PGLYRP1/Tag-7/PGRP-S is one of mammalian peptidoglycan recognition proteins (PGRPs). Here, we demonstrate that human recombinant PGLYRP1/Tag-7/PGRP-S potentiates the response of murine macrophage-like ANA-1 cells and human macrophages to facultative intracellular pathogen Listeria monocytogenes. PGLYRP1/Tag-7/PGRP-S binds to the surface of L. monocytogenes and other bacterial cells but has no effect on their growth in culture. While PGLYRP1/Tag-7/PGRP-S treatment modestly enhanced phagocytosis of bacteria by ANA-1 cells, the intracellular survival of PGLYRP1/Tag-7/PGRP-S treated L. monocytogenes was strongly inhibited 2 h after internalization. PGLYRP1/Tag-7/PGRP-S treatment of bacteria boosted oxidative burst induction and increased the level of proinflammatory cytokine IL-6 produced by ANA-1, however, these effects happened too late to be responsible for decreased intracellular survival of bacteria. Our results thus suggest that PGLYRP1/Tag-7/PGRP-S acts as a molecular sensor for detection of L. monocytogenes infection of mammalian cells that leads to increased killing through a mechanism(s) that remains to be defined.

PGLYRP1 / Tag-7 / PGRP-S是哺乳动物肽聚糖识别蛋白（PGRP）之一。在这里，我们证明了人类重组PGLYRP1 / Tag-7 / PGRP-S增强了鼠巨噬细胞样ANA-1细胞和人类巨噬细胞对兼性细胞内病原体的反应李斯特菌。PGLYRP1 / Tag-7 / PGRP-S结合到单核细胞增生李斯特菌和其他细菌细胞，但对其培养没有影响。尽管PGLYRP1 / Tag-7 / PGRP-S处理适度增强了ANA-1细胞的吞噬作用，但PGLYRP1 / Tag-7 / PGRP-S处理后的细胞内存活率单核细胞增生李斯特菌内化2小时后，其被强烈抑制。PGLYRP1 / Tag-7 / PGRP-S对细菌的处理增强了氧化爆发诱导并增加了ANA-1产生的促炎性细胞因子IL-6的水平，但是，这些作用发生得太晚了，无法减少细菌的细胞内存活。因此，我们的结果表明PGLYRP1 / Tag-7 / PGRP-S充当分子传感器来检测单核细胞增生李斯特菌 通过尚待确定的一种或多种机制导致哺乳动物细胞杀伤的增加。