Phagosome–lysosome (P–L) fusion is one of the central immune-effector responses of host. It is known that phagosome maturation process is associated with numerous signaling cascades and among these, important role of calcium (Ca²⁺) signaling has been realized recently. Ca²⁺ plays key roles in actin rearrangement, activation of NADPH oxidase and protein kinase C (PKC). Involvement of Ca²⁺ in these cellular processes directs phagosomal maturation process. Some of the intracellular pathogens have acquired the strategies to modulate Ca²⁺ associated pathways to block P–L fusion process. In this review we have described the mechanism of Ca²⁺ signals that influence P–L fusion by controlling ROS, actin and PKC signaling cascades. We have also discussed the strategies implemented by the intracellular pathogens to manipulate Ca²⁺ signaling to consequently subvert P–L fusion. A detail study of factors associated in manipulating Ca²⁺ signaling may provide new insights for the development of therapeutic tools for more effective treatment options against infectious diseases.

吞噬体-溶酶体（PL）融合是宿主的主要免疫效应反应之一。众所周知，吞噬体的成熟过程与许多信号级联有关，其中，钙（Ca ²⁺）信号的重要作用最近已经实现。Ca ²⁺在肌动蛋白重排，NADPH氧化酶激活和蛋白激酶C（PKC）中起关键作用。Ca ²⁺参与这些细胞过程指导吞噬体成熟过程。一些细胞内病原体已经获得了调节Ca ²⁺相关途径以阻断P–L融合过程的策略。在这篇综述中，我们描述了Ca ²⁺的机制通过控制ROS，肌动蛋白和PKC信号级联反应影响PL融合的信号。我们还讨论了细胞内病原体实施的操纵Ca ²⁺信号传导从而破坏P–L融合的策略。有关操纵Ca ²⁺信号传导的因素的详细研究可能会为开发针对感染性疾病的更有效治疗选择的治疗工具提供新的见解。