Interleukin 17A Promotes Lymphocytes Adhesion and Induces CCL2 and CXCL1 Release from Brain Endothelial Cells

Wójkowska, Dagmara; Szpakowski, Piotr; Głąbiński, Andrzej

doi:10.3390/ijms18051000

Cited by 64 publications

(46 citation statements)

References 44 publications

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“…32,33 Pro-inflammatory interleukins IL-17A 34 and IL-9, 35 as well as TNF 36 are suggested to be involved in neuroinflammation after experimental severe (IL-17A and IL-9) and clinical repeated mTBI (TNF), by stimulating and controlling recruitment of neutrophils. 37 To our knowledge, IL-9 has not been reported in clinical studies assessing TBI patients, yet. This may be due to pre-selection of known cytokines in previous studies.…”

mentioning

confidence: 92%

Systemic Inflammation Persists the First Year after Mild Traumatic Brain Injury: Results from the Prospective Trondheim Mild Traumatic Brain Injury Study

Chaban

Clarke

Skandsen

et al. 2020

Journal of Neurotrauma

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Innate immune activation has been attributed a key role in traumatic brain injury (TBI) and successive morbidity. In mild TBI (mTBI), however, the extent and persistence of innate immune activation are unknown. We determined plasma cytokine level changes over 12 months after an mTBI in hospitalized and non-hospitalized patients compared with community controls; and examined their associations to injury-related and demographic variables at admission. Prospectively, 207 patients presenting to the emergency department (ED) or general practitioner with clinically confirmed mTBI and 82 matched community controls were included. Plasma samples were obtained at admission, after 2 weeks, 3 months, and 12 months. Cytokine levels were analysed with a 27-plex beads-based immunoassay. Brain magnetic resonance imaging (MRI) was performed on all participants. Twelve cytokines were reliably detected. Plasma levels of interferon gamma (IFN-c), interleukin 8 (IL-8), eotaxin, macrophage inflammatory protein-1-beta (MIP-1b), monocyte chemoattractant protein 1 (MCP-1), IL-17A, IL-9, tumor necrosis factor (TNF), and basic fibroblast growth factor (FGFbasic) were significantly increased at all time-points in patients compared with controls, whereas IFN-c-inducing protein 10 (IP-10), platelet-derived growth factor (PDGF), and IL-1ra were not. IL-17A and FGF-basic showed significant increases in patients from admission to follow-up at 3 months, and remained increased at 12 months compared with admission. Interestingly, MRI findings were negatively associated with four cytokines: eotaxin, MIP-1b, IL-9, and IP-10, whereas age was positively associated with nine cytokines: IL-8, eotaxin, MIP-1b, MCP-1, IL-17A, IL-9, TNF, FGFbasic, and IL-1ra. TNF was also increased in those with presence of other injuries. In conclusion, mTBI activated the innate immune system consistently and this is the first study to show that several inflammatory cytokines remain increased for up to 1 year post-injury.

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confidence: 92%

Systemic Inflammation Persists the First Year after Mild Traumatic Brain Injury: Results from the Prospective Trondheim Mild Traumatic Brain Injury Study

Chaban

Clarke

Skandsen

et al. 2020

Journal of Neurotrauma

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“…cantonensis infection. In the previous study, there were strong indications pointing to a role for IL-17 in the pathogenesis of MS and EAE, major causes of demyelination diseases [ 20 , 21 ]. As a result, we applied IL-17A-neutralizing antibody to treat the demyelination caused by A .…”

Section: Discussionmentioning

confidence: 99%

Inhibiting Interleukin 17 Can Ameliorate the Demyelination Caused by A. cantonensis via iNOS Inhibition

Feng

Zheng

Feng

et al. 2017

Mediators of Inflammation

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Angiostrongylus cantonensis (A. cantonensis) is an important food-borne parasitic disease. Previous study showed that A. cantonensis infection can cause demyelination in the central nerve system, but the mechanism of action has not been understood. To explore the mechanism and to look for effective therapeutic methods, interleukin 17A (IL-17A) and iNOS expressions were detected during A. cantonensis infection. In addition, IL-17A-neutralizing antibody was applied to treat A. cantonensis-infected mice. In our results, we found that IL-17A and iNOS RNA expressions increased gradually in the process of A. cantonensis infection. When infected mice were treated with IL-17A-neutralizing antibody, the pathologic changes of demyelination alleviated obviously, followed with the elevation of myelin basic protein (MBP) in the brain. In addition, the iNOS expression of the brain in infected animals also showed a decrease in astrocytes. Our study provided evidence that IL-17A may take part in the demyelination caused by A. cantonensis and inhibiting IL-17A expression can ameliorate the pathologic changes of demyelination. Moreover, the decreasing of iNOS expression may be the key reason for the effect of IL-17A inhibition on demyelination caused by A. cantonensis.

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“…In humans, CCL2 is increased in the cerebrospinal fluid of patients with severe human enterovirus 71 encephalitis. 10,11 In addition, CCL2 is produced by human brain microvascular endothelial cells infected with dengue virus. 7 CCL2 and CCR2 are also involved in the pathogenesis of neurodegenerative disorders including Alzheimer's disease, multiple sclerosis and ischemic brain injury.…”

Section: Introductionmentioning

confidence: 99%

“…In brain endothelial cells, the production of CCL2 is increased by inflammatory cytokines, including tumor-necrosis factor-a, interleukin-1b, interferon (IFN)-c and interleukin-17. 10,11 In addition, CCL2 is produced by human brain microvascular endothelial cells infected with dengue virus. 12 Recognition of the molecular pattern of microbes by pattern recognition receptors is the first step in the response of the innate immune system.…”

Section: Introductionmentioning

confidence: 99%

Induction of C‐C motif chemokine ligand 2 through Toll‐like receptor 3 signaling in human cerebral microvascular endothelial cell/D3 cells: possible regulation by nuclear factor‐κB

Sassa

Hirono

Shiratori

et al. 2019

Clinical & Exp Neuroim

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Objective C-C motif chemokine ligand 2 (CCL2) is a potent chemokine that plays an important role in host defense and inflammatory diseases in the central nervous system. Toll-like receptor 3 (TLR3) is a pattern recognition receptor that recognizes viral double-stranded RNAs. In the present study, we examined whether a TLR3 agonist induces CCL2 expression in brain microvascular endothelial cells, and investigated the mechanism underlying upregulation of CCL2 expression through TLR3 signaling. Methods A human brain microvascular endothelial cell line, human cerebral microvascular endothelial cell (hCMEC)/D3 was treated with a TLR3 agonist, polyinosinic-polycytidylic acid (poly IC). The mRNA and protein expression of CCL2 were evaluated using real-time reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The role of TLR3 and nuclear factor-jB (NF-jB) were examined with RNA interference. We also examined the effect of pretreatment with an NF-jB inhibitor, SN50, an interferon regulatory factor 3 inhibitor MR67307 and human type I interferon neutralizing antibody mixture on poly IC-induced CCL2 expression. Results Expression of CCL2 was induced by poly IC. Poly IC-induced CCL2 expression was decreased by knockdown of TLR3 or NF-jB p65 and by pretreatment with SN50. Neither MR67307 nor human type I interferon neutralizing antibody mixture affected the CCL2 expression induced by poly IC. Conclusions CCL2 expression was induced by poly IC through TLR3 signaling, and NF-jB is involved in this reaction. CCL2 produced by human brain endothelial cells might induce the infiltration of monocytes followed by immune and inflammatory reactions in the brain, and could be involved in the pathogenesis of viral encephalitis.

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Interleukin 17A Promotes Lymphocytes Adhesion and Induces CCL2 and CXCL1 Release from Brain Endothelial Cells

Cited by 64 publications

References 44 publications

Systemic Inflammation Persists the First Year after Mild Traumatic Brain Injury: Results from the Prospective Trondheim Mild Traumatic Brain Injury Study

Systemic Inflammation Persists the First Year after Mild Traumatic Brain Injury: Results from the Prospective Trondheim Mild Traumatic Brain Injury Study

Inhibiting Interleukin 17 Can Ameliorate the Demyelination Caused by A. cantonensis via iNOS Inhibition

Induction of C‐C motif chemokine ligand 2 through Toll‐like receptor 3 signaling in human cerebral microvascular endothelial cell/D3 cells: possible regulation by nuclear factor‐κB

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