Apolipoprotein A-I diminishes acute lung injury and sepsis in mice induced by lipoteichoic acid

作者：Jiao Yan ling; Wu Man Ping^*

来源：Cytokine, 2008, 43(1): 83-87.

DOI：10.1016/j.cyto.2008.04.002

• apolipoprotein A-I (ApoA-I)
• lipotechoic acid (LTA)
• acute lung injury
• cytokines
• sepsis

Lipoteichoic acid (LTA), as a primary immunostimulus, triggers the systematic inflammatory responses. Our hypothesis is that ApoA-I can neutralize LTA toxicity, like its effect on LPS. BALB/c mice were challenged with LTA, followed by human ApoA-I administration. We found that ApoA-I could attenuate LTA-induced acute lung injury and inflammation and significantly inhibit LTA-induced IL-1 beta and TNF-alpha accumulation in the serum (P < 0.01 and P < 0.05, respectively), as well as in bronchoalveolar lavage (BAL) fluid (P < 0.01 and P < 0.05, respectively). Moreover, ApoA-I could significantly reduce the L-929 cell mortality caused by LTA-activated macrophages in a dose-dependent fashion. Furthermore, ApoA-I treatment could diminish LTA-mediated NF(B kappa) nuclear translocation in macrophages. An in vitro binding assay indicated that ApoA-I can bind LTA. These results clearly indicated that ApoA-I can effectively protect against LTA-induced sepsis and acute lung damage. The mechanism might be related to the binding and neutralization of LTA.

• 出版日期2008-7
• 单位复旦大学