The role of peripheral monocytes and macrophages in ischemic stroke
- PDF / 803,960 Bytes
- 19 Pages / 595.276 x 790.866 pts Page_size
- 26 Downloads / 228 Views
REVIEW ARTICLE
The role of peripheral monocytes and macrophages in ischemic stroke Dong Han 1 & Hang Liu 1 & Yan Gao 1 Received: 13 July 2020 / Accepted: 26 September 2020 # Fondazione Società Italiana di Neurologia 2020
Abstract After acute ischemic stroke (AIS), peripheral monocytes infiltrate into the lesion site within 24 h, peak at 3 to 7 days, and then differentiate into macrophages. Traditionally, monocytes/macrophages (MMs) are thought to play a deleterious role in AIS. Depletion of MMs in the acute phase can alleviate brain injury induced by ischemia. However, several studies have shown that MMs have anti-inflammatory functions, participate in angiogenesis, phagocytose necrotic neurons, and promote neurovascular repair. Therefore, MMs play dual roles in ischemic stroke, depending mainly upon the MM microenvironment and the window of time post-stroke. Because activated microglia and MMs are similar in morphology and function, previous studies have often investigated them together. However, recent studies have used special methods to distinguish MMs from microglia and have found that MMs have properties which differ from microglia. Here, we review the unique role of MMs and the interaction between MMs and neurovascular units, including neurons, astrocytes, microglia, and microvessels. Future therapeutics targeting MMs should regulate the polarization and subset transformation of the MMs at different stages of AIS rather than comprehensively suppressing MM infiltration and differentiation. In addition, more studies are needed to elucidate the cellular and molecular mechanisms of MM subsets and polarization during ischemic stroke. Keywords Ischemic stroke . Monocytes/macrophages . Polarization . Neurovascular units . Therapy
Introduction Acute ischemic stroke (AIS) is caused by a focal decrease or interruption of cerebral blood flow. This initiates an ischemic cascade, which results in neuronal death and rapid loss of neurological function. Dying neurons and debris cause a sterile inflammatory response in the ischemic brain [1]. This inflammatory response contributes to poor prognosis after AIS. Ischemia leads to the destruction of the blood-brain barrier (BBB), aggravation of brain edema, and inflammation in the subacute phase of AIS [2, 3]. Large amounts of material are released by dead neurons, including modified or oxidized lipids, cytoplasmic proteins, DNA, RNA, and modified extracellular matrix components. These are referred to as damage-associated molecular patterns (DAMPs), and * Yan Gao [email protected] 1
Department of Neurology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Heping District, Shenyang 110004, Liaoning, People’s Republic of China
their release results in inflammation. DAMPs first activate microglia in the brain. With the destruction of the BBB, circulating immune cells, such as monocytes, neutrophils, and lymphocytes, are recruited to the injury site and aggravate inflammation [4]. However, increasing evidence shows that inflammation has dual effects in the acu
Data Loading...
