The effect of extracellular ATP on LPS-induced endotoxin shock in mice.

细胞外的三磷酸腺苷能在多种细胞类型(如巨噬细胞、T细胞)和组织中引起免疫反应。然而，目前尚不清楚这种由ATP激活的巨噬细胞是否调节了对实际组织损伤的免疫反应的幅度。因此，我们研究了三磷酸腺苷介导的巨噬细胞炎症反应在内毒素休克中的作用。这项研究表明，细胞外的ATP与巨噬细胞上的P_2嘌呤能受体结合，通过产生MIP-2来增加中性粒细胞的渗透。然而，在这条通路中，由于具有多种类型的P_2嘌呤能受体是相关的，因此还需要进一步的研究。

Extracellular ATP leads to immune responses in a wide spectrum of cell types (e.g., macrophages, T cells) and tissues. However, it remains unclear whether such ATP-activated macrophages modulate the magnitude of immune responses to actual tissue injury. Thus, we investigated the role of ATP-mediated inflammatory response by macrophages in LPS-induced endotoxin shock. This study indicated that the binding of extracellular ATP to P2purinergic receptors on macrophages increases neutrophil infiltration via the production of MIP-2. However, in this pathway, further examination was required because P2purinergic receptor of the having many kinds was related.