Department of Rheumatology, School of Medicine, Collegium Medicum, University of Warmia and Mazury, 10-900 Olsztyn, Poland.
Department of Pediatrics, Faculty of Medicine and Health Sciences, Andrzej Frycz Modrzewski Kraków University, 30-705 Kraków, Poland.
Int J Mol Sci. 2022 Feb 23;23(5):2433. doi: 10.3390/ijms23052433.
Macrophage activation syndrome (MAS) is one of the few entities in rheumatology with the potential to quickly cause multiple organ failure and loss of life, and as such, requires urgent clinical intervention. It has a broad symptomatology, depending on the organs it affects. One especially dangerous aspect of MAS's course of illness is myocarditis leading to acute heart failure and possibly death. Research in recent years has proved that macrophages settled in different organs are not a homogenous group, with particular populations differing in both structure and function. Within the heart, we can determine two major groups, based on the presence of the C-C 2 chemokine receptor (CCR2): CCR2+ and CCR2-. There are a number of studies describing their function and the changes in the population makeup between normal conditions and different illnesses; however, to our knowledge, there has not been one touching on the matter of changes occurring in the populations of heart macrophages during MAS and their possible consequences. This review summarizes the most recent knowledge on heart macrophages, the influence of select cytokines (those particularly significant in the development of MAS) on their activity, and both the immediate and long-term consequences of changes in the makeup of specific macrophage populations-especially the loss of CCR2- cells that are responsible for regenerative processes, as well as the substitution of tissue macrophages by the highly proinflammatory CCR2+ macrophages originating from circulating monocytes. Understanding the significance of these processes may lead to new discoveries that could improve the therapeutic methods in the treatment of MAS.
巨噬细胞活化综合征 (MAS) 是风湿病学中少数几个有潜力导致多器官衰竭和死亡的实体之一，因此需要紧急临床干预。它的症状广泛，取决于受影响的器官。MAS 病程的一个特别危险的方面是心肌炎导致急性心力衰竭和可能死亡。近年来的研究证明，定居在不同器官中的巨噬细胞不是一个同质群体，其结构和功能在特定人群中存在差异。在心脏中，我们可以根据 C-C 2 趋化因子受体 (CCR2) 的存在确定两个主要群体：CCR2+和 CCR2-。有许多研究描述了它们的功能以及在正常条件和不同疾病之间群体组成的变化；然而，据我们所知，还没有一项研究涉及 MAS 期间心脏巨噬细胞群体变化及其可能后果的问题。这篇综述总结了心脏巨噬细胞的最新知识，选择细胞因子（特别是在 MAS 发展中起重要作用的细胞因子）对其活性的影响，以及特定巨噬细胞群体组成变化的直接和长期后果，特别是负责再生过程的 CCR2-细胞的丧失，以及起源于循环单核细胞的高度促炎 CCR2+巨噬细胞取代组织巨噬细胞。了解这些过程的意义可能会导致新的发现，从而改善 MAS 的治疗方法。
