Chen Guoqian, Chen Da-Zhi, Li Jianhua, Czura Christopher J, Tracey Kevin J, Sama Andrew E, Wang Haichao
Department of Emergency Medicine, North Shore University Hospital, New York University School of Medicine, Manhasset, NY 11030, USA.
Med Hypotheses. 2004;63(4):691-5. doi: 10.1016/j.mehy.2004.01.037.
High mobility group box 1 protein (HMGB1) is released by necrotic cells or activated macrophages/monocytes, and functions as a late mediator of lethal systemic and local pulmonary inflammation. Passive immunization with anti-HMGB1 antibodies confers significant protection against lethal endotoxemia, sepsis, and acute lung injury, even when antibodies are administered after the onset of these diseases. In light of observations that three Chinese herbal formulations recommended for treatment of severe acute respiratory syndrome (SARS) specifically inhibited the release of HMGB1 from innate immune cells, we hypothesize that HMGB1 might occupy a pathogenic role in SARS by mediating an injurious pulmonary inflammatory response.
高迁移率族蛋白B1(HMGB1)由坏死细胞或活化的巨噬细胞/单核细胞释放,作为致死性全身和局部肺部炎症的晚期介质发挥作用。用抗HMGB1抗体进行被动免疫可显著保护机体免受致死性内毒素血症、败血症和急性肺损伤,即使在这些疾病发作后给予抗体也有效。鉴于有观察表明,三种推荐用于治疗严重急性呼吸综合征(SARS)的中药配方可特异性抑制先天免疫细胞释放HMGB1,我们推测HMGB1可能通过介导有害的肺部炎症反应在SARS中起致病作用。