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Article ; Online: Neuroinflammation is a player in coma, but in which role?

Tenovuo, Olli / Loane, David J

2024 Volume 147, Issue 4, Page(s) 1121–1123

MeSH term(s)	Humans ; Coma ; Neuroinflammatory Diseases ; Coma, Post-Head Injury ; Inflammation
Language	English
Publishing date	2024-04-04
Publishing country	England
Document type	Editorial ; Comment
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awae082
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Article ; Online: MAnGLed astrocytes in traumatic brain injury: astrocytic 2-AG metabolism as a new therapeutic target.

Loane, David J

Brain : a journal of neurology

2022 Volume 145, Issue 1, Page(s) 7–10

MeSH term(s)	Astrocytes/metabolism ; Brain Injuries ; Brain Injuries, Traumatic/metabolism ; Humans
Language	English
Publishing date	2022-03-30
Publishing country	England
Document type	Editorial ; Comment
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awac014
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Article: Targeting chronic and evolving neuroinflammation following traumatic brain injury to improve long-term outcomes: insights from microglial-depletion models.

Henry, Rebecca J / Loane, David J

Neural regeneration research

2020 Volume 16, Issue 5, Page(s) 976–977

Language	English
Publishing date	2020-11-23
Publishing country	India
Document type	Journal Article
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.297068
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Article ; Online: Experimental Models of Hospital-Acquired Infections After Traumatic Brain Injury: Challenges and Opportunities.

Gandasasmita, Natasha / Li, Jian / Loane, David J / Semple, Bridgette D

Journal of neurotrauma

2023 Volume 41, Issue 7-8, Page(s) 752–770

Abstract: Patients hospitalized after a moderate or severe traumatic brain injury (TBI) are at increased risk of nosocomial infections, including bacterial pneumonia and other upper respiratory tract infections. Infections represent a secondary immune challenge ... ...

Abstract	Patients hospitalized after a moderate or severe traumatic brain injury (TBI) are at increased risk of nosocomial infections, including bacterial pneumonia and other upper respiratory tract infections. Infections represent a secondary immune challenge for vulnerable TBI patients that can lead to increased morbidity and poorer long-term prognosis. This review first describes the clinical significance of infections after TBI, delving into the known mechanisms by which a TBI can alter systemic immunological responses towards an immunosuppressive state, leading to promotion of increased vulnerability to infections. Pulmonary dysfunction resulting from respiratory tract infections is considered in the context of neurotrauma, including the bidirectional relationship between the brain and lungs. Turning to pre-clinical modeling, current laboratory approaches to study experimental TBI and lung infections are reviewed, to highlight findings from the limited key studies to date that have incorporated both insults. Then, practical decisions for the experimental design of animal studies of post-injury infections are discussed. Variables associated with the host animal, the infectious agent (e.g., species, strain, dose, and administration route), as well as the timing of the infection relative to the injury model are important considerations for model development. Together, the purpose of this review is to highlight the significant clinical need for increased pre-clinical research into the two-hit insult of a hospital-acquired infection after TBI to encourage further scientific enquiry in the field.
MeSH term(s)	Animals ; Humans ; Brain Injuries, Traumatic/complications ; Brain Injuries ; Cross Infection ; Disease Models, Animal ; Hospitals
Language	English
Publishing date	2023-12-26
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	645092-1
ISSN	1557-9042 ; 0897-7151
ISSN (online)	1557-9042
ISSN	0897-7151
DOI	10.1089/neu.2023.0453
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Article ; Online: Fundamental Neurochemistry Review: Microglial immunometabolism in traumatic brain injury.

Strogulski, Nathan R / Portela, Luis V / Polster, Brian M / Loane, David J

Journal of neurochemistry

2023 Volume 167, Issue 2, Page(s) 129–153

Abstract: Traumatic brain injury (TBI) is a devastating neurological disorder caused by a physical impact to the brain that promotes diffuse damage and chronic neurodegeneration. Key mechanisms believed to support secondary brain injury include mitochondrial ... ...

Abstract	Traumatic brain injury (TBI) is a devastating neurological disorder caused by a physical impact to the brain that promotes diffuse damage and chronic neurodegeneration. Key mechanisms believed to support secondary brain injury include mitochondrial dysfunction and chronic neuroinflammation. Microglia and brain-infiltrating macrophages are responsible for neuroinflammatory cytokine and reactive oxygen species (ROS) production after TBI. Their production is associated with loss of homeostatic microglial functions such as immunosurveillance, phagocytosis, and immune resolution. Beyond providing energy support, mitochondrial metabolic pathways reprogram the pro- and anti-inflammatory machinery in immune cells, providing a critical immunometabolic axis capable of regulating immunologic response to noxious stimuli. In the brain, the capacity to adapt to different environmental stimuli derives, in part, from microglia's ability to recognize and respond to changes in extracellular and intracellular metabolite levels. This capacity is met by an equally plastic metabolism, capable of altering immune function. Microglial pro-inflammatory activation is associated with decreased mitochondrial respiration, whereas anti-inflammatory microglial polarization is supported by increased oxidative metabolism. These metabolic adaptations contribute to neuroimmune responses, placing mitochondria as a central regulator of post-traumatic neuroinflammation. Although it is established that profound neurometabolic changes occur following TBI, key questions related to metabolic shifts in microglia remain unresolved. These include (a) the nature of microglial mitochondrial dysfunction after TBI, (b) the hierarchical positions of different metabolic pathways such as glycolysis, pentose phosphate pathway, glutaminolysis, and lipid oxidation during secondary injury and recovery, and (c) how immunometabolism alters microglial phenotypes, culminating in chronic non-resolving neuroinflammation. In this basic neurochemistry review article, we describe the contributions of immunometabolism to TBI, detail primary evidence of mitochondrial dysfunction and metabolic impairments in microglia and macrophages, discuss how major metabolic pathways contribute to post-traumatic neuroinflammation, and set out future directions toward advancing immunometabolic phenotyping in TBI.
MeSH term(s)	Animals ; Mice ; Microglia/metabolism ; Neurochemistry ; Neuroinflammatory Diseases ; Brain Injuries, Traumatic/metabolism ; Anti-Inflammatory Agents ; Mice, Inbred C57BL
Chemical Substances	Anti-Inflammatory Agents
Language	English
Publishing date	2023-09-27
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.15959
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Article ; Online: Understanding microglial responses in large animal models of traumatic brain injury: an underutilized resource for preclinical and translational research.

Grovola, Michael R / von Reyn, Catherine / Loane, David J / Cullen, D Kacy

Journal of neuroinflammation

2023 Volume 20, Issue 1, Page(s) 67

Abstract: Traumatic brain injury (TBI) often results in prolonged or permanent brain dysfunction with over 2.8 million affected annually in the U.S., including over 56,000 deaths, with over 5 million total survivors exhibiting chronic deficits. Mild TBI (also ... ...

Abstract	Traumatic brain injury (TBI) often results in prolonged or permanent brain dysfunction with over 2.8 million affected annually in the U.S., including over 56,000 deaths, with over 5 million total survivors exhibiting chronic deficits. Mild TBI (also known as concussion) accounts for over 75% of all TBIs every year. Mild TBI is a heterogeneous disorder, and long-term outcomes are dependent on the type and severity of the initial physical event and compounded by secondary pathophysiological consequences, such as reactive astrocytosis, edema, hypoxia, excitotoxicity, and neuroinflammation. Neuroinflammation has gained increasing attention for its role in secondary injury as inflammatory pathways can have both detrimental and beneficial roles. For example, microglia-resident immune cells of the central nervous system (CNS)-influence cell death pathways and may contribute to progressive neurodegeneration but also aid in debris clearance and neuroplasticity. In this review, we will discuss the acute and chronic role of microglia after mild TBI, including critical protective responses, deleterious effects, and how these processes vary over time. These descriptions are contextualized based on interspecies variation, sex differences, and prospects for therapy. We also highlight recent work from our lab that was the first to describe microglial responses out to chronic timepoints after diffuse mild TBI in a clinically relevant large animal model. The scaled head rotational acceleration of our large animal model, paired with the gyrencephalic architecture and appropriate white:gray matter ratio, allows us to produce pathology with the same anatomical patterns and distribution of human TBI, and serves as an exemplary model to examine complex neuroimmune response post-TBI. An improved understanding of microglial influences in TBI could aid in the development of targeted therapeutics to accentuate positive effects while attenuating detrimental post-injury responses over time.
MeSH term(s)	Animals ; Female ; Humans ; Male ; Microglia/metabolism ; Neuroinflammatory Diseases ; Translational Research, Biomedical ; Brain Injuries, Traumatic/pathology ; Brain Concussion/complications ; Disease Models, Animal
Language	English
Publishing date	2023-03-09
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-023-02730-z
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Article ; Online: Brain-gut axis dysfunction in the pathogenesis of traumatic brain injury.

Hanscom, Marie / Loane, David J / Shea-Donohue, Terez

The Journal of clinical investigation

2021 Volume 131, Issue 12

Abstract: Traumatic brain injury (TBI) is a chronic and progressive disease, and management requires an understanding of both the primary neurological injury and the secondary sequelae that affect peripheral organs, including the gastrointestinal (GI) tract. The ... ...

Abstract	Traumatic brain injury (TBI) is a chronic and progressive disease, and management requires an understanding of both the primary neurological injury and the secondary sequelae that affect peripheral organs, including the gastrointestinal (GI) tract. The brain-gut axis is composed of bidirectional pathways through which TBI-induced neuroinflammation and neurodegeneration impact gut function. The resulting TBI-induced dysautonomia and systemic inflammation contribute to the secondary GI events, including dysmotility and increased mucosal permeability. These effects shape, and are shaped by, changes in microbiota composition and activation of resident and recruited immune cells. Microbial products and immune cell mediators in turn modulate brain-gut activity. Importantly, secondary enteric inflammatory challenges prolong systemic inflammation and worsen TBI-induced neuropathology and neurobehavioral deficits. The importance of brain-gut communication in maintaining GI homeostasis highlights it as a viable therapeutic target for TBI. Currently, treatments directed toward dysautonomia, dysbiosis, and/or systemic inflammation offer the most promise.
MeSH term(s)	Animals ; Brain/metabolism ; Brain/microbiology ; Brain/pathology ; Brain Injuries, Traumatic/metabolism ; Brain Injuries, Traumatic/microbiology ; Brain Injuries, Traumatic/pathology ; Gastrointestinal Microbiome ; Humans ; Inflammation/metabolism ; Inflammation/microbiology ; Inflammation/pathology ; Intestinal Mucosa/metabolism ; Intestinal Mucosa/microbiology ; Intestinal Mucosa/pathology
Language	English
Publishing date	2021-06-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI143777
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Article ; Online: Traumatic meningeal injury and repair mechanisms.

Loane, David J / Faden, Alan I

Nature immunology

2018 Volume 19, Issue 5, Page(s) 431–432

MeSH term(s)	Brain Concussion ; Humans ; Meninges ; Myeloid Cells ; Myeloid Progenitor Cells
Language	English
Publishing date	2018-04-18
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/s41590-018-0093-3
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Zs.A 5294: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 42: Show issues

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Article ; Online: Mesenchymal stromal cell secretome for traumatic brain injury: Focus on immunomodulatory action.

Pischiutta, Francesca / Caruso, Enrico / Cavaleiro, Helena / Salgado, Antonio J / Loane, David J / Zanier, Elisa R

Experimental neurology

2022 Volume 357, Page(s) 114199

Abstract: The severity and long-term consequences of brain damage in traumatic brain injured (TBI) patients urgently calls for better neuroprotective/neuroreparative strategies for this devastating disorder. Mesenchymal stromal cells (MSCs) hold great promise and ... ...

Abstract	The severity and long-term consequences of brain damage in traumatic brain injured (TBI) patients urgently calls for better neuroprotective/neuroreparative strategies for this devastating disorder. Mesenchymal stromal cells (MSCs) hold great promise and have been shown to confer neuroprotection in experimental TBI, mainly through paracrine mechanisms via secreted bioactive factors (i.e. secretome), which indicates significant potential for a cell-free neuroprotective approach. The secretome is composed of cytokines, chemokines, growth factors, proteins, lipids, nucleic acids, metabolites, and extracellular vesicles; it may offer advantages over MSCs in terms of delivery, safety, and variability of therapeutic response for brain injury. Immunomodulation by molecular factors secreted by MSCs is considered to be a key mechanism involved in their multi-potential therapeutic effects. Regulated neuroinflammation is required for healthy remodeling of central nervous system during development and adulthood. Moreover, immune cells and their secreted factors can also contribute to tissue repair and neurological recovery following acute brain injury. However, a chronic and maladaptive neuroinflammatory response can exacerbate TBI and contribute to progressive neurodegeneration and long-term neurological impairments. Here, we review the evidence for MSC-derived secretome as a therapy for TBI. Our framework incorporates a detailed analysis of in vitro and in vivo studies investigating the effects of the secretome on clinically relevant neurological and histopathological outcomes. We also describe the activation of immune cells after TBI and the immunomodulatory properties exerted by mediators released in the secretome. We then describe how ageing modifies central and systemic immune responses to TBI and discuss challenges and opportunities of developing secretome based neuroprotective therapies for elderly TBI populations. Finally, strategies aimed at modulating the secretome in order to boost its efficacy for TBI will also be discussed.
MeSH term(s)	Adult ; Aged ; Brain Injuries/pathology ; Brain Injuries, Traumatic/pathology ; Humans ; Immunity ; Immunomodulation ; Mesenchymal Stem Cells/metabolism ; Secretome
Language	English
Publishing date	2022-08-08
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2022.114199
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Article ; Online: Bi-directional neuro-immune dysfunction after chronic experimental brain injury.

Ritzel, Rodney M / Li, Yun / Jiao, Yun / Doran, Sarah J / Khan, Niaz / Henry, Rebecca J / Brunner, Kavitha / Loane, David J / Faden, Alan I / Szeto, Gregory L / Wu, Junfang

Journal of neuroinflammation

2024 Volume 21, Issue 1, Page(s) 83

Abstract: Background: It is well established that traumatic brain injury (TBI) causes acute and chronic alterations in systemic immune function and that systemic immune changes contribute to posttraumatic neuroinflammation and neurodegeneration. However, how TBI ... ...

Abstract	Background: It is well established that traumatic brain injury (TBI) causes acute and chronic alterations in systemic immune function and that systemic immune changes contribute to posttraumatic neuroinflammation and neurodegeneration. However, how TBI affects bone marrow (BM) hematopoietic stem/progenitor cells chronically and to what extent such changes may negatively impact innate immunity and neurological function has not been examined. Methods: To further understand the role of BM cell derivatives on TBI outcome, we generated BM chimeric mice by transplanting BM from chronically injured or sham (i.e., 90 days post-surgery) congenic donor mice into otherwise healthy, age-matched, irradiated CD45.2 C57BL/6 (WT) hosts. Immune changes were evaluated by flow cytometry, multiplex ELISA, and NanoString technology. Moderate-to-severe TBI was induced by controlled cortical impact injury and neurological function was measured using a battery of behavioral tests. Results: TBI induced chronic alterations in the transcriptome of BM lineage Conclusions: TBI causes chronic activation and progressive dysfunction of the BM stem/progenitor cell pool, which drives long-term deficits in hematopoiesis, innate immunity, and neurological function, as well as altered sensitivity to subsequent brain injury.
MeSH term(s)	Mice ; Animals ; Neuroinflammatory Diseases ; Mice, Inbred C57BL ; Brain Injuries, Traumatic/pathology ; Brain Injuries/pathology ; Brain/metabolism
Language	English
Publishing date	2024-04-05
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-024-03082-y
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