Abstract
Acute lung injury (ALI) is an acute inflammatory disease. Leukocyte immunoglobulin-like receptor B4 (LILRB4) is an immunoreceptor tyrosine-based inhibitory motif (ITIM)-bearing inhibitory receptor that is implicated in various pathological processes. However, the function of LILRB4 in ALI remains largely unknown. The aim of the present study was to explore the role of LILRB4 in ALI. LILRB4 knockout mice (LILRB4 KO) were used to construct a model of ALI. Bone marrow cell transplantation was used to identify the cell source of the LILRB4 deficiency-aggravated inflammatory response in ALI. The effect on ALI was analyzed by pathological and molecular analyses. Our results indicated that LILRB4 KO exacerbated ALI triggered by LPS. Additionally, LILRB4 deficiency can enhance lung inflammation. According to the results of our bone marrow transplant model, LILRB4 regulates the occurrence and development of ALI by bone marrow-derived macrophages (BMDMs) rather than by stromal cells in the lung. The observed inflammation was mainly due to BMDM-induced NF-κB signaling. In conclusion, our study demonstrates that LILRB4 deficiency plays a detrimental role in ALI-associated BMDM activation by prompting the NF-κB signal pathway.
Highlights
Acute lung injury (ALI) is a serious respiratory illness with a high mortality
In the present study, using Leukocyte immunoglobulin-like receptor B4 (LILRB4) knockout mice (LILRB4 KO), we found that the LILRB4 expression was up-regulated in our model of ALI, and LILRB4 deficiency enhanced the inflammatory response in ALI
The HE stain showed more inflammatory cell infiltration and tissue damage in the lung tissue from the mice treated with LPS (Figure 1B).CD31 was used as a marker of vascular endothelial cells and the immunofluorescence staining showed that the structure of endothelial cells was destroyed significantly compared with sham group (Figure 1C)
Summary
Acute lung injury (ALI) is a serious respiratory illness with a high mortality It results in acute diffuse inflammatory lung tissue injury that is caused by various pathogenic factors [1]; the pathogenesis of ALI has not been fully characterized [2]. The inflammatory cytokines and chemokines can recruit neutrophils and other inflammatory cells to further release inflammatory factors and cytokines that promote inflammation in the lungs. Harmful molecules, such as proteolytic enzymes and reactive oxygen species, damage pulmonary capillary endothelial cells and alveolar epithelial cells, leading to the development of ALI. It is important to discover new targets to treat inflammation in ALI
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