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Traumatic brain injury in aged animals increases lesion size and chronically alters microglial/macrophage classical and alternative activation states
Open accessAbstract
Traumatic brain injury (TBI) causes chronic microglial activation that contributes to subsequent neurodegeneration, with clinical outcomes declining as a function of aging. Microglia/macrophages (MG/Mɸ) have multiple phenotypes, including a classically activated, proinflammatory (M1) state that might contribute to neurotoxicity, and an alternatively activated (M2) state that might promote repair. In this study we used gene expression, immunohistochemical, and stereological analyses to show that TBI in aged versus young mice caused larger lesions associated with an M1/M2 balance switch and increased numbers of reactive (bushy and hypertrophic) MG/Mɸ in the cortex, hippocampus, and thalamus. Chitinase3-like 3 (Ym1), an M2 phenotype marker, displayed heterogeneous expression after TBI with amoeboid-like Ym1-positive MG/Mɸ at the contusion site and ramified Ym1-positive MG/Mɸ at distant sites; this distribution was age-related. Aged-injured mice also showed increased MG/Mɸ expression of major histocompatibility complex II and NADPH oxidase, and reduced antioxidant enzyme expression which was associated with lesion size and neurodegeneration. Thus, altered relative M1/M2 activation and an nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase)-mediated shift in redox state might contribute to worse outcomes observed in older TBI animals by creating a more proinflammatory M1 MG/Mɸ activation state.
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“The mode of activation following TBI is somewhat age-dependent and may be less neuroprotective and more toxic in older animals [109].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [109]
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“Elderly individuals are at greater risk to suffer significant cognitive impairment and early morbidity following TBI, potentially due to an already present dysfunction in the microglial compartment [109,122,123].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [109]
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Citations
Cites
The chemokine system in diverse forms of macrophage activation and polarization
MANTOVANI, A., SICA, A., SOZZANI, S., ALLAVENA, P., VECCHI, A., & LOCATI, M. (2004) · Trends in Immunology · doi:10.1016/j.it.2004.09.015 · Cited by 6,534
Alternative activation of macrophages
Gordon, S. (2003) · Nature Reviews Immunology · doi:10.1038/nri978 · Cited by 6,189
Microglia-mediated neurotoxicity: uncovering the molecular mechanisms
Block, M. L., Zecca, L., & Hong, J.-S. (2007) · Nature Reviews Neuroscience · doi:10.1038/nrn2038 · Cited by 4,110
National Center for Injury Prevention and Control (U.S.). Division of Injury Response., Faul, M., Wald, M. M., Wu, L., & Coronado, V. G. (2010) · doi:10.15620/cdc.5571 · Cited by 3,494
Kigerl, K. A., Gensel, J. C., Ankeny, D. P., Alexander, J. K., Donnelly, D. J., & Popovich, P. G. (2009) · The Journal of Neuroscience · doi:10.1523/jneurosci.3257-09.2009 · Cited by 2,130
Microglia and inflammation-mediated neurodegeneration: Multiple triggers with a common mechanism
Block, M. L., & Hong, J.-S. (2005) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2005.06.004 · Cited by 1,557
Microglial Activation and Chronic Neurodegeneration
Lull, M. E., & Block, M. L. (2010) · Neurotherapeutics · doi:10.1016/j.nurt.2010.05.014 · Cited by 1,047 · cited 4×
“…species (ROS) by phagocytic cells including MG. NADPH oxidase has been implicated as a common and essential mechanism of MGmediated neurotoxicity (Lull and Block, 2010), and NADPH oxidase plays a critical role in the modulation of MG/MΦ activation phenotype and subsequent inflammatory…”
BackgroundInfluentialHeterogeneity of Microglial Activation in the Innate Immune Response in the Brain
Colton, C. A. (2009) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-009-9164-4 · Cited by 916
Godbout, J. P., Chen, J., Abraham, J., Richwine, A. F., Berg, B. M., Kelley, K. W., & Johnson, R. W. (2005) · The FASEB Journal · doi:10.1096/fj.05-3776fje · Cited by 813
Neuroinflammation after traumatic brain injury: Opportunities for therapeutic intervention
Kumar, A., & Loane, D. J. (2012) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2012.06.008 · Cited by 710
Self-citationRole of Microglia in Neurotrauma
Loane, D. J., & Byrnes, K. R. (2010) · Neurotherapeutics · doi:10.1016/j.nurt.2010.07.002 · Cited by 657
Self-citationWu, D., Teismann, P., Tieu, K., Vila, M., Jackson-Lewis, V. R., Ischiropoulos, H., & Przedborski, S. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0937239100 · Cited by 634
Th1/Th2-regulated expression of arginase isoforms in murine macrophages and dendritic cells.
Munder, M., Eichmann, K., Morán, J., Centeno, F., Soler, G., & Modolell, M. (1999) · Journal of Immunology · doi:10.4049/jimmunol.163.7.3771 · Cited by 619
Differential expression of FIZZ1 and Ym1 in alternatively versus classically activated macrophages
Raes, G., BAETSELIER, P. D., Noël, W., Beschin, A., Brombacher, F., & Gh., G. H. (2002) · Journal of Leukocyte Biology · doi:10.1189/jlb.71.4.597 · Cited by 443
Redox regulation of glial inflammatory response to lipopolysaccharide and interferonγ
Pawate, S., Shen, Q., Fan, F., & Bhat, N. R. (2004) · Journal of Neuroscience Research · doi:10.1002/jnr.20180 · Cited by 428
Ponomarev, E. D., Maresz, K., Tan, Y., & Dittel, B. N. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.1922-07.2007 · Cited by 396
Expression profiles for macrophage alternative activation genes in AD and in mouse models of AD.
(2006) · Journal of Neuroinflammation · doi:10.1186/1742-2094-3-27 · Cited by 393
Antioxidant Therapies for Traumatic Brain Injury
Hall, E. D., Vaishnav, R. A., & Mustafa, A. G. (2010) · Neurotherapeutics · doi:10.1016/j.nurt.2009.10.021 · Cited by 390 · cited 2×
“Neuroinflammation, oxidative stress, and MG/MΦ activation are important secondary injury mechanisms that lead to progressive neuronal damage and tissue loss after TBI (Byrnes et al., 2012; Hall et al., 2010; Kumar and Loane, 2012).”
BackgroundJimenez, S., Baglietto-Vargas, D., Caballero, C., Moreno-Gonzalez, I., Torres, M., Sanchez-Varo, R., Ruano, D., Vizuete, M., Gutierrez, A., & Vitorica, J. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.3024-08.2008 · Cited by 383 · cited 2×
“Interestingly, a recent study demonstrated an agedependent phenotypic change of MG/MΦ activation in the hippocampus of AD transgenic (PS1M146L/APP751SL) mice from an M2 activation state with Aβ phagocytic capabilities to a M1 and neurotoxic phenotype, which promoted high levels of soluble Aβ oligomers and significant…”
BackgroundChieppa, M., Bianchi, G., Doni, A., Prete, A. D., Sironi, M., Laškarin, G., Monti, P., Piemonti, L., Biondi, A., Mantovani, A., et al. (2003) · The Journal of Immunology · doi:10.4049/jimmunol.171.9.4552 · Cited by 372
The mannose receptor: linking homeostasis and immunity through sugar recognition
TAYLOR, P., GORDON, S., & MARTINEZPOMARES, L. (2005) · Trends in Immunology · doi:10.1016/j.it.2004.12.001 · Cited by 368
Critical Role for Microglial NADPH Oxidase in Rotenone-Induced Degeneration of Dopaminergic Neurons
Gao, H., Liu, B., & Hong, J. (2003) · Journal of Neuroscience · doi:10.1523/jneurosci.23-15-06181.2003 · Cited by 338
Oxidative stress and modification of synaptic proteins in hippocampus after traumatic brain injury
Ansari, M. A., Roberts, K. N., & Scheff, S. W. (2008) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2008.04.038 · Cited by 327
Fox, G. B., Fan, L., LeVasseur, R. A., & Faden, A. I. (1998) · Journal of Neurotrauma · doi:10.1089/neu.1998.15.599 · Cited by 320
Self-citationQin, L., Liu, Y., Cooper, C. L., Liu, B., Wilson, B. C., & Hong, J. (2002) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2002.01210.x · Cited by 294
Activation of NADPH Oxidase in Alzheimer’s Disease Brains
Shimohama, S., Tanino, H., Kawakami, N., Okamura, N., Kodama, H., Yamaguchi, T., Hayakawa, T., Nunomura, A., Chiba, S., Perry, G., et al. (2000) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.2000.2897 · Cited by 292
Inhibition of NADPH Oxidase is Neuroprotective after Ischemia—Reperfusion
Chen, H., Song, Y. S., & Chan, P. H. (2009) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/jcbfm.2009.47 · Cited by 291
Nair, M. G., Du, Y., Perrigoue, J., Zaph, C., Taylor, J. J., Goldschmidt, M. H., Swain, G. P., Yancopoulos, G. D., Valenzuela, D. M., Murphy, A. J., et al. (2009) · The Journal of Experimental Medicine · doi:10.1084/jem.20082048 · Cited by 278
The multifaceted profile of activated microglia
Lynch, M. A. (2009) · Molecular Neurobiology · doi:10.1007/s12035-009-8077-9 · Cited by 268
Amyloid precursor protein secretases as therapeutic targets for traumatic brain injury
Loane, D. J., Pocivavsek, A., Moussa, C. E.-H., Thompson, R., Matsuoka, Y., Faden, A. I., Rebeck, G. W., & Burns, M. P. (2009) · Nature Medicine · doi:10.1038/nm.1940 · Cited by 246
Self-citationChoi, S., Aïd, S., Kim, H., Jackson, S. H., & Bosetti, F. (2011) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2011.07572.x · Cited by 228
Accelerated Glial Reactivity to Stroke in Aged Rats Correlates with Reduced Functional Recovery
Badan, I., Buchhold, B., Hamm, A. O., Gratz, M., Walker, L. C., Platt, D., Kessler, C., & Popa‐Wagner, A. (2003) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1097/01.wcb.0000071883.63724.a7 · Cited by 216
Retnla (Relmα/Fizz1) Suppresses Helminth-Induced Th2-Type Immunity
Pesce, J. T., Ramalingam, T. R., Wilson, M. S., Mentink-Kane, M. M., Thompson, R. W., Cheever, A. W., Urban, J. F., & Wynn, T. A. (2009) · PLoS Pathogens · doi:10.1371/journal.ppat.1000393 · Cited by 213
Zhang, Q.-G., Laird, M. D., Han, D., Nguyen, K., Scott, E., Dong, Y., Dhandapani, K. M., & Brann, D. W. (2012) · PLoS ONE · doi:10.1371/journal.pone.0034504 · Cited by 211
Microglia Proliferation Is Regulated by Hydrogen Peroxide from NADPH Oxidase
Mander, P. K., Jekabsone, A., & Brown, G. C. (2006) · The Journal of Immunology · doi:10.4049/jimmunol.176.2.1046 · Cited by 206
Fenn, A. M., Henry, C. J., Huang, Y., Dugan, A., & Godbout, J. P. (2012) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2011.10.003 · Cited by 198
The CDC Traumatic Brain Injury Surveillance System
Coronado, V. G., Thomas, K. E., Sattin, R. W., & Johnson, R. L. (2005) · Journal of Head Trauma Rehabilitation · doi:10.1097/00001199-200505000-00005 · Cited by 196
Gp91phox (NOX2) in classically activated microglia exacerbates traumatic brain injury
Dohi, K., Ohtaki, H., Nakamachi, T., Yofu, S., Satoh, K., Miyamoto, K., Song, D., Tsunawaki, S., Shioda, S., & Aruga, T. (2010) · Journal of Neuroinflammation · doi:10.1186/1742-2094-7-41 · Cited by 188
Exacerbated glial response in the aged mouse hippocampus following controlled cortical impact injury
Sandhir, R., Onyszchuk, G., & Berman, N. E. J. (2008) · Experimental Neurology · doi:10.1016/j.expneurol.2008.06.013 · Cited by 183
Ansari, M. A., Roberts, K. N., & Scheff, S. W. (2008) · Journal of Neurotrauma · doi:10.1089/neu.2007.0451 · Cited by 181
FIZZ1 Stimulation of Myofibroblast Differentiation
Liu, T., Dhanasekaran, S. M., Jin, H., Hu, B., Tomlins, S. A., Chinnaiyan, A. M., & Phan, S. H. (2004) · American Journal Of Pathology · doi:10.1016/s0002-9440(10)63218-x · Cited by 179
Traumatic Brain Injury in an Aging Population
Stocchetti, N., Paternò, R., Citerio, G., Beretta, L., & Colombo, A. (2012) · Journal of Neurotrauma · doi:10.1089/neu.2011.1995 · Cited by 178
Byrnes, K. R., Loane, D. J., Stoica, B. A., Zhang, J., & Faden, A. I. (2012) · Journal of Neuroinflammation · doi:10.1186/1742-2094-9-43 · Cited by 175
Self-citationSedgwick, J. D., Ford, A. L., Foulcher, E., & Airriess, R. (1998) · The Journal of Immunology · doi:10.4049/jimmunol.160.11.5320 · Cited by 134
The Response of the Aged Brain to Stroke: Too Much, Too Soon?
Popa‐Wagner, A., Carmichael, S. T., Kokaia, Z., Kessler, C., & Walker, L. C. (2007) · Current Neurovascular Research · doi:10.2174/156720207781387213 · Cited by 134
The effects of aging, injury and disease on microglial function: a case for cellular senescence
Miller, K. R., & Streit, W. J. (2007) · Neuron Glia Biology · doi:10.1017/s1740925x08000136 · Cited by 134
Livingston, D. H., Lavery, R. F., Mosenthal, A. C., Knudson, M. M., Lee, S., Morabito, D. J., Manley, G. T., Nathens, A. B., Jurkovich, G. J., Hoyt, D. B., et al. (2005) · The Journal of Trauma: Injury, Infection, and Critical Care · doi:10.1097/01.ta.0000196002.03681.18 · Cited by 131
Survival After Severe Brain Injury in the Aged
Pennings, J. L. (1993) · Archives of Surgery · doi:10.1001/archsurg.1993.01420190083011 · Cited by 125
Onyszchuk, G., He, Y., Berman, N. E. J., & Brooks, W. M. (2008) · Journal of Neurotrauma · doi:10.1089/neu.2007.0430 · Cited by 120
Kyrkanides, S., O’Banion, M. K., Whiteley, P. E., Daeschner, J., & Olschowka, J. A. (2001) · Journal of Neuroimmunology · doi:10.1016/s0165-5728(01)00404-0 · Cited by 118
NADPH oxidase is involved in post-ischemic brain inflammation
Chen, H., Kim, G. S., Okami, N., Narasimhan, P., & Chan, P. H. (2011) · Neurobiology of Disease · doi:10.1016/j.nbd.2011.01.027 · Cited by 117
Outcome After Traumatic Brain Injury: Effects of Aging on Recovery
Testa, J. A., Malec, J. F., Moessner, A. M., & Brown, A. W. (2005) · Archives of Physical Medicine and Rehabilitation · doi:10.1016/j.apmr.2005.03.010 · Cited by 115
Oxidative stress in head trauma in aging
Shao, C., Roberts, K. N., Markesbery, W. R., Scheff, S. W., & Lovell, M. A. (2006) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2006.03.007 · Cited by 111
NOX Activity Is Increased in Mild Cognitive Impairment
Bruce‐Keller, A. J., Gupta, S., Parrino, T. E., Knight, A. G., Ebenezer, P. J., Weidner, A. M., LeVine, H., Keller, J. N., & Markesbery, W. R. (2009) · Antioxidants and Redox Signaling · doi:10.1089/ars.2009.2823 · Cited by 101
Chung, W., Chang, A. C., Kato, I., & Chang, N.-C. A. (2002) · Journal of Leukocyte Biology · doi:10.1189/jlb.72.1.72 · Cited by 88
Interleukin-4 mediates the neuroprotective effects of rosiglitazone in the aged brain
Loane, D. J., Deighan, B. F., Clarke, R. M., Griffin, R. J., Lynch, A. M., & Lynch, M. A. (2007) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2007.09.001 · Cited by 87
Self-citationEffect of aging on the microglial response to peripheral nerve injury
Conde, J. R., & Streit, W. J. (2006) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2005.07.012 · Cited by 86
Macrosialin increases during normal brain aging are attenuated by caloric restriction
Wong, A. M., Patel, N. V., Patel, N. K., Wei, M., Morgan, T. E., de Beer, M. C., de Villiers, W. J. S., & Finch, C. E. (2005) · Neuroscience Letters · doi:10.1016/j.neulet.2005.07.058 · Cited by 85 · cited 2×
“MG/MΦ in the aged brain are primed and have a ‘reactive’ phenotype (Miller and Streit, 2007), which is characterized by increased expression of M1 and pro-inflammatory markers such as ED1 (Wong et al., 2005), CD86 (Downer et al.”
BackgroundThe Effect of Age on Motor and Cognitive Deficits after Traumatic Brain Injury in Rats
Hamm, R. J., White-Gbadebo, D. M., Lyeth, B. G., Jenkins, L. W., & Hayes, R. L. (1992) · Neurosurgery · doi:10.1227/00006123-199212000-00013 · Cited by 84
A novel anti-inflammatory role of NCAM-derived mimetic peptide, FGL
Downer, E. J., Cowley, T. R., Lyons, A., Mills, K. H. G., Berezin, V., Bock, E., & Lynch, M. A. (2008) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2008.03.017 · Cited by 81
Emerging roles for telomerase in neuronal development and apoptosis
Mattson, M. P., & Klapper, W. (2001) · Journal of Neuroscience Research · doi:10.1002/1097-4547(20010101)63:1 · Cited by 76
Age-Related Mitochondrial Changes after Traumatic Brain Injury
Gilmer, L. K., Ansari, M. A., Roberts, K. N., & Scheff, S. W. (2010) · Journal of Neurotrauma · doi:10.1089/neu.2009.1181 · Cited by 69
Outcome After Traumatic Brain Injury Sustained in Older Adulthood: A One-Year Longitudinal Study
Rapoport, M. J., Herrmann, N., Shammi, P., Kiss, A., Phillips, A., & Feinstein, A. (2006) · American Journal of Geriatric Psychiatry · doi:10.1097/01.jgp.0000199339.79689.8a · Cited by 63
Anderson, J., Sandhir, R., Hamilton, E. S., & Berman, N. E. J. (2009) · Journal of Neurotrauma · doi:10.1089/neu.2008.0765 · Cited by 62
The effect of age on outcome following traumatic brain injury in rats
Hamm, R. J., Jenkins, L. W., Lyeth, B. G., White-Gbadebo, D. M., & Hayes, R. L. (1991) · Journal of neurosurgery · doi:10.3171/jns.1991.75.6.0916 · Cited by 62
Kabadi, S. V., Stoica, B. A., Hanscom, M., Loane, D. J., Kharebava, G., Murray, M. G., II, Cabatbat, R. M., & Faden, A. I. (2011) · Neurotherapeutics · doi:10.1007/s13311-011-0095-4 · Cited by 59
Self-citationAge-dependent response of CCAAT/enhancer binding proteins following traumatic brain injury in mice
Sandhir, R., & Berman, N. E. J. (2009) · Neurochemistry International · doi:10.1016/j.neuint.2009.10.002 · Cited by 56
Impairment of the ability of the injured aged brain in elevating urate and ascorbate
MOOR, E., Shohami, E., Kanevsky, E., Grigoriadis, N. K., Symeonidou, C., & Kohen, R. (2006) · Experimental Gerontology · doi:10.1016/j.exger.2005.12.006 · Cited by 31
Galbraith, S. (1987) · BMJ · doi:10.1136/bmj.294.6568.325 · Cited by 24
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DiSabato, D. J., Quan, N., & Godbout, J. P. (2016) · Journal of Neurochemistry · doi:10.1111/jnc.13607 · Cited by 1,640
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Jurga, A. M., Paleczna, M., & Kuter, K. Z. (2020) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2020.00198 · Cited by 1,000
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Lan, X., Han, X., Li, Q., Yang, Q.-W., & Wang, J. (2017) · Nature Reviews Neurology · doi:10.1038/nrneurol.2017.69 · Cited by 915
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Metadata
- Authors
- Kumar, A., Stoica, B. A., Sabirzhanov, B., Burns, M. P., Faden, A. I., & Loane, D. J.
- Affiliations
- University of Maryland, Baltimore (US)
- Georgetown University Medical Center (US)
- Corresponding author
- Loane, David J.
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2013-05
- Volume
- 34
- Issue
- 5
- Pages
- 1397-1411
- ISSN
- 0197-4580 (ISSN-L)
- PMC
- PMC3572914
- OpenAlex
- W2043020388
- Cited by
- 244
- References
- 69
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 13 · 2023: 10 · 2022: 14 · 2021: 16 · 2020: 21 · 2019: 15 · 2018: 21 · 2017: 24 · 2016: 33 · 2015: 27 · 2014: 25 · 2013: 10
- FWCI
- 12.91
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Capital Area Rehabilitation Research Network (R24HD050845)
- 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, aging, microglial activation, macrophages, macrophage polarization, Ym1, NADPH oxidase, MHC class II, antioxidant enzymes, neurodegeneration, lesion size, reactive microglia, redox state, proinflammation
- MeSH terms
- Aging, Animals, Brain, Brain Injuries, Cells, Cultured, Chronic Disease, Macrophage Activation, Macrophages, Male, Mice, Inbred C57BL, Microglia, Mice
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