AI Article Synopsis
- Cigarette smoking is a major cause of death globally and has been shown to increase the infectivity of Streptococcus pneumoniae, a harmful bacteria that often affects the respiratory system.
- This study utilized cigarette smoke extract (CSE) to examine how it impacts the innate immune response, specifically in mouse macrophage models.
- Findings revealed that CSE exposure reduces the production of key immune signaling molecules and disrupts macrophage functions, ultimately weakening the body's defense against pneumococcal infections.
Article Abstract
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.
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| http://dx.doi.org/10.1016/j.jmii.2024.10.001 | DOI Listing |
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