Low doses of lipopolysaccharide cause chronic inflammation in mice with chronic lung injury: specific roles for AMPK α2 knockout

Abstract

Abstract Background Chronic inflammation leads to the activation of inflammatory signaling pathways, cause a long-term vicious cycle of inflammation. It exacerbates tissue and cellular damage in the body, especially in the lungs. Long-term treatment of Lipopolysaccharide (LPS) can cause this systemic chronic inflammation. It was recently proposed that 5’-AMP-activated kinase (AMPK), as an energy sensor, which regulates metabolic pathways and the response to cell stress. AMPK consists of three subunits containing α, β and γ subunits. Rare reports have been made regarding the role of AMPK α2 as a catalytic subunit of AMPK in lung injury caused by LPS. Methods Experimental validation was performed using mouse lung sections. HE staining was used to detect pathological and microstructural changes. Western blot, immunofluorescence, and enzyme-linked immunosorbent assay were used to evaluate protein expression. Results The structural alterations of the lung tissue in the AMPK α2 knockout group were noticeably better than those in the LPS group. IL-1, IL-6, IL-18, and TNF-α were all significantly lowered as well. Additionally, after AMPK α2 knockout, M-CSF, a marker of macrophage differentiation, was remarkable decreased. The relative levels of M2 type macrophage were significantly increased. Conclusion The results showed that AMPK α2 knockout reduces chronic inflammatory damage in the lung caused by LPS. This effect may be achieved by promoting macrophage differentiation into M2 type.