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PM2.5 Promotes Macrophage-Mediated Inflammatory Response Through Airway Epithelial Cell-Derived Exosomal miR-155-5p
1The First School of Clinical Medicine, Lanzhou University, Lanzhou, Gansu, People's Republic of China.
Background:
Airway epithelial cells (AECs) and alveolar macrophages are involved in airway inflammation. The direct effects of atmospheric fine-particulate-matter (PM2.5) on airway cells, such as AECs and alveolar macrophages, have been widely investigated, but the effect of cell-cell interaction on inflammatory response remains unclear. Exosomes play a crucial role in intercellular communication. However, the cellular interaction of exosomes in PM2.5-induced airway inflammation is unclear.
Methods:
The PM2.5-induced human bronchial epithelial (BEAS-2B) cells and phorbol 12-myristate 13-acetate-induced macrophages (Mφ) were co-cultured and then the expression of IL-6, IL-1β, TNF-α and miRNA-155-5p were detected. Exosomes from PM2.5-exposed BEAS-2B cells were then co-cultured with Mφ to detect the expression of miR-155-5p and inflammatory cytokines, as well as cytokine signaling inhibitor-1 (SOCS1)/NFκB, and to detect the effect of the exosome inhibitor GW4869.
Results:
After the co-culture of PM2.5-induced BEAS-2B cells and Mφ, the expression of Mφ-derived IL-6, IL-1β, and TNF-α, as well as miRNA-155-5p were upregulated. The expression of miRNA-155-5p was upregulated in BEAS-2B and BEAS-2B cell-derived exosomes after exposure to PM2.5. Furthermore, co-culturing exosomes derived from PM2.5-exposed BEAS-2B cells with Mφ, upregulated miR-155-5p and inflammatory cytokines, decreased cytokine signaling inhibitor-1 (SOCS1) expression, and activated NF-κB. In addition, adding exosome inhibitor GW4869 to PM2.5-interfered BEAS-2B cells co-culture with Mφ downregulated miRNA-155-5p expression, inhibited NF-κB, and reduced the levels of inflammatory factors.
Conclusion:
PM2.5 promotes Mφ inflammation by upregulating miRNA-155-5P in exosomes obtained from BEAS-2B cells through miR-155-5P/SOCS1/NF-κB pathway. Exosomal miRNAs mediate cellular communication between BEAS-2B cells and Mφ, which may be a new mechanism of PM2.5-stimulated pulmonary inflammatory response.
Insights
Fine particulate matter (PM2.5) exposure increases airway inflammation by promoting macrophage activation via exosomes. These exosomes transfer microRNA-155-5p from bronchial epithelial cells to macrophages, activating the miR-155-5p/SOCS1/NF-κB pathway and exacerbating inflammation.
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Environmental Health
Background:
- Airway epithelial cells (AECs) and alveolar macrophages are key players in airway inflammation.
- While PM2.5 effects on individual cells are studied, cell-cell interactions in PM2.5-induced inflammation are unclear.
- Exosomes mediate intercellular communication, but their role in PM2.5-induced airway inflammation is not well understood.
Purpose of the Study:
- To investigate the role of exosomes in PM2.5-induced airway inflammation.
- To elucidate the mechanism of intercellular communication between airway epithelial cells and macrophages mediated by exosomes.
- To determine the specific molecular pathways involved in PM2.5-induced inflammation.
Main Methods:
- Co-culture of PM2.5-exposed human bronchial epithelial cells (BEAS-2B) with macrophages (Mφ).
- Detection of inflammatory cytokines (IL-6, IL-1β, TNF-α) and miRNA-155-5p expression.
- Co-culture of exosomes from PM2.5-exposed BEAS-2B cells with Mφ, assessing miR-155-5p, inflammatory cytokines, SOCS1/NF-κB signaling, and the effect of exosome inhibitor GW4869.
Main Results:
- PM2.5 exposure upregulated Mφ-derived IL-6, IL-1β, TNF-α, and miRNA-155-5p.
- PM2.5 increased miRNA-155-5p in BEAS-2B cells and their exosomes.
- Exosomes from PM2.5-exposed BEAS-2B cells upregulated miR-155-5p and inflammation in Mφ, decreasing SOCS1 and activating NF-κB; GW4869 inhibited these effects.
Conclusions:
- PM2.5 promotes Mφ inflammation via exosomes from BEAS-2B cells, mediated by the miR-155-5P/SOCS1/NF-κB pathway.
- Exosomal miRNAs facilitate intercellular communication between BEAS-2B cells and Mφ.
- This exosome-mediated pathway represents a novel mechanism in PM2.5-induced pulmonary inflammation.
