Cited by 253Traumatic Brain Injury and Neurovascular DisturbancesNeuroinflammation and Neurodegeneration MechanismsTraumatic Brain Injury Research

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CCR2 Antagonism Alters Brain Macrophage Polarization and Ameliorates Cognitive Dysfunction Induced by Traumatic Brain Injury

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Morganti, Josh M., Jopson, Timothy D., Liu, Sharon, Riparip, Lara-Kirstie, Guandique, Cristian K., Gupta, Nalin, Ferguson, Adam R., Rosi, Susanna·2015·The Journal of Neuroscience

DOI 10.1523/jneurosci.2405-14.2015PMC PMC4293420

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Abstract

Traumatic brain injury (TBI) is a major risk factor for the development of multiple neurodegenerative diseases. With respect to the increasing prevalence of TBI, new therapeutic strategies are urgently needed that will prevent secondary damage to primarily unaffected tissue. Consistently, neuroinflammation has been implicated as a key mediator of secondary damage following the initial mechanical insult. Following injury, there is uncertainty regarding the role that accumulating CCR2 + macrophages play in the injury-induced neuroinflammatory sequelae and cognitive dysfunction. Using CX3CR1 GFP /+ CCR2 RFP /+ reporter mice, we show that TBI initiated a temporally restricted accumulation of peripherally derived CCR2 + macrophages, which were concentrated in the hippocampal formation, a region necessary for learning and memory. Multivariate analysis delineated CCR2 + macrophages' neuroinflammatory response while identifying a novel therapeutic treatment window. As a proof of concept, targeting CCR2 + macrophages with CCX872, a novel Phase I CCR2 selective antagonist, significantly reduced TBI-induced inflammatory macrophage accumulation. Concomitantly, there was a significant reduction in multiple proinflammatory and neurotoxic mediators with this treatment paradigm. Importantly, CCR2 antagonism resulted in a sparing of TBI-induced hippocampal-dependent cognitive dysfunction and reduced proinflammatory activation profile 1 month after injury. Thus, therapeutically targeting the CCR2 + subset of monocytes/macrophages may provide a new avenue of clinical intervention following TBI.

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Singer, B. H., Newstead, M. W., Zeng, X., Cooke, C. L., Thompson, R. C., Singer, K., Ghantasala, R., Parent, J. M., Murphy, G. G., Iwashyna, T. J., et al. (2016) · PLoS ONE · doi:10.1371/journal.pone.0149136 · Cited by 104
Triggering Receptor Expressed on Myeloid Cells 2 Deficiency Alters Acute Macrophage Distribution and Improves Recovery after Traumatic Brain Injury
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“65 Another study showed that impairing macrophage inﬁltration using CCR2 deﬁcient mice is beneﬁcial for TBI recovery and cognitive outcome after TBI.”
Activation of Alpha 7 Cholinergic Nicotinic Receptors Reduce Blood–Brain Barrier Permeability following Experimental Traumatic Brain Injury
Dash, P. K., Zhao, J., Kobori, N., Redell, J. B., Hylin, M. J., Hood, K. N., & Moore, A. N. (2016) · Journal of Neuroscience · doi:10.1523/jneurosci.3197-15.2016 · Cited by 93
“, 2008), we also examined the expression of C-C chemokine receptor type 2 (CCR2), as this receptor is expressed only by circulating monocytes/ macrophages and not by resident microglia (Morganti et al., 2015).”
Background
Resolution of neuroinflammation: mechanisms and potential therapeutic option
Dokalis, N., & Prinz, M. (2019) · Seminars in Immunopathology · doi:10.1007/s00281-019-00764-1 · Cited by 91
Plasma dilution improves cognition and attenuates neuroinflammation in old mice
Mehdipour, M., Mehdipour, T., Skinner, C. M., Wong, N., Liu, C., Chen, C.-C., Jeon, O. H., Zuo, Y., Conboy, M. J., & Conboy, I. M. (2021) · GeroScience · doi:10.1007/s11357-020-00297-8 · Cited by 77
Inhibition of miR-155 Limits Neuroinflammation and Improves Functional Recovery After Experimental Traumatic Brain Injury in Mice
Henry, R. J., Doran, S. J., Barrett, J. P., Meadows, V. E., Sabirzhanov, B. E., Stoica, B. A., Loane, D. J., & Faden, A. I. (2018) · Neurotherapeutics · doi:10.1007/s13311-018-0665-9 · Cited by 84
“Morganti and colleagues [47] recently demonstrated that inhibition of CCL2–CCR2 signaling following TBI, using a selective CCR2 antagonist, attenuated pro-inflammatory signaling.”
Background
The immune system in traumatic brain injury
Plesnila, N. (2015) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2015.10.008 · Cited by 85
Understanding Immune‐Driven Brain Aging by Human Brain Organoid Microphysiological Analysis Platform
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Monocytes promote acute neuroinflammation and become pathological microglia in neonatal hypoxic-ischemic brain injury
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“Elucidating these issues has implications for both basic science and clinical practice, since the influx of monocytes may be impeded by targeting the MCP1-CCR2 chemo-attraction axis as shown in several past studies [17-19 , 43-46”
Result
Macrophage depletion reduced brain injury following middle cerebral artery occlusion in mice
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“Both peripheral infiltrated macrophages and brain resident microglia activation were implicated in demyelinationassociated diseases such as globoid cell leukodystrophy, multiple sclerosis, spinal cord injury, and traumatic brain injury [28–31].”
Background
Interleukin-13 immune gene therapy prevents CNS inflammation and demyelination via alternative activation of microglia and macrophages: Modulation of CNS Inflammation by Interkeukin-13
Guglielmetti, C., Le Blon, D., Santermans, E., Salas-Perdomo, A., Daans, J., De Vocht, N., Shah, D., Hoornaert, C., Praet, J., Peerlings, J., et al. (2016) · Glia · doi:10.1002/glia.23053 · Cited by 76
“Furthermore, in the past years, numerous studies have reported the beneficial effect operated by the shift from M1to M2-polarized immune cells in other preclinical models of MS and other models of neuroinflammation (Cash et al., 1994; Janssens et al,. 2015; Liu et al., 2013; Miro-Mur et al., 2016; Miron et al., 2013;…”
Background
Novel microglia-mediated mechanisms underlying synaptic loss and cognitive impairment after traumatic brain injury
Krukowski, K., Nolan, A., Becker, M., Picard, K., Vernoux, N., Frias, E. S., Feng, X., Tremblay, M., & Rosi, S. (2021) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2021.08.210 · Cited by 87
“While acutely microglia contribute to restoring homeostasis after the injury, persistently reactive microglia produce pro-inflammatory/cytotoxic molecules contributing to neuronal damage (18-20).”
BackgroundSelf-citation
Age exacerbates the CCR2/5-mediated neuroinflammatory response to traumatic brain injury
Morganti, J. M., Riparip, L., Chou, A., Liu, S., Gupta, N. M., & Rosi, S. (2016) · Journal of Neuroinflammation · doi:10.1186/s12974-016-0547-1 · Cited by 86
“These data align with our previous work implicating CCR2 macrophages as the predominant source for NOX2 gene expression following TBI [13].”
BackgroundMethodResultInfluentialSelf-citation
Macrophages play an essential role in trauma-induced sterile inflammation and tissue repair
Peiseler, M., & Kubes, P. (2018) · European Journal of Trauma and Emergency Surgery · doi:10.1007/s00068-018-0956-1 · Cited by 79
Cellular players that shape evolving pathology and neurodegeneration following traumatic brain injury
Puntambekar, S. S., Saber, M., Lamb, B. T., & Kokiko‐Cochran, O. N. (2018) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2018.03.033 · Cited by 79
“kinetics of the macrophage response following TBI (22) .”
BackgroundInfluential
Persistent Infiltration and Impaired Response of Peripherally-Derived Monocytes after Traumatic Brain Injury in the Aged Brain
Chou, A., Krukowski, K., Morganti, J. M., Riparip, L., & Rosi, S. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19061616 · Cited by 78
“The prevention of CCR2+ monocyte infiltration in young animals significantly reduces both proand anti-inflammatory markers and ultimately improves cognitive outcomes after TBI [17,18].”
BackgroundMethodResultInfluentialSelf-citation
Analysis of monocyte infiltration in MPTP mice reveals that microglial CX3CR1 protects against neurotoxic over-induction of monocyte-attracting CCL2 by astrocytes
Parillaud, V. R., Lornet, G., Monnet, Y., Privat, A., Haddad, A. T., Brochard, V., Bekaert, A., de Chanville, C. B., Hirsch, E., Combadière, C., et al. (2017) · Journal of Neuroinflammation · doi:10.1186/s12974-017-0830-9 · Cited by 68
“, in traumatic brain injury models [41, 42], they are protective in motor neuron disease ALS mice [43].”
Background
CCR2 deficiency alters activation of microglia subsets in traumatic brain injury
Somebang, K., Rudolph, J. D., Imhof, I., Li, L., Niemi, E. C., Shigenaga, J. K., Tran, H., Gill, T. M., Lo, I., Zabel, B. A., et al. (2021) · Cell Reports · doi:10.1016/j.celrep.2021.109727 · Cited by 77
“, 2018), CCX872, improved TBI outcomes in WT mice (Morganti et al., 2015) when it is administered prior to trauma.”
BackgroundResult
Microglia Receptors in Animal Models of Traumatic Brain Injury
Younger, D., Murugan, M., Rao, K. V. R., Wu, L., & Chandra, N. (2018) · Molecular Neurobiology · doi:10.1007/s12035-018-1428-7 · Cited by 69
Intranasal delivery of exosomes from human adipose derived stem cells at forty-eight hours post injury reduces motor and cognitive impairments following traumatic brain injury
Moss, L. D., Sode, D., Patel, R. S., Lui, A., Hudson, C., Patel, N. A., & Bickford, P. C. (2021) · Neurochemistry International · doi:10.1016/j.neuint.2021.105173 · Cited by 63
“Prevention of aspects of the secondary inflammatory response have been shown to modulate recovery (Bachstetter et al., 2015, 2016; Morganti et al., 2015, 2019; Chou et al., 2018; Rowe et al., 2018).”
Background
Chemokine receptors CCR2 and CX3CR1 regulate viral encephalitis-induced hippocampal damage but not seizures
Käufer, C., Chhatbar, C., Bröer, S., Waltl, I., Ghita, L., Gerhauser, I., Kalinke, U., & Löscher, W. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1806754115 · Cited by 61
“CCR2 antagonists are efficacious after traumatic brain injury (47) and have entered clinical trials for the treatment of neuropathic pain (48).”
Background
An Agonist of the Protective Factor SIRT1 Improves Functional Recovery and Promotes Neuronal Survival by Attenuating Inflammation after Spinal Cord Injury
Chen, H., Ji, H., Zhang, M., Liu, Z., Lao, L., Deng, C., Chen, J., & Zhong, G. (2017) · Journal of Neuroscience · doi:10.1523/jneurosci.3046-16.2017 · Cited by 76
“Hsieh et al. (2014), Ka et al. (2015), and Morganti et al. (2015) reported that increased CCR2 expression may directly trigger the recruitment of macrophages to the CNS and that decreased expression impaired macrophage infiltration into the CNS.”
Background
Microglia moonlighting after traumatic brain injury: aging and interferons influence chronic microglia reactivity
Wangler, L. M., & Godbout, J. P. (2023) · Trends in Neurosciences · doi:10.1016/j.tins.2023.08.008 · Cited by 61
Deletion of p38α MAPK in microglia blunts trauma-induced inflammatory responses in mice
Morganti, J. M., Goulding, D. S., & Eldik, L. J. V. (2019) · Journal of Neuroinflammation · doi:10.1186/s12974-019-1493-5 · Cited by 59
Self-citation
Traumatic Brain Injury: An Age-Dependent View of Post-Traumatic Neuroinflammation and Its Treatment
Delage, C., Taib, T., Mamma, C., Lerouet, D., & Besson, V. C. (2021) · Pharmaceutics · doi:10.3390/pharmaceutics13101624 · Cited by 72
“Following TBI, inhibition of monocyte/macrophage infiltration in aged mice prevents spatial memory deficits [203] to a greater extent than in young adult mice [104].”
Background
The CCL2/CCL7/CCL12/CCR2 pathway is substantially and persistently upregulated in mice after traumatic brain injury, and CCL2 modulates the complement system in microglia
Popiołek-Barczyk, K., Ciechanowska, A., Ciapała, K., Pawlik, K., Oggioni, M., Mercurio, D., Simoni, M. G. D., & Mika, J. (2020) · Molecular and Cellular Probes · doi:10.1016/j.mcp.2020.101671 · Cited by 68
Comparison of the detrimental features of microglia and infiltrated macrophages in traumatic brain injury: A study using a hypnotic bromovalerylurea
Abe, N., Choudhury, M. E., Watanabe, M., Kawasaki, S., Nishihara, T., Yano, H., Matsumoto, S., Kunieda, T., Kumon, Y., Yorozuya, T., et al. (2018) · Glia · doi:10.1002/glia.23469 · Cited by 63
Role of infiltrating monocytes/macrophages in acute and chronic neuroinflammation: Effects on cognition, learning and affective behaviour
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“cesses required to limit tissue damage (Kapellos et al., 2016; Kumar et al., 2015, 2016; Morganti et al., 2015).”
Influential
Effects of advanced age upon astrocyte-specific responses to acute traumatic brain injury in mice
Early, A. N., Gorman, A. A., Eldik, L. J. V., Bachstetter, A. D., & Morganti, J. M. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01800-w · Cited by 64
“17 multivariate methods to delineate the effect of injury and time [32].”
BackgroundMethodSelf-citation
In vivo metabolic imaging of Traumatic Brain Injury
Guglielmetti, C., Chou, A., Krukowski, K., Najac, C., Feng, X., Riparip, L., Rosi, S., & Chaumeil, M. M. (2017) · Scientific Reports · doi:10.1038/s41598-017-17758-4 · Cited by 53
Self-citation
C-C chemokine receptor type 2-overexpressing exosomes alleviated experimental post-stroke cognitive impairment by enhancing microglia/macrophage M2 polarization
Yang, H., Zhang, M., Wu, R. T., Zheng, H., Zhang, L., Luo, J., Li, L., & Hu, X. (2020) · World Journal of Stem Cells · doi:10.4252/wjsc.v12.i2.152 · Cited by 54
STAT6 mediates the effect of ethanol on neuroinflammatory response in TBI
Heuvel, F. O., Holl, S., Chandrasekar, A., Li, Z., Wang, Y., Rehman, R., Förstner, P., Sinske, D., Palmer, A., Wiesner, D., et al. (2019) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2019.06.019 · Cited by 56
Interleukin-6 in Traumatic Brain Injury: A Janus-Faced Player in Damage and Repair
Ciryam, P., Gerzanich, V., & Simard, J. M. (2023) · Journal of Neurotrauma · doi:10.1089/neu.2023.0135 · Cited by 55
“226 Using ﬂow cytometry, Li and colleagues sought to identify IL-6 expression in speciﬁc cell types in the brains of mice subjected to CCI.”
Inflammatory Regulation of CNS Barriers After Traumatic Brain Injury: A Tale Directed by Interleukin-1
Garnett, C. N., Watson, J. B., Higgins, E. K., Quan, N., & Bachstetter, A. D. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.688254 · Cited by 62
Gene co-expression networks identify Trem2 and Tyrobp as major hubs in human APOE expressing mice following traumatic brain injury
Castranio, E. L., Mounier, A., Wolfe, C. M., Nam, K. N., Fitz, N. F., Letronne, F., Schug, J., Koldamova, R. P., & Lefterov, I. M. (2017) · Neurobiology of Disease · doi:10.1016/j.nbd.2017.05.006 · Cited by 56
“Studies have shown that the expression levels of themajority of those inflammatory factors are associated with severity of injury and outcome in TBI patients, the reduction of neurobehavioral impairments and injury volume as well as the survival rates in rodent models (Morganti et al., 2015; Yang et al., 2013).”
Background
Spinal motor circuit synaptic plasticity after peripheral nerve injury depends on microglia activation and a CCR2 mechanism
Rotterman, T. M., Akhter, E. T., Lane, A. R., MacPherson, K. P., García, V. V., Tansey, M. G., & Álvarez, F. J. (2019) · Journal of Neuroscience · doi:10.1523/jneurosci.2945-17.2019 · Cited by 51
“…models (Ajami et al., 2011; Prinz et al., 2011; Shi and Pamer, 2011), after spinal cord injury (Donnelly et al., 2011; Evans et al., 2014) and after traumatic brain injury (Morganti et al., 2015; Katsumoto et al., 2018), and to study dorsal horn pain mechanisms after PNI (Gu et al., 2016).”
Background
Microglia-specific deletion of histone deacetylase 3 promotes inflammation resolution, white matter integrity, and functional recovery in a mouse model of traumatic brain injury
Zhao, Y., Mu, H., Huang, Y., Li, S., Wang, Y., Stetler, R. A., Bennett, M. V. L., Dixon, C. E., Chen, J., & Shi, Y. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-022-02563-2 · Cited by 47
“Since CX3CR1 is expressed by microglia and peripheral monocytes [17], and both cells are present in the brain after TBI [29], we employed a tamoxifen pulse knockout strategy to restrict CX3CR1CreER-mediated HDAC3 knockout to microglia [17].”
Background
Fibrin promotes oxidative stress and neuronal loss in traumatic brain injury via innate immune activation
Dean, T., Mendiola, A. S., Yan, Z., Meza-Acevedo, R., Cabriga, B., Akassoglou, K., & Ryu, J. K. (2024) · Journal of Neuroinflammation · doi:10.1186/s12974-024-03092-w · Cited by 53
“These sequelae are likely responsible for TBI-induced oxidative damage and cortical loss observed in our study, and provides an underlying mechanism triggering monocyte and microglia post-TBI neurotoxicity [16, 46–49].”
BackgroundMethod
Links between thrombosis and inflammation in traumatic brain injury
Hubbard, W. B., Dong, J., Crúz, M. A., & Rumbaut, R. E. (2020) · Thrombosis Research · doi:10.1016/j.thromres.2020.10.041 · Cited by 57
Evaluation of M2-like macrophage enrichment after diffuse traumatic brain injury through transient interleukin-4 expression from engineered mesenchymal stromal cells
Enam, S. F., Kader, S. R., Bodkin, N., Lyon, J. G., Calhoun, M. A., Azrak, C., Tiwari, P. M., Vanover, D. A., Wang, H., Santangelo, P. J., et al. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01860-y · Cited by 55
Preclinical chorioamnionitis dysregulates CXCL1/CXCR2 signaling throughout the placental-fetal-brain axis
Yellowhair, T. R., Noor, S., Maxwell, J. R., Anstine, C. V., Oppong, A. Y., Robinson, S., Milligan, E. D., & Jantzie, L. L. (2017) · Experimental Neurology · doi:10.1016/j.expneurol.2017.11.002 · Cited by 57
“Notably, limiting neutrophils and macrophages improves neuropathological and functional outcomes following stroke and TBI (Semple et al., 2010; Morganti et al., 2015),”
Background
Intracerebral transplantation of interleukin 13-producing mesenchymal stem cells limits microgliosis, oligodendrocyte loss and demyelination in the cuprizone mouse model
Blon, D. L., Guglielmetti, C., Hoornaert, C., Quarta, A., Daans, J., Dooley, D., Lemmens, E., Praet, J., Vocht, N. D., Reekmans, K., et al. (2016) · Journal of Neuroinflammation · doi:10.1186/s12974-016-0756-7 · Cited by 56
“Although microglia and CNS-invading peripheral monocytes both act as phagocytic cells of the brain, it is currently becoming accepted that these two cell types are more distinct than generally assumed [2, 5].”
Background
Acute peripheral inflammation and post‐traumatic sleep differ between sexes after experimental diffuse brain injury
Saber, M., Giordano, K. R., Hur, Y., Ortiz, J. B., Morrison, H., Godbout, J. P., Murphy, S. M., Lifshitz, J., & Rowe, R. K. (2020) · European Journal of Neuroscience · doi:10.1111/ejn.14611 · Cited by 46
“In male mice or mixed sex studies, monocyte-derived macrophages have increased in the brain after TBI, as have peripheral monocytes and neutrophils in the blood long-term (Morganti et al., 2015; Ritzel et al., 2018; Saber et al., 2016; Schwulst et al., 2013).”
BackgroundInfluential
The role of macrophage polarization in tendon healing and therapeutic strategies: Insights from animal models
Wang, Y., Xiao, L., Lu, J., Hernigou, P., & Jin, F. (2024) · Frontiers in Bioengineering and Biotechnology · doi:10.3389/fbioe.2024.1366398 · Cited by 42
Dwellers and Trespassers: Mononuclear Phagocytes at the Borders of the Central Nervous System
Ivan, D. C., Walthert, S., Berve, K., Steudler, J., & Locatelli, G. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2020.609921 · Cited by 55
The Immune System's Role in the Consequences of Mild Traumatic Brain Injury (Concussion)
Verboon, L. N., Patel, H. C., & Greenhalgh, A. D. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.620698 · Cited by 63
A novel antagonist of p75NTR reduces peripheral expansion and CNS trafficking of pro-inflammatory monocytes and spares function after traumatic brain injury
Lee, S., Mattingly, A. J., Lin, A., Sacramento, J. A., Mannent, L., Castel, M., Canolle, B., Delbary-Gossart, S., Ferzaz, B., Morganti, J. M., et al. (2016) · Journal of Neuroinflammation · doi:10.1186/s12974-016-0544-4 · Cited by 55
“transgenic is a heterozygous mouse with bi-allelic expression of RFP and CCR2 [20, 50].”
BackgroundInfluentialSelf-citation
Differential fracture response to traumatic brain injury suggests dominance of neuroinflammatory response in polytrauma
Morioka, K., Marmor, Y., Sacramento, J. A., Lin, A., Shao, T., Miclau, K. R., Clark, D. R., Beattie, M. S., Marcucio, R., Miclau, T., et al. (2019) · Scientific Reports · doi:10.1038/s41598-019-48126-z · Cited by 44
Self-citation
Evidence of a distinct peripheral inflammatory profile in sport-related concussion
Battista, A. P. D., Churchill, N. W., Rhind, S. G., Richards, D. W., & Hutchison, M. G. (2019) · Journal of Neuroinflammation · doi:10.1186/s12974-019-1402-y · Cited by 51
Frontal Traumatic Brain Injury in Rats Causes Long-Lasting Impairments in Impulse Control That Are Differentially Sensitive to Pharmacotherapeutics and Associated with Chronic Neuroinflammation
Haar, C. V., Lam, F. C. W., Adams, W. K., Riparip, L., Kaur, S., Muthukrishna, M., Rosi, S., & Winstanley, C. A. (2016) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.6b00166 · Cited by 45
Self-citation

Authors: Morganti, J. M., Jopson, T. D., Liu, S., Riparip, L.-K., Guandique, C. K., Gupta, N., Ferguson, A. R., & Rosi, S.
Affiliations: University of California, San Francisco (US)
ORCID: Morganti, Josh M.
Gupta, Nalin
Ferguson, Adam R.
Rosi, Susanna
Venue: The Journal of Neuroscience
Publisher: Society for Neuroscience
Published: 2015-01-14
Volume: 35
Issue: 2
Pages: 748-760
ISSN: 0270-6474 (ISSN-L)
1529-2401
DOI: 10.1523/jneurosci.2405-14.2015
PMC: PMC4293420
OpenAlex: W2140178129
Cited by: 253
References: 71
Citations by year: 2026: 13 · 2025: 11 · 2024: 17 · 2023: 15 · 2022: 21 · 2021: 30 · 2020: 35 · 2019: 26 · 2018: 32 · 2017: 19 · 2016: 23 · 2015: 10
FWCI: 19.74
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 181 d)
Locations: Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
eScholarship (California Digital Library) (submittedVersion)
Funders: Alzheimer's Association (IIRG-11-202064)
National Institutes of Health
National Institute on Aging (R21AG042016)
National Cancer Institute (R01CA133216)
National Institute of Neurological Disorders and Stroke (R21NS087458, R01NS067092, F32NS090805)
Topics: Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
Keywords: traumatic brain injury, CCR2+ macrophages, macrophage polarization, neuroinflammation, cognitive impairment, hippocampus, monocytes, secondary injury, pro-inflammatory mediators
MeSH terms: CX3C Chemokine Receptor 1, Animals, Brain Injuries, Cognition, Female, Hippocampus, Macrophage Activation, Macrophages, Male, Mice, Inbred C57BL, Receptors, Chemokine, Mice, Receptors, CCR2

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CCR2 Antagonism Alters Brain Macrophage Polarization and Ameliorates Cognitive Dysfunction Induced by Traumatic Brain Injury

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