Virginia Via Research Day Book 2026

Graduate Student Research Biomedical

04 COMM TREATMENT TO DIRECT IL-6 TRAFFICKING INTO THE LYMPHATIC SYSTEM AFTER BLAST INDUCED NEUROTRAUMA

Nora Ahmed 2 ; Susan Murphy, PhD2; Andrew Krueger, DO1; Gunnar Brolinson, DO1; and Pamela VandeVord, PhD2 Corresponding author: noraa23@vt.edu

1VCOM-Virginia, Blacksburg, Virginia 2Department of Biomedical Engineering and Mechanics, Virginia Tech

lymph nodes. These lymph nodes play a central role in coordinating neuroimmune interactions between the CNS and peripheral lymphatic system. However, IL-6 trafficking into the peripheral lymphatics after blast exposure remains understudied. Currently, no therapies directly target glymphatic dysfunction. For this study, the proposed treatment is cranial osteopathic manipulative medicine (cOMM), a non-invasive, manual-force-based technique that enhances cerebral fluid dynamics. The main technique of cOMM involves applying manual force to the occipital squama and manipulating the bones and sutures of the skull to encourage homeostatic CSF flow, ultimately balancing the body’s overall fluid response. Hypothesis: We hypothesize that cOMM treatment will enhance IL-6 trafficking via lymphatics, resulting in a decrease in pain behaviors. Methods: To test our hypothesis, we performed a pilot study with four groups (n = 6 per group): sham ± cOMM treatment and blast ± cOMM treatment. Blast-exposed animals received three blasts separated by one hour, while sham animals underwent identical experimental procedures without blast exposure. cOMM treatments were administered on days 1, 2, and

3 post-blast. Pain assessments were conducted using manual Von-Frey and an automated rat grimace scale at baseline, 1, 4 and 7 days post-blast. The cervical lymph nodes were collected at day 7 for IL-6 quantification using automated western blot. Results: Based on the proposed methodology, we are in the process of assessing IL-6 protien expression in the cervical lymphatic system following blast injury and are planning to evaluate nociceptive outcomes with cOMM treatment. Conclusion and Potential Impact: As data collection in underway, the application of these approaches may provide new insight into the interplay between neuroinflammation and pain after bTBI, as well as the potential for cOMM to restore lymphatic homeostasis and mitigate early nociceptive signaling.

Background: Within the military population, more than 500,000 service members have sustained a traumatic brain injury (TBI), with approximately one third of cases being attributed to blast exposure (bTBI). Neuroinflammation is a hallmark of TBI, characterized by dysregulated cytokine and chemokine release, and its spatiotemporal distribution has been suggested to influence the onset and severity of behavioral symptoms. Among these symptoms, heightened pain sensitivity in the form of post-traumatic headaches is one of the most common. Previous studies have shown that activation of neuroimmune cells contributes to the production of proinflammatory mediators after injury; however, the acute development of nociception after bTBI, particularly in relation to tissue-specific cytokine trafficking, remains poorly understood. Interleukin-6 (IL-6) is a cytokine that contributes to and can exacerbate neuroinflammation post-TBI. IL-6 can interact with various cell types within the central nervous system (CNS) and the periphery to induce an inflammatory response, yet its trafficking following blast TBI remains unclear. The glymphatic system serves as a major communication pathway between the CNS and peripheral tissues by transporting metabolic waste and excess fluid to the deep cervical

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