Skip to main content

Neuroimmune and Neuroinflammatory Mechanisms in Traumatic Brain Injury

Guest Editors:

David J. Loane, PhD, Trinity College Dublin, Ireland
Lee A Shapiro, PhD, Texas A&M University College of Medicine, United States of America 

Submission Status: Closed   |   Submission Deadline: 15 February 2024


This collection is no longer accepting submissions.


Journal of Neuroinflammation is calling for submissions to our Collection on "Neuroimmune and Neuroinflammatory Mechanisms in Traumatic Brain Injury".



Image credit: idealeksis / stock.adobe.com

  1. Chronic neuroinflammation and microglial activation are key mediators of the secondary injury cascades and cognitive impairment that follow exposure to repetitive mild traumatic brain injury (r-mTBI). Peroxiso...

    Authors: Andrew Pearson, Milica Koprivica, Max Eisenbaum, Camila Ortiz, Mackenzie Browning, Tessa Vincennie, Cooper Tinsley, Michael Mullan, Fiona Crawford and Joseph Ojo
    Citation: Journal of Neuroinflammation 2024 21:194
  2. Therapeutics for traumatic brains injuries constitute a global unmet medical need. Despite the advances in neurocritical care, which have dramatically improved the survival rate for the ~ 70 million patients a...

    Authors: James Dooley, Jasmine G. Hughes, Edward J. Needham, Katerina A. Palios and Adrian Liston
    Citation: Journal of Neuroinflammation 2024 21:183
  3. Traumatic brain injury (TBI) is a significant risk factor for Alzheimer’s disease (AD), and accumulating evidence supports a role for adaptive immune B and T cells in both TBI and AD pathogenesis. We previousl...

    Authors: Jaclyn Iannucci, Reagan Dominy, Shreya Bandopadhyay, E. Madison Arthur, Brenda Noarbe, Amandine Jullienne, Margret Krkasharyan, Richard P. Tobin, Aleksandr Pereverzev, Samantha Beevers, Lavanya Venkatasamy, Karienn A. Souza, Daniel C. Jupiter, Alan Dabney, Andre Obenaus, M. Karen Newell-Rogers…
    Citation: Journal of Neuroinflammation 2024 21:165
  4. Repetitive mild traumatic brain injuries (rmTBI) sustained within a window of vulnerability can result in long term cognitive deficits, depression, and eventual neurodegeneration associated with tau pathology,...

    Authors: Alyssa F. Pybus, Sara Bitarafan, Rowan O. Brothers, Alivia Rohrer, Arushi Khaitan, Felix Rivera Moctezuma, Kareena Udeshi, Brae Davies, Sydney Triplett, Martin N. Griffin, Eric B. Dammer, Srikant Rangaraju, Erin M. Buckley and Levi B. Wood
    Citation: Journal of Neuroinflammation 2024 21:156
  5. Uncontrolled neuroinflammation mediates traumatic brain injury (TBI) pathology and impairs recovery. Interleukin-6 (IL-6), a pleiotropic inflammatory regulator, is associated with poor clinical TBI outcomes. I...

    Authors: Ian G. Gober, Ashley L. Russell, Tyler J. Shick, Vincent A. Vagni, Jenna C. Carlson, Patrick M. Kochanek and Amy K. Wagner
    Citation: Journal of Neuroinflammation 2024 21:149
  6. White matter injury (WMI) represents a significant etiological factor contributing to neurological impairment subsequent to Traumatic Brain Injury (TBI). CD36 receptors are recognized as pivotal participants i...

    Authors: Xiaoxiang Hou, Xiaolin Qu, Wen Chen, Xianzheng Sang, Yichao Ye, Chengqing Wang, Yangu Guo, Hantong Shi, Chengzi Yang, Kaixin Zhu, Yelei Zhang, Haoxiang Xu, Liquan Lv, Danfeng Zhang and Lijun Hou
    Citation: Journal of Neuroinflammation 2024 21:148
  7. The gut microbiota plays a critical role in regulating brain function through the microbiome-gut-brain axis (MGBA). Dysbiosis of the gut microbiota is associated with neurological impairment in Traumatic brain...

    Authors: Nina Gu, Jin Yan, Wei Tang, Zhaosi Zhang, Lin Wang, Zhao Li, Yingwen Wang, Yajun Zhu, Shuang Tang, Jianjun Zhong, Chongjie Cheng, Xiaochuan Sun and Zhijian Huang
    Citation: Journal of Neuroinflammation 2024 21:147
  8. The lectin pathway (LP) of complement mediates inflammatory processes linked to tissue damage and loss of function following traumatic brain injury (TBI). LP activation triggers a cascade of proteolytic events...

    Authors: Domenico Mercurio, Francesca Pischiutta, Serena Seminara, Francesca Tribuzio, Ilaria Lisi, Laura Pasetto, Valentina Bonetto, Maria-Grazia De Simoni, Wilhelm Schwaeble, Sadam Yaseen, Thomas Dudler, Elisa R. Zanier and Stefano Fumagalli
    Citation: Journal of Neuroinflammation 2024 21:141
  9. Perihematomal edema (PHE) after post-intracerebral hemorrhage (ICH) has complex pathophysiological mechanisms that are poorly understood. The complicated immune response in the post-ICH brain constitutes a cru...

    Authors: Peng Zhang, Cong Gao, Qiang Guo, Dongxu Yang, Guangning Zhang, Hao Lu, Liman Zhang, Guorong Zhang and Daojing Li
    Citation: Journal of Neuroinflammation 2024 21:140
  10. Epidemiological studies have unveiled a robust link between exposure to repetitive mild traumatic brain injury (r-mTBI) and elevated susceptibility to develop neurodegenerative disorders, notably chronic traum...

    Authors: Camila Ortiz, Andrew Pearson, Robyn McCartan, Shawn Roche, Nolan Carothers, Mackenzie Browning, Sylvia Perez, Bin He, Stephen D. Ginsberg, Michael Mullan, Elliott J. Mufson, Fiona Crawford and Joseph Ojo
    Citation: Journal of Neuroinflammation 2024 21:130
  11. Traumatic brain injury (TBI) is a chronic and debilitating disease, associated with a high risk of psychiatric and neurodegenerative diseases. Despite significant advancements in improving outcomes, the lack o...

    Authors: Mahmoud G. El Baassiri, Zachariah Raouf, Sarah Badin, Alejandro Escobosa, Chhinder P. Sodhi and Isam W. Nasr
    Citation: Journal of Neuroinflammation 2024 21:124
  12. Pneumonia is a common comorbidity in patients with severe traumatic brain injury (TBI), and is associated with increased morbidity and mortality. In this study, we established a model of intratracheal Klebsiella ...

    Authors: Ali Shad, Sarah S. J. Rewell, Matthew Macowan, Natasha Gandasasmita, Jiping Wang, Ke Chen, Ben Marsland, Terence J. O’Brien, Jian Li and Bridgette D. Semple
    Citation: Journal of Neuroinflammation 2024 21:122
  13. Obesity increases the morbidity and mortality of traumatic brain injury (TBI). Detailed analyses of transcriptomic changes in the brain and adipose tissue were performed to elucidate the interactive effects be...

    Authors: Rebecca J. Henry, James P. Barrett, Maria Vaida, Niaz Z. Khan, Oleg Makarevich, Rodney M. Ritzel, Alan I. Faden and Bogdan A. Stoica
    Citation: Journal of Neuroinflammation 2024 21:113
  14. Traumatic encephalopathy syndrome (TES) is defined as the clinical manifestation of the neuropathological entity chronic traumatic encephalopathy (CTE). A core feature of TES is neurobehavioral dysregulation (...

    Authors: Suzan van Amerongen, Surya V. Pulukuri, Fatima Tuz-Zahra, Yorghos Tripodis, Jonathan D. Cherry, Charles Bernick, Yonas E. Geda, Jennifer V. Wethe, Douglas I. Katz, Michael L. Alosco, Charles H. Adler, Laura J. Balcer, Nicholas J. Ashton, Kaj Blennow, Henrik Zetterberg, Daniel H. Daneshvar…
    Citation: Journal of Neuroinflammation 2024 21:46
  15. Monocytes represent key cellular elements that contribute to the neurological sequela following brain injury. The current study reveals that trauma induces the augmented release of a transcriptionally distinct...

    Authors: Erwin K. Gudenschwager Basso, Jing Ju, Eman Soliman, Caroline de Jager, Xiaoran Wei, Kevin J. Pridham, Michelle L. Olsen and Michelle H. Theus
    Citation: Journal of Neuroinflammation 2024 21:41
  16. Traumatic brain injury (TBI) is a key contributor to global morbidity that lacks effective treatments. Microbial infections are common in TBI patients, and their presence could modify the physiological respons...

    Authors: Tamara L. Baker, David K. Wright, Alessandro D. Uboldi, Christopher J. Tonkin, Anh Vo, Trevor Wilson, Stuart J. McDonald, Richelle Mychasiuk, Bridgette D. Semple, Mujun Sun and Sandy R. Shultz
    Citation: Journal of Neuroinflammation 2024 21:14
  17. Efferocytosis is a process that removes apoptotic cells and cellular debris. Clearance of these cells alleviates neuroinflammation, prevents the release of inflammatory molecules, and promotes the production o...

    Authors: Eman Soliman, John Leonard, Erwin Kristobal Gudenschwager Basso, Ilana Gershenson, Jing Ju, Jatia Mills, Caroline de Jager, Alexandra M. Kaloss, Mohamed Elhassanny, Daniela Pereira, Michael Chen, Xia Wang and Michelle H. Theus
    Citation: Journal of Neuroinflammation 2023 20:256
  18. Childhood represents a period of significant growth and maturation for the brain, and is also associated with a heightened risk for mild traumatic brain injuries (mTBI). There is also concern that repeated-mTB...

    Authors: Katie J. Neale, Hannah M. O. Reid, Barbara Sousa, Erin McDonagh, Jamie Morrison, Sandy Shultz, Eric Eyolfson and Brian R. Christie
    Citation: Journal of Neuroinflammation 2023 20:250
  19. Neuroinflammation contributes to secondary injury cascades following traumatic brain injury (TBI), with alternating waves of inflammation and resolution. Interleukin-1 (IL-1), a critical neuroinflammatory medi...

    Authors: Jonathan C. Vincent, Colleen N. Garnett, James B. Watson, Emma K. Higgins, Teresa Macheda, Lydia Sanders, Kelly N. Roberts, Ryan K. Shahidehpour, Eric M. Blalock, Ning Quan and Adam D. Bachstetter
    Citation: Journal of Neuroinflammation 2023 20:248

    The Correction to this article has been published in Journal of Neuroinflammation 2023 20:287

  20. Traumatic brain injury (TBI) is a significant worldwide public health concern that necessitates attention. Apoptosis signal-regulating kinase 1 (ASK1), a key player in various central nervous system (CNS) dise...

    Authors: Shan Meng, Hui Cao, Yichen Huang, Ziyu Shi, Jiaying Li, Yana Wang, Yue Zhang, Shuning Chen, Hong Shi and Yanqin Gao
    Citation: Journal of Neuroinflammation 2023 20:244
  21. Understanding the microglial neuro-immune interactions in the primate brain is vital to developing therapeutics for cortical injury, such as stroke or traumatic brain injury. Our previous work showed that mese...

    Authors: Yuxin Zhou, Hrishti Bhatt, Chromewell A. Mojica, Hongqi Xin, Monica A. Pessina, Douglas L. Rosene, Tara L. Moore and Maria Medalla
    Citation: Journal of Neuroinflammation 2023 20:201
  22. Individuals who have experienced mild traumatic brain injuries (mTBIs) suffer from several comorbidities, including chronic pain. Despite extensive studies investigating the underlying mechanisms of mTBI-assoc...

    Authors: Tyler Nguyen, Natalie Nguyen, Ashlyn G. Cochran, Jared A. Smith, Mohammed Al-Juboori, Andrew Brumett, Saahil Saxena, Sarah Talley, Edward M. Campbell, Alexander G. Obukhov and Fletcher A. White
    Citation: Journal of Neuroinflammation 2023 20:196
  23. Traumatic brain injury (TBI) remains a major cause of death and severe disability worldwide. We found previously that treatment with exogenous naïve B cells was associated with structural and functional neurop...

    Authors: Liam J. Dwyer, Saumya Maheshwari, Emily Levy, Mark C. Poznansky, Michael J. Whalen and Ruxandra F. Sîrbulescu
    Citation: Journal of Neuroinflammation 2023 20:133

About the collection

The neuroinflammatory hypothesis of traumatic brain injury (TBI) broadly states that neuroinflammatory mechanisms underlie many of the negative sequela of TBI. Each year, millions of people experience a TBI, with worldwide estimates suggesting as many as 69 million people suffer a TBI annually. In the United States alone, more than 40 million Americans over 40 years of age are living with TBI. Suffering a TBI increases the 30-year mortality rate by 2.2 – 2.9x, and it frequently induces depression, cognitive impairment, and other neurobehavioral dysfunction. TBI also increases susceptibility to acute and chronic neurodegenerative disorders, including epilepsy, Parkinson’s disease, and Alzheimer’s disease. Although clinical trials for TBI biomarkers and therapeutics have largely failed, major advances in the identification of functional neuroimmune and neuroinflammatory mechanisms hold renewed promise as important post-traumatic therapeutic targets. This Collection seeks to explore these novel functional mechanisms after TBI with an eye towards elucidating and modifying the pathogenic progression to the various post-traumatic syndromes.

As part of this Collection, we invite articles that include:

• Innate immune and neuroimmune mechanisms, including DAMP’s and complement signaling
• Adaptive immune and neuroimmune mechanisms
• Meningeal lymphatics, glymphatic, lymphatic dysfunction in TBI
• Gut/neuroinflammatory axis
• Vascular/neuroimmune axis
• Immune cell/brain cell interactions
• Immunometabolism and TBI
• Neuroinflammatory biomarkers of TBI severity and outcomes
• Sex as a biological variable in the neuroimmune response to injury
• Translational human immune mechanisms
• Astrocyte and microglial mechanisms and function

Submission Guidelines

Back to top

This Collection welcomes submission of original Research Articles. Should you wish to submit a different article type, please read our submission guidelines to confirm that type is accepted by the journal. Articles for this Collection should be submitted via our submission system, Snapp. During the submission process you will be asked whether you are submitting to a Collection, please select "Neuroimmune and Neuroinflammatory Mechanisms in Traumatic Brain Injury" from the dropdown menu.

Articles will undergo the journal’s standard peer-review process and are subject to all of the journal’s standard policies. Articles will be added to the Collection as they are published.

The Guest Editors have no competing interests with the submissions which they handle through the peer review process. The peer review of any submissions for which the Guest Editors have competing interests is handled by another Editorial Board Member who has no competing interests.