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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Colony-Stimulating Factor-1 Receptor Inhibition Transiently Attenuated the Peripheral Immune Response to Experimental Traumatic Brain Injury
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“Similar to SCI, mice following TBI also showed accumulation of CCR2-positive macrophages derived from peripheral blood.”
BackgroundInfluential
Repetitive injury and absence of monocytes promote astrocyte self‐renewal and neurological recovery
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Inhibiting α5 Subunit-Containing γ-Aminobutyric Acid Type A Receptors Attenuates Cognitive Deficits After Traumatic Brain Injury
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Macrophages: Redefining extracellular matrix architecture through phenotypic switches as therapeutic targets
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MethodSelf-citation
Inhibition of MALT1 paracaspase activity improves lesion recovery following spinal cord injury
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BackgroundMethod
The NOX2-ROS-NLRP3 inflammasome axis in traumatic brain injury
Laabei, J., Vegliante, G., Strogulski, N., Douglas, C., Threja, S., Pearson, A., Nkiliza, A., Hanscom, M., Emediato, I. D. F., Crawford, F., et al. (2025) · bioRxiv · doi:10.1101/2025.05.16.654460 · Cited by 5
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BackgroundInfluential
Autophagy in neuroinflammation after traumatic brain injury
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“…of pro-inflammatory markers like NOS2/iNOS (nitric oxide synthase 2, inducible), NLRP3, and CYBB/NOX2 (cytochrome b-245, beta polypeptide) and cytokines like tumor necrosis factor-α and interleukin-1β (Morganti et al., 2015), indicating that inhibition of autophagy is associated with inflammation.”
Background
Ccr2 Gene Ablation Does Not Influence Seizure Susceptibility, Tissue Damage, or Cellular Inflammation after Murine Pediatric Traumatic Brain Injury
Sharma, R., Chu, E., Dill, L. K., Shad, A., Zamani, A., O'Brien, T. J., Casillas-Espinosa, P. M., Shultz, S. R., & Semple, B. D. (2022) · Journal of Neurotrauma · doi:10.1089/neu.2022.0033 · Cited by 5
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“CCR2 is a chemokine receptor expressed in blood derived monocytes but not in brain resident microglia (Morganti et al., 2015) and activation of the CCR2-CCL2 signaling axis has been shown to recruit CCR2-expressing monocytes (“inflammatory monocytes”) into the injured tissue where they become activated macrophages, ex…”
BackgroundSelf-citation
Temporally-regulated genetic access to IL-1β-expressing cellular networks in homeostasis and following peripheral or central immune stimuli
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Open Data Commons for Preclinical Traumatic Brain Injury Research: Empowering Data Sharing and Big Data Analytics
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Tumor Necrosis Factor α as a Potential Mediator of the Effects of Phosphodiesterase 4B Inhibition on Cognition after Traumatic Brain Injury
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“…chronic cognitive dysfunction, including impaired LTP (Titus et al., 2013), cholinergic (Arciniegas, 2003) and catecholaminergic (Jenkins et al., 2016) signaling disturbances, neuroinflammation (Morganti et al., 2015), and dysfunctions of white matter and neural connectivity (Hayes et al., 2016).”
Background
Interleukin-1 receptor-1 signaling mediates neuroinflammation, neuronal injury, and cognitive decline after diffuse traumatic brain injury
Davis, A. C., Goodman, E. J., Wangler, L. M., Packer, J. M., Thammachack, R., Yildiz, V. O., Sharma, P., Pietrzak, M., Xiaokui, M., Quan, N., et al. (2026) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2026.106524 · Cited by 3
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Target mitochondrial pyroptosis with sequential delivery of nanoliposomes to alleviate secondary injury following traumatic brain injury
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Background
Colony stimulating factor-1 receptor as a treatment for cognitive deficits postfractionated whole-brain irradiation
Rosi, S. (2017) · Brain Circulation · doi:10.4103/bc.bc_25_17 · Cited by 2
“[12] CCR2 is a chemokine receptor absent from brain microglia[2] and the stimulation of CCR2-CCL2 signaling causes the accumulation of CCR2-expressing monocytes (also known as “inflammatory monocytes”) in the injured tissue.”
BackgroundSelf-citation
The role of persistent inflammation in failed recovery after perinatal brain injury: is resolution the cure?
Helmbrecht, H., Ardalan, M., Kelly, L. A., Robinson, S., Fleiss, B., Doherty, D. G., Gressèns, P., Mallard, C. E., Molloy, E. J., & Jantzie, L. L. (2026) · Journal of Neuroinflammation · doi:10.1186/s12974-026-03900-5 · Cited by 3
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Traumatic brain injury and post-injury sleep fragmentation differentially alter the microglial transcriptome
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“This chemokine receptor plays an important role in the recruitment of macrophages to damaged tissues and their activation.(27,28) It was reported that the amounts of CD11b+CCR2+ cells and the number of macrophages infiltrating an injured site from the periphery temporarily increase and induce inflammation within 12 to…”
Background
The Fluid Percussion Injury Model of Traumatic Brain Injury: Insights into Post-Traumatic Epilepsy and Comorbidities
Iannucci, J., Sentmanat, A., Dickerson, K., Obaid, M., Bandopadhyay, S., Houghton, A., Arisi, G. M., & Shapiro, L. A. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27209127
“CCL2 signaling through its receptor CCR2 helps regulate monocyte entry into the brain after TBI [225], and CCR2-associated macrophage responses are increased after injury [226–228].”

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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