Systemic innate myeloid responses to acute ischaemic and haemorrhagic stroke

Abstract

Acute ischaemic and haemorrhagic stroke account for significant disability and morbidity burdens worldwide. The myeloid arm of the peripheral innate immune system is critical in the immunological response to acute ischaemic and haemorrhagic stroke. Neutrophils, monocytes, and dendritic cells (DC) contribute to the evolution of pathogenic local and systemic inflammation, whilst maintaining a critical role in ongoing immunity protecting against secondary infections. This review aims to summarise the key alterations to myeloid immunity in acute ischaemic stroke, intracerebral haemorrhage (ICH), and subarachnoid haemorrhage (SAH). By integrating clinical and preclinical research, we discover how myeloid immunity is affected across multiple organ systems including the brain, blood, bone marrow, spleen, and lung, and evaluate how these perturbations associate with real-world outcomes including infection. These findings are placed in the context of the rapidly developing field of human immunology, which offers a wealth of opportunity for further research.

Multifunctional Carbon Quantum Dots: Iron Clearance and Antioxidation for Neuroprotection in Intracerebral Hemorrhage Mice

“…CCL2, IL-1β, and TNF-α are crucial inflammatory factors involved in ICH, playing significant roles in the recruitment and activation of microglia and macrophages . Our study used to assess the inflammatory factor content in the meningeal tissue.…”

“…CCL2, IL-1β, and TNF-α are crucial inflammatory factors involved in ICH, playing significant roles in the recruitment and activation of microglia and macrophages. 35 Our study used to assess the inflammatory factor content in the meningeal tissue. Compared with the sham group, there was a marked increase in CCL2, IL-1β, and TNF-α levels on day 3 post-ICH (Figure 5D−F).…”

Macrophage and monocyte subsets in response to ischemic stroke

“…Ischemic stroke is a sterile neuroinflammatory disease causing local and systemic inflammation [6]. Stroke is caused either by an undersupply of blood in the case of cerebral ischemia or by the extravasated blood into the brain parenchyma, subarachnoid space, and cerebrospinal fluid (CSF) in a hemorrhagic stroke [1,7]. Both pathologies require a rapid initial response to minimize tissue damage.…”

“…All macrophage populations are acting in a specific temporal order of post-stroke phases, starting in the first acute phase within minutes to hours, followed by a subacute phase in the next hours to days, reaching out to a chronic phase lasting days to months [4,[9][10][11]. Microglia, as the primary CNS-resident immune cells, are directly located in the parenchyma at the peri-infarct or perihaematomal region and are the first local immune cell responders [7,12]. BAMs represent a smaller macrophage population, but due to their subtissular niche, they are naturally sitting ing the acute poststroke phase, dying cells release damage-associated molecular patterns (DAMPs), and responding microglia release anti-inflammatory factors in the infarct core, whereas P2RY12-expressing microglia switch to responding microglia associated with proinflammatory signals with downregulated P2RY12 expression in the peri-infarct region.…”

“…All macrophage populations are acting in a specific temporal order of post‐stroke phases, starting in the first acute phase within minutes to hours, followed by a subacute phase in the next hours to days, reaching out to a chronic phase lasting days to months [4, 9–11]. Microglia, as the primary CNS‐resident immune cells, are directly located in the parenchyma at the peri‐infarct or perihaematomal region and are the first local immune cell responders [7, 12]. BAMs represent a smaller macrophage population, but due to their subtissular niche, they are naturally sitting in proximity to the infarct area and are thereby contributing to the early immune response upon stroke [13].…”