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In normal human lung tissue, only alveolar macrophages synthesize and secrete HMGB1. However, HMGB1 expression levels were significantly higher in inflammatory cells and injured epithelial nuclei in patients with idiopathic pulmonary fibrosis and allergic pneumonia. The HMGB1 polyclonal antibody or A-box protein could improve the acute lung injury induced by lipopolysaccharide and reduce the pulmonary edema and inflammation caused by hyperoxia response. HMGB1 can also reduce bleeding-induced proinflammatory cytokines and neutrophil aggregation and inhibit bleomycin-induced lung injury in mice with pulmonary fibrosi. Recently, a number of studies have shown that ethyl pyruvate can also reduce the level of HMGB1 expression, reduce airway neutrophil infiltration, thereby reducing hyperoxia-induced lung injury in mice model or asthma model of lung injury. Thus, HMGB1 is involved in a variety of respiratory diseases such as pulmonary fibrosis, acute lung injury, chronic obstructive pulmonary disease, pneumonia and other pathophysiological processes, the application of the corresponding antagonist or antibody intervention in its pathological process is expected for its clinical application to provide theoretical basis.
EnglertJM, KlimentCR, RamsgaardL, et al. Paradoxical function for the receptor for advanced glycation end products in mouse models of pulmonary fibrosis. Int J Clin Exp Pathol, 2011,4(3):241–254.
This study confirms paradoxical responses to two different models of pulmonary fibrosis and suggests a further role for RAGE in cellular migration.