The triggering receptor expressed by myeloid cells-1 activates TLR4-MyD88-NF-κB-dependent signaling to aggravate ventilation-induced lung inflammation and injury in mice
| Autor: | Xiao-Xia Wang, Deng-Ge Pang, Bijun Luo, Yan-Yan Lu, Jian-Lan Mo, Jianqiu Zheng, Hui Huang, Ji-Feng Feng |
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| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Histology Myeloid business.industry medicine.medical_treatment Inflammation NF-κB Cell Biology respiratory system Lung injury respiratory tract diseases Pathology and Forensic Medicine 03 medical and health sciences chemistry.chemical_compound 030104 developmental biology medicine.anatomical_structure Cytokine chemistry medicine TLR4 Cancer research Myeloid Differentiation Factor 88 medicine.symptom Receptor business |
| Zdroj: | Cell and Tissue Research. 374:137-148 |
| ISSN: | 1432-0878 0302-766X |
| Popis: | The triggering receptor expressed by myeloid cells-1 (TREM-1) plays an important role in infectious and autoimmune diseases but how it contributes to ventilation-induced lung injury (VILI) and inflammation is unclear. Here, we examine the possibility that TREM-1 activates signaling dependent on Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (Myd88) and nuclear factor (NF)-κB, which leads in turn to VILI. In a mouse model of VILI, which we validated based on lung edema and histopathology as well as cytokine levels, we examine mRNA and protein levels of TREM-1, TLR4, MyD88, NF-κB and its inhibitory protein I-κB in animals subjected to ventilation at normal or high tidal volume. The extent of lung edema, injury and inflammation were higher in the high tidal volume animals, as were the expression levels of all proteins examined. Treatment with TREM-1 agonist aggravated these effects, whereas treatment with TREM-1 antagonist attenuated them. Our results suggest that aggravation of VILI by TREM-1 in mice may be associated with TLR4-MyD88-NF-κB-dependent signaling. |
| Databáze: | OpenAIRE |
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