GodboutJonathanAssistant Director for Basic Science, Institute for Behavioral Medicine Research
Professor, Center for Brain and Spinal Cord Repair
Professor, Department of Neuroscience
Faculty Director, Chronic Brain Injury

College of Medicine
Department of Neuroscience

Google scholar articles
PubMed articles

231 Institute for Behavioral Medicine Research Building
460 Medical Center Drive
Columbus, OH 43210

My Research Lab: Godbout Lab for Neuroimmunology, Neurotrauma, and Behavior

Current Research:
1. Aging and Neuroimmunology
Microglia and astrocytes are key cells that recognize, interpret, propagate and regulate immune responses. In the elderly, peripheral infections can trigger delirium and behavioral disturbances. Moreover, ongoing inflammatory processes in the elderly are associated with depressive-like complications. These complications are not a normal part of aging and negatively affect quality of life and life-span. Impaired regulation of microglia could cause this altered communication between the immune system and the aged brain. 

Dr. Godbout's lab has identified astrocytes as the pivotal cell in the failure to resolve microglial activation in the aged brain following immune challenge. Activated astrocytes in the aged brain have reduced sensitivity to IL-10, an anti-inflammatory cytokine and decreased IL-10 receptor-1 expression. This IL-10 insensitivity of aged astrocytes results in failure to produce TGFα and attenuate microglial activation. They are testing the hypothesis that prolonged neuroinflammation in the aged brain following a peripheral inflammatory challenge is caused by impaired astrocyte-dependent regulation of microglia. Understanding how impaired IL-10 re-programming of astrocytes contributes to neuroinflammation and depressive-like behavior will lead to new interventions that target astrocytes in order to reduce neuropsychiatric complications associated with inflammatory challenge in the aged. 

2. Brain Injury and Intervention Project
Traumatic brain injury (TBI) can lead to secondary neuropsychiatric complications that develop and persist years after injury. Mounting evidence indicates that neuroinflammatory processes continue to advance after the initial head injury and can worsen with time and are likely mediated by microglia and astrocytes. Therefore, it is critical to identify interventions that can be provided immediately after TBI that reduce glia-mediated inflammation, facilitate functional recovery, and reduce the development of TBI-induced long-term complications in behavior, cognition, and pathology.

Immediate intervention with methylene blue (MB), an antioxidant and anti-inflammatory agent, reduces neuroinflammation in mice after moderate and diffuse TBI, improves functional recovery, and limits the development of a primed and reactive microglia one month after injury. They are investigating the degree to which MB intervention shifts the activation profile of microglia and astrocytes and protects against secondary complications following TBI including cognitive decline, glia-mediated inflammation and glial reactivity to immune challenge. 

3. Stress Neuroimmunology 
Brain region dependent trafficking of myeloid cells following repeated social defeat

Project Summary/Abstract: Psychosocial stressors are associated with an increased prevalence of mental health complications including anxiety and depression. Although chronic stressors negatively affect health and influence quality of life, the mechanisms that underlie these neurobehavioral deficits are not well understood. Repeated social defeat (RSD)-induced anxiety-like behavior is associated with the egress and trafficking of bone marrow (BM)-derived, glucocorticoid (GC)-insensitive myeloid cells to the brain. Moreover, RSD promotes the infiltration of CD11b+/Ly6Chigh/CCR2+ myeloid cells to specific brain regions associated with fear and threat appraisal.  IL-1 receptor type-1 (IL-1R1) and -adrenergic receptor (-ADR)-dependent pathways are critical in the development of behavioral and immunological alterations promoted by RSD. They are testing our hypothesis that repeated social defeat stimulates trafficking of primed GC-insensitive, CD11b+/LyC6high/CCR2+ myeloid cells from the bone marrow to fear and threat appraisal regions in the brain to promote prolonged anxiety-like behavior.

To address this hypothesis, they are using a mouse model of repeated social defeat to understand how stress-associated promotion of myeloid cell trafficking contributes to neuroinflammation and the promotion of long-lasting anxiety-like behavior. This understanding could lead to novel interventions to target myeloid cell trafficking and attenuate prolonged neurobehavioral complications associated with chronic stress.

Research Techniques: Cell flow cytometry; FAC-Sorting; immunohistochemistry; neurochemistry; RNA analyses; ELISA; bone marrow chimeras; microglia; astrocyte, and macrophage specific isolations; fluid percussion injury; glia cultures; behavioral and cognitive analyses

Active Funding:

1.  Principal investigator, R01, NIH/NIA 
8/1/2016- 7/31/2021
Consequences of Age-Related Impairments in the Dynamic Regulation of Active Microglia by Astrocytes

2.  Principal investigator, R56, NIH/NINDS
8/1/2017- 7/31/2018
Acute and Long-Term Benefits of Methylene Blue Intervention after TBI on Neuroinflammation, Glial Dysfunction, and Neuropsychiatric Complications

3. Co-investigator, R01, NIH/NIMH 
4/01/13 – 3/31/18
Brain region dependent trafficking of myeloid cells following repeated social defeat 

4. Co-investigator, R01, NIH/NIMH 
1/01/12 -12/30/17 (extension)
Source: NIH/National Institute of Mental Health
Brain region dependent trafficking of myeloid cells following repeated social defeat 

5. Co-investigator, R01, NIH/NINDS 
10/2016- 9/31/2021        
Behavioral and cellular determinants of treadmill training and recovery after SCI 

6. Co-investigator, R01, NIH/NIMH 
Anxiety, IL-1R1, and Neuroinflammation

7. Co-investigator, R01, NIH/NINDS
Glucocorticoids and Sensory Neuron Plasticity 

8. Co-investigator, R21, NIH/NINDS
08/15/2016 – 07/31/2019
Neuroprotective role of Vitamin D during Childhood

9. Co-investigator, R01, NIH/NCI
Affective Consequences of Chemotherapy

PhD: Biochemistry/Signal Transduction, University of Illinois

Fellowship: Research, Rodney Johnson, PhD, University of Illinois; Ruth Kirschstein NRSA Postdoctoral Fellowship

Dr. Godbout is partially funded by the Chronic Brain Injury program, a part of Ohio State’s Discovery Themes Initiative.

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