摘要
SARS作为急性呼吸道传染病,其肺损伤的早期与急性呼吸窘迫综合征(ARDS)有关,后期表现为肺纤维化。患者体内免疫防御机制可出现什对SARS病毒的过度激活,造成肺部白细胞免疫炎性损伤。粘附分子及其介导的白细胞粘附可能参与了SARS的急性肺损伤。设想在病毒感染早期,通过抗粘附免疫调节,抑制患者过激的免疫防御机制,阻抑活化白细胞的粘附级联反应,进而减轻肺损伤;以减轻或延缓病变的进一步发展。
Severe acute respiratory syndrome(SARS) , known as acute respiratory contagion, can induce lung injury relating to acute respiratory distress syndrome(ARDS) in earlier period, and lung fibrosis in later period. During its progression, there has been immune defence overactivity followed by leukocytic immune damage. Adhesion molecules mediating cell-cell adhesion plays a key role in SARS acute lung injury. The lung injury might be reduced by blocking the overactivated immune defence reaction and leukocytic adhesion cascades with anti-adhesion immunotherapy in earlier stage of this disease.
出处
《生命科学》
CSCD
2003年第3期134-136,188,共4页
Chinese Bulletin of Life Sciences