Chemokines play complex roles in cerebral ischemia

Chen, Chen; Chu, Shifeng; Liu, Dandan; Zhang, Zhao; Kong, Ling-Lei; Zhou, Xin; Chen, Nai‐Hong

doi:10.1016/j.neuint.2017.06.008

Cited by 46 publications

(39 citation statements)

References 146 publications

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“…Pro-inflammatory effects of cytokines like CCL11 in the post-ischemic tissue lead to acute brain injury through their ability to recruit and activate inflammatory cells [3]. Herein, the administration of ectopic CCL11 in adolescent mice had no effect on post-stroke brain injury and on microglia.…”

Section: Discussionmentioning

confidence: 81%

“…Hence, the cytokine CCL11, known to also pass the intact blood-brain barrier (BBB), has recently been recognized as an interesting target under conditions of CNS diseases not limited to cerebral ischemia alone [2]. CCL11, which is also referred to as eotaxin-1, belongs to the CC-chemokine family known for its role in chemoattracting eosinophils [3]. The latter represents the pro-inflammatory properties of CCL11 which have been reported for the peripheral immune system under various pathophysiological conditions [4].…”

Section: Introductionmentioning

confidence: 99%

“…Cytokines, like CCL11, have a differential impact on the CNS exposed to noxious stimuli, ranging from pro-inflammatory and harmful actions towards promoting neurorestorative processes as indicated by the stimulation of endogenous neural progenitor cells (NPCs) within the stem cell niche [3]. As a matter of fact, endogenous neurogenesis persists within the adult mammalian brain, possibly contributing to neurological recovery under defined circumstances, albeit the majority of NPCs suffers from both low survival rates and reduced differentiation rates [9].…”

Section: Introductionmentioning

confidence: 99%

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CCL11 Differentially Affects Post-Stroke Brain Injury and Neuroregeneration in Mice Depending on Age

Lieschke

Zechmeister

Haupt

et al. 2019

Cells

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CCL11 has recently been shown to differentially affect cell survival under various pathological conditions including stroke. Indeed, CCL11 promotes neuroregeneration in neonatal stroke mice. The impact of CCL11 on the adult ischemic brain, however, remains elusive. We therefore studied the effect of ectopic CCL11 on both adolescent (six-week) and adult (six-month) C57BL6 mice exposed to stroke. Intraperitoneal application of CCL11 significantly aggravated acute brain injury in adult mice but not in adolescent mice. Likewise, post-stroke neurological recovery after four weeks was significantly impaired in adult mice whilst CCL11 was present. On the contrary, CCL11 stimulated gliogenesis and neurogenesis in adolescent mice. Flow cytometry analysis of blood and brain samples revealed a modification of inflammation by CCL11 at subacute stages of the disease. In adolescent mice, CCL11 enhances microglial cell, B and T lymphocyte migration towards the brain, whereas only the number of B lymphocytes is increased in the adult brain. Finally, the CCL11 inhibitor SB297006 significantly reversed the aforementioned effects. Our study, for the first time, demonstrates CCL11 to be a key player in mediating secondary cell injury under stroke conditions. Interfering with this pathway, as shown for SB297006, might thus be an interesting approach for future stroke treatment paradigms.

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Section: Discussionmentioning

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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CCL11 Differentially Affects Post-Stroke Brain Injury and Neuroregeneration in Mice Depending on Age

Lieschke

Zechmeister

Haupt

et al. 2019

Cells

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“…The third family, consisting of a single member is Fraktalkine (CX3CL1) which is one of the two transmembrane chemokines and has two isoforms, one binds to the membrane and the other is a soluble form. According to its isoform, it may have different functions, the form that is anchored to the membrane serves as adhesion molecule for cells expressing CX3CR1, while the soluble form possesses a potent chemotactic activity [169]. The fourth family has only one member lymphotoxin (XCL1); this chemokine is similar to members of the CC and CXC families, but the lack of two of the four cysteine residues are characteristic of this chemokine.…”

Section: Chemokinesmentioning

confidence: 99%

Physiology and Pathology of Innate Immune Response Against Pathogens

Muñoz‐Carrillo¹,

García²,

Coronado³

et al. 2017

Physiology and Pathology of Immunology

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Pathogen infections are recognized by the immune system, which consists of two types of responses: an innate immune response and an antigen-specific adaptive immune response. The innate response is characterized by being the first line of defense that occurs rapidly in which leukocytes such as neutrophils, monocytes, macrophages, eosinophils, mast cells, dendritic cells, etc., are involved. These cells recognize the pathogen-associated molecular patterns (PAMPs), which have been evolutionarily conserved by the diversity of microorganisms that infect humans. Recognition of these pathogen-associated molecular patterns occurs through pattern recognition receptors such as Toll-like receptors and some other intracellular receptors such as nucleotide oligomerization domain (NOD), with the aim of amplifying the inflammation and activating the adaptive cellular immune response, through the antigenic presentation. In the present chapter, we will review the importance of the main components involved in the innate immune response, such as different cell types, inflammatory response, soluble immune mediators and effector mechanisms exerted by the immune response against bacteria, viruses, fungi, and parasites; all with the purpose of eliminating them and eradicating the infection of the host.

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“…8 In addition, CKLF1 has a role in neuronal apoptosis after cerebral ischemia and reperfusion, and the production of inflammatory mediators and adhesion molecules are decreased in rats by treatment with an anti-CKLF1 antibody. 9 The two secreted forms of CKLF1 (C19 and C27) can stimulate antigen-presenting capability of immature dendritic cells via CCR4, and the C19 can inhibit chemotaxis induced by CKLF1. 10 In addition, CKLF1 regulates vascular smooth muscle cell migration and proliferation and facilitates neointima hyperplasia and atherosclerosis.…”

mentioning

confidence: 99%