Impact of autophagy on LMPs-induced airway inflammation in C57/BL6 mice

Objectives: The impacts of LMPs and autophagy on the development of chronic obstructive pulmonary disease and the corresponding mechanism were investigated with the constructed C57/BL6 mouse airway inflammation model. Methods: LMPs were produced by human T lymphocyte leukemia cell line 6T-CEM stimulated by actinomycin D and identified by flow cytometry, and then used to induce C57/BL6 mice in various concentrations and induction times. The optimum induction conditions were determined via the detection of IL-1 beta and IL-18 in bronchoalveolar lavage fluid of the mice, and the inflammation response was confirmed via HE staining on the lung tissues, whereby the C57/BL6 mouse airway inflammation model was constructed. The impacts of LMPs and autophagy on the development of COPD and the corresponding mechanism were investigated through the detection of the mRNA and protein expression of TLR4, PI3K, AKT, LC-3, NLRP3, caspase-1, etc. in the lung tissues of the mice. Results: The C57/BL6 mouse airway inflammation model was successfully constructed with the optimum induction concentration of LMPs of 50 mu g/ml and the optimum induction time of 24 h. In the lung tissues of the mice, the mRNA and protein expressions of TLR4, PI3K, AKT, NLRP3 and caspase-1 were up-regulated to varying degrees except LC-3. Conclusions: NLRP3 is a key protein in LMPs-induced airway inflammation. Autophagy negatively regulates the activation of NLRP3 inflammasomes.