
| spelling | doaj.art-bf88f6eaaef440328efdd98757159f792022-12-22T03:53:20ZengElsevierInternational Journal of Infectious Diseases1201-97122022-12-01125103113Prokineticin 2 promotes macrophages-mediated antibacterial host defense against bacterial pneumoniaQianqian Tu0Xiaoyan Yu1Wei Xie2Yetao Luo3Hong Tang4Kai Chen5Yanting Ruan6Yue Li7Jie Zhou8Yibing Yin9Dapeng Chen10Zhixin Song11Department of Clinical Laboratory, Children's Hospital of Chongqing Medical University; National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University. Chongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China; Department of Laboratory Medicine, Key Laboratory of Diagnostic Medicine, Chongqing Medical University, Chongqing, ChinaDepartment of Clinical Laboratory, Children's Hospital of Chongqing Medical University; National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University. Chongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, ChinaDepartment of Clinical Laboratory, Children's Hospital of Chongqing Medical University; National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University. Chongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, ChinaDepartment of Nosocomial Infection Control, Second affiliated Hospital, Army Medical University, Chongqing, ChinaDepartment of Critical Care Medicine, Department of Surgical Intensive Care Unit, the First Affiliated Hospital of Chongqing Medical University, Chongqing, ChinaDepartment of Laboratory Medicine, Key Laboratory of Diagnostic Medicine, Chongqing Medical University, Chongqing, ChinaDepartment of Clinical Laboratory, Children's Hospital of Chongqing Medical University; National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University. Chongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, ChinaMolecular Medicine and Cancer Research Center, College of Basic Medical Sciences, Chongqing Medical University, Chongqing, ChinaDepartment of Clinical Laboratory, Children's Hospital of Chongqing Medical University; National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University. Chongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, ChinaDepartment of Laboratory Medicine, Key Laboratory of Diagnostic Medicine, Chongqing Medical University, Chongqing, ChinaDepartment of Clinical Laboratory, Children's Hospital of Chongqing Medical University; National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University. Chongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China; Corresponding authors: Department of Clinical Laboratory, Children's Hospital of Chongqing Medical University; NO 136 Zhongshaner Road, Yuzhong District, Chongqing, 400014, P.R. China; Tel: +86-023-63633384Department of Clinical Laboratory, Children's Hospital of Chongqing Medical University; National Clinical Research Center for Child Health and Disorders, Children's Hospital of Chongqing Medical University; Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital of Chongqing Medical University. Chongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China; Corresponding authors: Department of Clinical Laboratory, Children's Hospital of Chongqing Medical University; NO 136 Zhongshaner Road, Yuzhong District, Chongqing, 400014, P.R. China; Tel: +86-023-63633384ABSTRACT: Objectives: Bacterial pneumonia is a common serious infectious disease with high morbidity and mortality. Prokineticin 2 (PK2) has recently been identified as a novel immunomodulator in a variety of diseases; however, its role in bacterial pneumonia remains unclear. Methods: The levels of PK2 were measured and analyzed in patients with pneumonia and healthy controls. The effects of PK2 on the host response to pneumonia were evaluated by in vivo animal experiments and in vitro cell experiments. Results: PK2 levels dramatically decreased in patients with pneumonia compared with healthy controls, and PK2 levels were lower in patients with severe pneumonia than in pneumonia. In a mouse model of bacterial pneumonia, transtracheal administration of recombinant PK2 significantly alleviated lung injury and improved the survival, which was associated with increased host's bacterial clearance capacity, as manifested by decreased pulmonary bacterial loads. PK2 enhanced the chemotaxis, phagocytosis, and killing ability of macrophages, whereas the protective efficacy of PK2 was abolished after macrophage depletion. Conclusion: Impaired alveolar macrophage function caused by decreased PK2 is a new endogenous cause of the occurrence and development of bacterial pneumonia. The administration of recombinant PK2 may be a potential adjuvant therapy for bacterial pneumonia.http://www.sciencedirect.com/science/article/pii/S1201971222005410Prokineticin 2PneumoniaImmune protectionMacrophages |
| spellingShingle | Qianqian Tu Xiaoyan Yu Wei Xie Yetao Luo Hong Tang Kai Chen Yanting Ruan Yue Li Jie Zhou Yibing Yin Dapeng Chen Zhixin Song Prokineticin 2 promotes macrophages-mediated antibacterial host defense against bacterial pneumonia International Journal of Infectious Diseases Prokineticin 2 Pneumonia Immune protection Macrophages |
| title | Prokineticin 2 promotes macrophages-mediated antibacterial host defense against bacterial pneumonia |
| title_full | Prokineticin 2 promotes macrophages-mediated antibacterial host defense against bacterial pneumonia |
| title_fullStr | Prokineticin 2 promotes macrophages-mediated antibacterial host defense against bacterial pneumonia |
| title_full_unstemmed | Prokineticin 2 promotes macrophages-mediated antibacterial host defense against bacterial pneumonia |
| title_short | Prokineticin 2 promotes macrophages-mediated antibacterial host defense against bacterial pneumonia |
| title_sort | prokineticin 2 promotes macrophages mediated antibacterial host defense against bacterial pneumonia |
| topic | Prokineticin 2 Pneumonia Immune protection Macrophages |
| url | http://www.sciencedirect.com/science/article/pii/S1201971222005410 |
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