Cigarette smoke compromises macrophage innate sensing in response to pneumococcal infection
Background: Cigarette smoking remains a leading cause of mortality worldwide. Streptococcus pneumoniae, also known as pneumococcus, is one of the most common pathogens that colonizes the human respiratory tract, causing life-threatening infections. Several studies have reported that cigarette smoke...
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Elsevier
2025-02-01
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| Series: | Journal of Microbiology, Immunology and Infection |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S1684118224001865 |
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| author | Wei-Chih Liao Chia-Huei Chou Mao-Wang Ho Jo-Tsen Chen Shu-Ling Chou Yu-Tsen Huang Ngoc-Niem Bui Hui-Yu Wu Chi-Fan Lee Wei-Chien Huang Chih-Ho Lai |
| author_facet | Wei-Chih Liao Chia-Huei Chou Mao-Wang Ho Jo-Tsen Chen Shu-Ling Chou Yu-Tsen Huang Ngoc-Niem Bui Hui-Yu Wu Chi-Fan Lee Wei-Chien Huang Chih-Ho Lai |
| author_sort | Wei-Chih Liao |
| collection | DOAJ |
| description | Background: Cigarette smoking remains a leading cause of mortality worldwide. Streptococcus pneumoniae, also known as pneumococcus, is one of the most common pathogens that colonizes the human respiratory tract, causing life-threatening infections. Several studies have reported that cigarette smoke (CS) exposure promotes pneumococcal infectivity; however, the underlying mechanisms remain to be illustrated. Methods: In this study, we prepared cigarette smoke extract (CSE) from tobacco containing nicotine (0.8 mg/cigarette) and tar (10 mg/cigarette) to investigate the effects of CSE on innate immune response using murine macrophage models. Results: The results from the cytokine array showed that the production of C-C Motif Chemokine Ligand 2 (CCL2), CCL4, CCL3, C-X-C Motif Chemokine Ligand 2 (CXCL2), and CXCL-10, in pneumococcus-infected cells was reduced upon 5 % CSE treatment. Our results further demonstrated that 5 % CSE exposure, followed by pneumococcal challenge, significantly decreased CCL2 and type I interferon (IFN) production in macrophages by inhibiting nuclear factor (NF)-κB and IFN regulatory factor 3 (IRF3) signaling pathways. Moreover, CSE disrupts macrophage polarization and impedes innate immune signaling to suppress pneumococcal phagocytosis by macrophages. Conclusion: Our results provide evidence that CS manipulates the signaling molecules to subvert macrophage functions, thereby hindering the innate response against pneumococcal infection. |
| format | Article |
| id | doaj-art-b18df428d35441d2b34b071a86b4a42c |
| institution | Kabale University |
| issn | 1684-1182 |
| language | English |
| publishDate | 2025-02-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Microbiology, Immunology and Infection |
| spelling | doaj-art-b18df428d35441d2b34b071a86b4a42c2025-02-06T05:11:20ZengElsevierJournal of Microbiology, Immunology and Infection1684-11822025-02-01581120127Cigarette smoke compromises macrophage innate sensing in response to pneumococcal infectionWei-Chih Liao0Chia-Huei Chou1Mao-Wang Ho2Jo-Tsen Chen3Shu-Ling Chou4Yu-Tsen Huang5Ngoc-Niem Bui6Hui-Yu Wu7Chi-Fan Lee8Wei-Chien Huang9Chih-Ho Lai10Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan; Center for Hyperbaric Oxygenation Therapy, China Medical University Hospital, Taichung, Taiwan; School of Medicine, China Medical University, Taichung, TaiwanSchool of Medicine, China Medical University, Taichung, Taiwan; Departments of Infectious Disease, China Medical University Hospital, Taichung, TaiwanSchool of Medicine, China Medical University, Taichung, Taiwan; Departments of Infectious Disease, China Medical University Hospital, Taichung, TaiwanGraduate Institute of Biomedical Sciences, Department of Microbiology and Immunology, Chang Gung University, Taoyuan, Taiwan; Department of Laboratory Medicine, Molecular Infectious Disease Research Center, Chang Gung Memorial Hospital, Linkou, TaiwanDepartment of Laboratory Medicine, Taichung Veterans General Hospital Chiayi Branch, Chiayi, TaiwanGraduate Institute of Biomedical Sciences, Department of Microbiology and Immunology, Chang Gung University, Taoyuan, TaiwanGraduate Institute of Biomedical Sciences, Department of Microbiology and Immunology, Chang Gung University, Taoyuan, Taiwan; Faculty of Medicine, Can Tho University of Medicine and Pharmacy, Can Tho, Viet NamGraduate Institute of Biomedical Sciences, Department of Microbiology and Immunology, Chang Gung University, Taoyuan, TaiwanGraduate Institute of Biomedical Sciences, Drug Development Center, China Medical University, Taichung, TaiwanGraduate Institute of Biomedical Sciences, Drug Development Center, China Medical University, Taichung, Taiwan; Center for Molecular Medicine, China Medical University Hospital, Taichung, Taiwan; Corresponding author. Graduate Institute of Biomedical Sciences, Drug Development Center, China Medical University, Taichung, Taiwan.School of Medicine, China Medical University, Taichung, Taiwan; Graduate Institute of Biomedical Sciences, Department of Microbiology and Immunology, Chang Gung University, Taoyuan, Taiwan; Department of Laboratory Medicine, Molecular Infectious Disease Research Center, Chang Gung Memorial Hospital, Linkou, Taiwan; Department of Nursing, Asia University, Taichung, Taiwan; Research Center for Emerging Viral Infections, Chang Gung University, Taoyuan, Taiwan; Corresponding author. Department of Microbiology and Immunology, Chang Gung University, Taiwan.Background: Cigarette smoking remains a leading cause of mortality worldwide. Streptococcus pneumoniae, also known as pneumococcus, is one of the most common pathogens that colonizes the human respiratory tract, causing life-threatening infections. Several studies have reported that cigarette smoke (CS) exposure promotes pneumococcal infectivity; however, the underlying mechanisms remain to be illustrated. Methods: In this study, we prepared cigarette smoke extract (CSE) from tobacco containing nicotine (0.8 mg/cigarette) and tar (10 mg/cigarette) to investigate the effects of CSE on innate immune response using murine macrophage models. Results: The results from the cytokine array showed that the production of C-C Motif Chemokine Ligand 2 (CCL2), CCL4, CCL3, C-X-C Motif Chemokine Ligand 2 (CXCL2), and CXCL-10, in pneumococcus-infected cells was reduced upon 5 % CSE treatment. Our results further demonstrated that 5 % CSE exposure, followed by pneumococcal challenge, significantly decreased CCL2 and type I interferon (IFN) production in macrophages by inhibiting nuclear factor (NF)-κB and IFN regulatory factor 3 (IRF3) signaling pathways. Moreover, CSE disrupts macrophage polarization and impedes innate immune signaling to suppress pneumococcal phagocytosis by macrophages. Conclusion: Our results provide evidence that CS manipulates the signaling molecules to subvert macrophage functions, thereby hindering the innate response against pneumococcal infection.http://www.sciencedirect.com/science/article/pii/S1684118224001865Cigarette smokePneumococcusMacrophageCytokineInflammation |
| spellingShingle | Wei-Chih Liao Chia-Huei Chou Mao-Wang Ho Jo-Tsen Chen Shu-Ling Chou Yu-Tsen Huang Ngoc-Niem Bui Hui-Yu Wu Chi-Fan Lee Wei-Chien Huang Chih-Ho Lai Cigarette smoke compromises macrophage innate sensing in response to pneumococcal infection Journal of Microbiology, Immunology and Infection Cigarette smoke Pneumococcus Macrophage Cytokine Inflammation |
| title | Cigarette smoke compromises macrophage innate sensing in response to pneumococcal infection |
| title_full | Cigarette smoke compromises macrophage innate sensing in response to pneumococcal infection |
| title_fullStr | Cigarette smoke compromises macrophage innate sensing in response to pneumococcal infection |
| title_full_unstemmed | Cigarette smoke compromises macrophage innate sensing in response to pneumococcal infection |
| title_short | Cigarette smoke compromises macrophage innate sensing in response to pneumococcal infection |
| title_sort | cigarette smoke compromises macrophage innate sensing in response to pneumococcal infection |
| topic | Cigarette smoke Pneumococcus Macrophage Cytokine Inflammation |
| url | http://www.sciencedirect.com/science/article/pii/S1684118224001865 |
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