Sara D. Johnson
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Sara D. Johnson has a total of 19 co-authors. Here are the top co-authors by number of shared publications:
- M. Rita I. Young
Research Service (151), Ralph H. Johnson Veterans Affairs Medical Center, 109 Bee Street, Charleston, SC 29401, USA
2 shared publications - Alexa Corker
College of Graduate Studies, Medical University of South Carolina, 171 Ashley Ave, Charleston, SC 29425, United States; Department of Medicine, Division of Cardiology, Medical University of South Carolina, 171 Ashley Ave, Charleston, SC 29425, United States; RResearch Service, Ralph H. Johnson Veterans Affairs Health Care System, 109 Bee St, Charleston, SC 29401, United States
1 shared publication - Amanda C. LaRue
Research Service, Ralph H. Johnson VA Health Care System, Charleston, USA
1 shared publication - Amber Hazzard
College of Graduate Studies, Medical University of South Carolina, 171 Ashley Ave, Charleston, SC 29425, United States; Department of Medicine, Division of Cardiology, Medical University of South Carolina, 171 Ashley Ave, Charleston, SC 29425, United States; RResearch Service, Ralph H. Johnson Veterans Affairs Health Care System, 109 Bee St, Charleston, SC 29401, United States
1 shared publication - Amy D. Bradshaw
Medical University of South Carolina
1 shared publication - An Van Laer
Department of Medicine, Division of Cardiology, Medical University of South Carolina, 171 Ashley Ave, Charleston, SC 29425, United States; RResearch Service, Ralph H. Johnson Veterans Affairs Health Care System, 109 Bee St, Charleston, SC 29401, United States
1 shared publication
Latest Publications
- Open Access
- 18 February 2025
- Published by Elsevier in Journal of Molecular and Cellular Cardiology
- Vol. 201, 32-43
Mouse model of post-traumatic stress disorder negatively impacts cardiac homeostasis
- 18 February 2025
- Published by Elsevier in Journal of Molecular and Cellular Cardiology
- Vol. 201, 32-43
Open AccessMouse model of post-traumatic stress disorder negatively impacts cardiac homeostasis
- Open Access
Cytokine and Adipokine Levels in Patients with Premalignant Oral Lesions or in Patients with Oral Cancer Who Did or Did Not Receive 1α,25-Dihydroxyvitamin D3 Treatment upon Cancer Diagnosis
Differences in levels of inflammation-modulating cytokines and adipokines in patients with premalignant oral lesions versus in patients that develop squamous cell carcinoma of the head and neck (HNSCC) were assessed. Also assessed was the impact of treating HNSCC patients with the immune regulatory mediator, 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3], on modulators of inflammation. Compared to healthy controls, patients with premalignant oral lesions had increases in their systemic levels of the inflammatory cytokines IL-6 and IL-17, and increases in the adipokine, leptin. However, levels of these pro-inflammatory cytokines and adipokine were reduced in patients with HNSCC. Treatment of HNSCC patients with 1,25(OH)2D3 increased levels of each of the measured immune mediators. Levels of the anti-inflammatory adipokine, adiponectin, were shifted inversely with the levels of the pro-inflammatory cytokines and with leptin. These studies demonstrate heightened immune reactivity in patients with premalignant lesions, which wanes in patients with HNSCC, but which is restored by treatment with 1,25(OH)2D3.
Open AccessCytokine and Adipokine Levels in Patients with Premalignant Oral Lesions or in Patients with Oral Cancer Who Did or Did Not Receive 1α,25-Dihydroxyvitamin D3 Treatment upon Cancer Diagnosis
Differences in levels of inflammation-modulating cytokines and adipokines in patients with premalignant oral lesions versus in patients that develop squamous cell carcinoma of the head and neck (HNSCC) were assessed. Also assessed was the impact of treating HNSCC patients with the immune regulatory mediator, 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3], on modulators of inflammation. Compared to healthy controls, patients with premalignant oral lesions had increases in their systemic levels of the inflammatory cytokines IL-6 and IL-17, and increases in the adipokine, leptin. However, levels of these pro-inflammatory cytokines and adipokine were reduced in patients with HNSCC. Treatment of HNSCC patients with 1,25(OH)2D3 increased levels of each of the measured immune mediators. Levels of the anti-inflammatory adipokine, adiponectin, were shifted inversely with the levels of the pro-inflammatory cytokines and with leptin. These studies demonstrate heightened immune reactivity in patients with premalignant lesions, which wanes in patients with HNSCC, but which is restored by treatment with 1,25(OH)2D3.
- Open Access
Effect of the Premalignant and Tumor Microenvironment on Immune Cell Cytokine Production in Head and Neck Cancer
Head and neck squamous cell carcinoma (HNSCC) is marked by immunosuppression, a state in which the established tumor escapes immune attack. However, the impact of the premalignant and tumor microenvironments on immune reactivity has yet to be elucidated. The purpose of this study was to determine how soluble mediators from cells established from carcinogen-induced oral premalignant lesions and HNSCC modulate immune cell cytokine production. It was found that premalignant cells secrete significantly increased levels of G-CSF, RANTES, MCP-1, and PGE2 compared to HNSCC cells. Splenocytes incubated with premalignant supernatant secreted significantly increased levels of Th1-, Th2-, and Th17-associated cytokines compared to splenocytes incubated with HNSCC supernatant. These studies demonstrate that whereas the premalignant microenvironment elicits proinflammatory cytokine production, the tumor microenvironment is significantly less immune stimulatory and may contribute to immunosuppression in established HNSCC.
Open AccessEffect of the Premalignant and Tumor Microenvironment on Immune Cell Cytokine Production in Head and Neck Cancer
Head and neck squamous cell carcinoma (HNSCC) is marked by immunosuppression, a state in which the established tumor escapes immune attack. However, the impact of the premalignant and tumor microenvironments on immune reactivity has yet to be elucidated. The purpose of this study was to determine how soluble mediators from cells established from carcinogen-induced oral premalignant lesions and HNSCC modulate immune cell cytokine production. It was found that premalignant cells secrete significantly increased levels of G-CSF, RANTES, MCP-1, and PGE2 compared to HNSCC cells. Splenocytes incubated with premalignant supernatant secreted significantly increased levels of Th1-, Th2-, and Th17-associated cytokines compared to splenocytes incubated with HNSCC supernatant. These studies demonstrate that whereas the premalignant microenvironment elicits proinflammatory cytokine production, the tumor microenvironment is significantly less immune stimulatory and may contribute to immunosuppression in established HNSCC.