CCL20-CCR6 axis modulated traumatic brain injury-induced visual pathologies.

Abstract:

BACKGROUND:Traumatic brain injury (TBI) is a major cause of death and disability in the USA and the world; it constitutes 30% of injury-related deaths (Taylor et al., MMWR Surveill Summ 66:1-16, 2017). Contact sports athletes often experience repetitive TBI (rTBI), which exerts a cumulative effect later in life. Visual impairment is a common after-effect of TBI. Previously, we have shown that C-C chemokine 20 (CCL20) plays a critical role in neurodegeneration and inflammation following TBI (Das et al., J Neuroinflammation 8:148, 2011). C-C chemokine receptor 6 (CCR6) is the only receptor that CCL20 interacts with. The objective of the present study was to investigate the role of CCL20-CCR6 axis in mediating rTBI-induced visual dysfunction (TVD). METHODS:Wild type (WT) or CCR6 knock out (CCR6-/-) mice were subjected to closed head rTBI. Pioglitazone (PG) is a peroxisome proliferator-activated receptor γ (PPARγ) agonist which downregulates CCL20 production. Subsets of WT mice were treated with PG following final rTBI. A subset of mice was also treated with anti-CCL20 antibody to neutralize the CCL20 produced after rTBI. Histopathological assessments were performed to show cerebral pathologies, retinal pathologies, and inflammatory changes induced by rTBI. RESULTS:rTBI induced cerebral neurodegeneration, retinal degeneration, microgliosis, astrogliosis, and CCL20 expression. CCR6-/- mice showed reduced retinal degeneration, microgliosis, and inflammation. Treatment with CCL20 neutralization antibody or PG showed reduced CCL20 expression along with reduced retinal degeneration and inflammation. rTBI-induced GFAP-positive glial activation in the optic nerve was not affected by knocking out CCR6. CONCLUSION:The present data indicate that rTBI-induced retinal pathology is mediated at least in part by CCL20 in a CCR6-dependent manner.

journal_name

J Neuroinflammation

authors

Das M,Tang X,Han JY,Mayilsamy K,Foran E,Biswal MR,Tzekov R,Mohapatra SS,Mohapatra S

doi

10.1186/s12974-019-1499-z

subject

Has Abstract

pub_date

2019-05-31 00:00:00

pages

115

issue

1

issn

1742-2094

pii

10.1186/s12974-019-1499-z

journal_volume

16

pub_type

杂志文章
  • Increased expression of cystine/glutamate antiporter in multiple sclerosis.

    abstract:BACKGROUND:Glutamate excitotoxicity contributes to oligodendrocyte and tissue damage in multiple sclerosis (MS). Intriguingly, glutamate level in plasma and cerebrospinal fluid of MS patients is elevated, a feature which may be related to the pathophysiology of this disease. In addition to glutamate transporters, level...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/1742-2094-8-63

    authors: Pampliega O,Domercq M,Soria FN,Villoslada P,Rodríguez-Antigüedad A,Matute C

    更新日期:2011-06-03 00:00:00

  • Correction to: Mild endoplasmic reticulum stress ameliorates lipopolysaccharide-induced neuroinflammation and cognitive impairment via regulation of microglial polarization.

    abstract::An amendment to this paper has been published and can be accessed via the original article. ...

    journal_title:Journal of neuroinflammation

    pub_type: 已发布勘误

    doi:10.1186/s12974-020-01990-3

    authors: Wang YW,Zhou Q,Zhang X,Qian QQ,Xu JW,Ni PF,Qian YN

    更新日期:2020-11-24 00:00:00

  • Suppression of MAPK attenuates neuronal cell death induced by activated glia-conditioned medium in alpha-synuclein overexpressing SH-SY5Y cells.

    abstract:BACKGROUND:Parkinson's disease (PD) is a neurodegenerative disease with characteristics and symptoms that are well defined. Nevertheless, its aetiology remains unknown. PD is characterized by the presence of Lewy bodies inside neurons. α-Synuclein (α-syn) is a soluble protein present in the pre-synaptic terminal of neu...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-015-0412-7

    authors: Yshii LM,Denadai-Souza A,Vasconcelos AR,Avellar MC,Scavone C

    更新日期:2015-10-26 00:00:00

  • Molecular and cellular neuroinflammatory status of mouse brain after systemic lipopolysaccharide challenge: importance of CCR2/CCL2 signaling.

    abstract:BACKGROUND:Genetic and environmental factors are critical elements influencing the etiology of major depression. It is now accepted that neuroinflammatory processes play a major role in neuropsychological disorders. Neuroinflammation results from the dysregulation of the synthesis and/or release of pro- and anti-inflam...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/1742-2094-11-132

    authors: Cazareth J,Guyon A,Heurteaux C,Chabry J,Petit-Paitel A

    更新日期:2014-07-28 00:00:00

  • Sesamin ameliorates oxidative stress and mortality in kainic acid-induced status epilepticus by inhibition of MAPK and COX-2 activation.

    abstract:BACKGROUND:Kainic acid (KA)-induced status epilepticus (SE) was involved with release of free radicals. Sesamin is a well-known antioxidant from sesame seeds and it scavenges free radicals in several brain injury models. However the neuroprotective mechanism of sesamin to KA-induced seizure has not been studied. METHO...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/1742-2094-8-57

    authors: Hsieh PF,Hou CW,Yao PW,Wu SP,Peng YF,Shen ML,Lin CH,Chao YY,Chang MH,Jeng KC

    更新日期:2011-05-24 00:00:00

  • Inhibition of myeloperoxidase oxidant production by N-acetyl lysyltyrosylcysteine amide reduces brain damage in a murine model of stroke.

    abstract:BACKGROUND:Oxidative stress plays an important and causal role in the mechanisms by which ischemia/reperfusion (I/R) injury increases brain damage after stroke. Accordingly, reducing oxidative stress has been proposed as a therapeutic strategy for limiting damage in the brain after stroke. Myeloperoxidase (MPO) is a hi...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-016-0583-x

    authors: Yu G,Liang Y,Huang Z,Jones DW,Pritchard KA Jr,Zhang H

    更新日期:2016-05-24 00:00:00

  • Hippocampal microglial activation triggers a neurotoxic-specific astrocyte response and mediates etomidate-induced long-term synaptic inhibition.

    abstract:BACKGROUND:Accumulating evidence has highlighted the importance of microglial and astrocyte responses in the pathological development of postoperative cognitive dysfunction (POCD). However, the mechanisms involved are not well understood. METHODS:A perioperative neurocognitive disorders (PND) mouse model was generated...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-020-01799-0

    authors: Li D,Chen M,Meng T,Fei J

    更新日期:2020-04-07 00:00:00

  • Differential neurovirulence of Usutu virus lineages in mice and neuronal cells.

    abstract:BACKGROUND:Usutu virus (USUV) is an emerging neurotropic arthropod-borne virus recently involved in massive die offs of wild birds predominantly reported in Europe. Although primarily asymptomatic or presenting mild clinical signs, humans infected by USUV can develop neuroinvasive pathologies (including encephalitis an...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-020-02060-4

    authors: Clé M,Constant O,Barthelemy J,Desmetz C,Martin MF,Lapeyre L,Cadar D,Savini G,Teodori L,Monaco F,Schmidt-Chanasit J,Saiz JC,Gonzales G,Lecollinet S,Beck C,Gosselet F,Van de Perre P,Foulongne V,Salinas S,Simonin Y

    更新日期:2021-01-06 00:00:00

  • Differential expression of Cathepsin E in transthyretin amyloidosis: from neuropathology to the immune system.

    abstract:BACKGROUND:Increasing evidence supports a key role for inflammation in the neurodegenerative process of familial amyloidotic polyneuropathy (FAP). While there seems to be an overactivation of the neuronal interleukin-1 signaling pathway, the immune response is apparently compromised in FAP. Accordingly, little immune c...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-017-0891-9

    authors: Gonçalves NP,Moreira J,Martins D,Vieira P,Obici L,Merlini G,Saraiva M,Saraiva MJ

    更新日期:2017-06-06 00:00:00

  • Complement activation at the motor end-plates in amyotrophic lateral sclerosis.

    abstract:BACKGROUND:Amyotrophic lateral sclerosis (ALS) is a fatal progressive neurodegenerative disease with no available therapy. Components of the innate immune system are activated in the spinal cord and central nervous system of ALS patients. Studies in the SOD1(G93A) mouse show deposition of C1q and C3/C3b at the motor en...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-016-0538-2

    authors: Bahia El Idrissi N,Bosch S,Ramaglia V,Aronica E,Baas F,Troost D

    更新日期:2016-04-07 00:00:00

  • Chemokine-mediated inflammation in the degenerating retina is coordinated by Müller cells, activated microglia, and retinal pigment epithelium.

    abstract:BACKGROUND:Monocyte infiltration is involved in the pathogenesis of many retinal degenerative conditions. This process traditionally depends on local expression of chemokines, though the roles of many of these in the degenerating retina are unclear. Here, we investigate expression and in situ localization of the broad ...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-014-0224-1

    authors: Rutar M,Natoli R,Chia RX,Valter K,Provis JM

    更新日期:2015-01-17 00:00:00

  • Anti-inflammatory and anti-oxidant mechanisms of an MMP-8 inhibitor in lipoteichoic acid-stimulated rat primary astrocytes: involvement of NF-κB, Nrf2, and PPAR-γ signaling pathways.

    abstract:BACKGROUND:Recent evidence suggests that reactive astrocytes play an important role in neuroinflammation and neurodegenerative diseases. Thus, controlling astrocyte reactivity has been suggested as a promising strategy for treating neurodegenerative diseases. In the present study, we investigated whether a matrix metal...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-018-1363-6

    authors: Lee EJ,Park JS,Lee YY,Kim DY,Kang JL,Kim HS

    更新日期:2018-11-23 00:00:00

  • The role of the complement system in traumatic brain injury: a review.

    abstract::Traumatic brain injury (TBI) is an important cause of disability and mortality in the western world. While the initial injury sustained results in damage, it is the subsequent secondary cascade that is thought to be the significant determinant of subsequent outcomes. The changes associated with the secondary injury do...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章,评审

    doi:10.1186/s12974-018-1066-z

    authors: Hammad A,Westacott L,Zaben M

    更新日期:2018-01-22 00:00:00

  • Combining nitric oxide release with anti-inflammatory activity preserves nigrostriatal dopaminergic innervation and prevents motor impairment in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's disease.

    abstract:BACKGROUND:Current evidence suggests a role of neuroinflammation in the pathogenesis of Parkinson's disease (PD) and in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of basal ganglia injury. Reportedly, nonsteroidal anti-inflammatory drugs (NSAIDs) mitigate DAergic neurotoxicity in rodent models of PD. ...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/1742-2094-7-83

    authors: L'Episcopo F,Tirolo C,Caniglia S,Testa N,Serra PA,Impagnatiello F,Morale MC,Marchetti B

    更新日期:2010-11-23 00:00:00

  • Therapeutic hypercapnia reduces blood-brain barrier damage possibly via protein kinase Cε in rats with lateral fluid percussion injury.

    abstract:BACKGROUND:This study investigated whether therapeutic hypercapnia (TH) ameliorated blood-brain barrier (BBB) damage and improved the neurologic outcome in a rat model of lateral fluid percussion injury (FPI), and explored the possible underlying mechanism. METHODS:Rats underwent lateral FPI and received inhalation of...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-019-1427-2

    authors: Yang WC,Wang Q,Chi LT,Wang YZ,Cao HL,Li WZ

    更新日期:2019-02-13 00:00:00

  • A central role for glial CCR5 in directing the neuropathological interactions of HIV-1 Tat and opiates.

    abstract:BACKGROUND:The collective cognitive and motor deficits known as HIV-associated neurocognitive disorders (HAND) remain high even among HIV+ individuals whose antiretroviral therapy is optimized. HAND is worsened in the context of opiate abuse. The mechanism of exacerbation remains unclear but likely involves chronic imm...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-018-1320-4

    authors: Kim S,Hahn YK,Podhaizer EM,McLane VD,Zou S,Hauser KF,Knapp PE

    更新日期:2018-10-10 00:00:00

  • Wnt canonical pathway activator TWS119 drives microglial anti-inflammatory activation and facilitates neurological recovery following experimental stroke.

    abstract:BACKGROUND:Ischemic stroke is a leading cause of disability worldwide and characteristically accompanied by downregulation of the Wnt/β-catenin signaling. Activation of Wnt/β-catenin signaling emerges to attenuate neuroinflammation after ischemic stroke; however, its effect on modulating microglial polarization is larg...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-019-1660-8

    authors: Song D,Zhang X,Chen J,Liu X,Xue J,Zhang L,Lan X

    更新日期:2019-12-06 00:00:00

  • A small peptide antagonist of the Fas receptor inhibits neuroinflammation and prevents axon degeneration and retinal ganglion cell death in an inducible mouse model of glaucoma.

    abstract:BACKGROUND:Glaucoma is a complex, multifactorial disease where apoptosis, microglia activation, and inflammation have been linked to the death of retinal ganglion cells (RGCs) and axon degeneration. We demonstrated previously that FasL-Fas signaling was required for axon degeneration and death of RGCs in chronic and in...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-019-1576-3

    authors: Krishnan A,Kocab AJ,Zacks DN,Marshak-Rothstein A,Gregory-Ksander M

    更新日期:2019-09-30 00:00:00

  • Hyperactivation of proprioceptors induces microglia-mediated long-lasting pain in a rat model of chronic fatigue syndrome.

    abstract:BACKGROUND:Patients diagnosed with chronic fatigue syndrome (CFS) or fibromyalgia experience chronic pain. Concomitantly, the rat model of CFS exhibits microglial activation in the lumbar spinal cord and pain behavior without peripheral tissue damage and/or inflammation. The present study addressed the mechanism underl...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-019-1456-x

    authors: Yasui M,Menjyo Y,Tokizane K,Shiozawa A,Tsuda M,Inoue K,Kiyama H

    更新日期:2019-03-30 00:00:00

  • Protease-activated receptor-1 activation by granzyme B causes neurotoxicity that is augmented by interleukin-1β.

    abstract:BACKGROUND:The cause of neurodegeneration in progressive forms of multiple sclerosis is unknown. We investigated the impact of specific neuroinflammatory markers on human neurons to identify potential therapeutic targets for neuroprotection against chronic inflammation. METHODS:Surface immunocytochemistry directly vis...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-017-0901-y

    authors: Lee PR,Johnson TP,Gnanapavan S,Giovannoni G,Wang T,Steiner JP,Medynets M,Vaal MJ,Gartner V,Nath A

    更新日期:2017-06-27 00:00:00

  • Virus-mediated EpoR76E gene therapy preserves vision in a glaucoma model by modulating neuroinflammation and decreasing oxidative stress.

    abstract:BACKGROUND:Glaucoma is a complex neurodegeneration and a leading cause of blindness worldwide. Current therapeutic strategies, which are all directed towards lowering the intraocular pressure (IOP), do not stop progression of the disease. We have demonstrated that recombinant adeno-associated virus (rAAV) gene delivery...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-016-0499-5

    authors: Hines-Beard J,Bond WS,Backstrom JR,Rex TS

    更新日期:2016-02-15 00:00:00

  • Pharmacological antagonism of interleukin-8 receptor CXCR2 inhibits inflammatory reactivity and is neuroprotective in an animal model of Alzheimer's disease.

    abstract:BACKGROUND:The chemokine interleukin-8 (IL-8) and its receptor CXCR2 contribute to chemotactic responses in Alzheimer's disease (AD); however, properties of the ligand and receptor have not been characterized in animal models of disease. The primary aim of our study was to examine effects of pharmacological antagonism ...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-015-0339-z

    authors: Ryu JK,Cho T,Choi HB,Jantaratnotai N,McLarnon JG

    更新日期:2015-08-09 00:00:00

  • Cerebral ischemic damage in diabetes: an inflammatory perspective.

    abstract::Stroke is one of the leading causes of death worldwide. A strong inflammatory response characterized by activation and release of cytokines, chemokines, adhesion molecules, and proteolytic enzymes contributes to brain damage following stroke. Stroke outcomes are worse among diabetics, resulting in increased mortality ...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章,评审

    doi:10.1186/s12974-016-0774-5

    authors: Shukla V,Shakya AK,Perez-Pinzon MA,Dave KR

    更新日期:2017-01-23 00:00:00

  • Three-dimensional morphometric analysis reveals time-dependent structural changes in microglia and astrocytes in the central amygdala and hypothalamic paraventricular nucleus of heart failure rats.

    abstract:BACKGROUND:Cardiovascular diseases, including heart failure, are the most common cause of death globally. Recent studies support a high degree of comorbidity between heart failure and cognitive and mood disorders resulting in memory loss, depression, and anxiety. While neuroinflammation in the hypothalamic paraventricu...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-020-01892-4

    authors: Althammer F,Ferreira-Neto HC,Rubaharan M,Roy RK,Patel AA,Murphy A,Cox DN,Stern JE

    更新日期:2020-07-23 00:00:00

  • Prevention of methamphetamine-induced microglial cell death by TNF-α and IL-6 through activation of the JAK-STAT pathway.

    abstract:BACKGROUND:It is well known that methamphetamine (METH) is neurotoxic and recent studies have suggested the involvement of neuroinflammatory processes in brain dysfunction induced by misuse of this drug. Indeed, glial cells seem to be activated in response to METH, but its effects on microglial cells are not fully unde...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/1742-2094-9-103

    authors: Coelho-Santos V,Gonçalves J,Fontes-Ribeiro C,Silva AP

    更新日期:2012-07-06 00:00:00

  • Effect of thymic stimulation of CD4+ T cell expansion on disease onset and progression in mutant SOD1 mice.

    abstract:BACKGROUND:The peripheral immune system is implicated in modulating microglial activation, neurodegeneration and disease progression in amyotrophic lateral sclerosis (ALS). Specifically, there is reduced thymic function and regulatory T cell (Treg) number in ALS patients and mutant superoxide dismutase 1 (SOD1) mice, w...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-015-0254-3

    authors: Sheean RK,Weston RH,Perera ND,D'Amico A,Nutt SL,Turner BJ

    更新日期:2015-02-27 00:00:00

  • Pro-inflammatory cytokines and their epistatic interactions in genetic susceptibility to schizophrenia.

    abstract:BACKGROUND:In schizophrenia, genetic background may provide a substrate for intrinsic maldevelopment of the brain through environmental influences, by recruiting neurotrophic factors and cytokines, to trigger the changes that lead to impaired neuronal functions. Cytokines being the key regulators of immune/inflammatory...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-016-0569-8

    authors: Srinivas L,Vellichirammal NN,Alex AM,Nair C,Nair IV,Banerjee M

    更新日期:2016-05-13 00:00:00

  • Repeated administration of the noradrenergic neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) modulates neuroinflammation and amyloid plaque load in mice bearing amyloid precursor protein and presenilin-1 mutant transgenes.

    abstract:BACKGROUND:Data indicates anti-oxidant, anti-inflammatory and pro-cognitive properties of noradrenaline and analyses of post-mortem brain of Alzheimer's disease (AD) patients reveal major neuronal loss in the noradrenergic locus coeruleus (LC), the main source of CNS noradrenaline (NA). The LC has projections to brain ...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/1742-2094-4-8

    authors: Pugh PL,Vidgeon-Hart MP,Ashmeade T,Culbert AA,Seymour Z,Perren MJ,Joyce F,Bate ST,Babin A,Virley DJ,Richardson JC,Upton N,Sunter D

    更新日期:2007-02-26 00:00:00

  • Pioglitazone inhibition of lipopolysaccharide-induced nitric oxide synthase is associated with altered activity of p38 MAP kinase and PI3K/Akt.

    abstract:BACKGROUND:Previous studies have suggested that peroxisome proliferator activated receptor-gamma (PPAR-gamma)-mediated neuroprotection involves inhibition of microglial activation and decreased expression and activity of inducible nitric oxide synthase (iNOS); however, the underlying molecular mechanisms have not yet b...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/1742-2094-5-4

    authors: Xing B,Xin T,Hunter RL,Bing G

    更新日期:2008-01-18 00:00:00

  • Evidence for the activation of pyroptotic and apoptotic pathways in RPE cells associated with NLRP3 inflammasome in the rodent eye.

    abstract:BACKGROUND:Age-related macular degeneration (AMD) is a devastating eye disease causing irreversible vision loss in the elderly. Retinal pigment epithelium (RPE), the primary cell type that is afflicted in AMD, undergoes programmed cell death in the late stages of the disease. However, the exact mechanisms for RPE degen...

    journal_title:Journal of neuroinflammation

    pub_type: 杂志文章

    doi:10.1186/s12974-018-1062-3

    authors: Gao J,Cui JZ,To E,Cao S,Matsubara JA

    更新日期:2018-01-12 00:00:00