alexa An Inflammatory Cytokine Milieu is Prominent in Premalignant Oral Lesions, but Subsides when Lesions Progress to Squamous Cell Carcinoma | OMICS International | Abstract
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Research Article

An Inflammatory Cytokine Milieu is Prominent in Premalignant Oral Lesions, but Subsides when Lesions Progress to Squamous Cell Carcinoma

Danielle Woodford1-3, Sara D Johnson1,2, Anna-Maria A De Costa1,2 and M Rita I Young1,2*
1Research Service, Ralph H. Johnson Veterans Affairs Medical Center, Charleston, SC, USA
2Department of Otolaryngology, Head and Neck Surgery, Medical University of South Carolina, Charleston, SC, USA
3Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA
Corresponding Author : M. Rita I. Young
Research Service (151), Ralph H. Johnson VA Medical Center
109 Bee Street, Charleston, SC 29401, USA
Tel: 843-789-6707
Fax: 478-274-5761
E-mail: [email protected]
Received: March 26, 2014; Accepted: June 20, 2014; Published: June 27, 2014
Citation: Woodford D, Johnson SD, De Costa AMA, Young MRI (2014) An Inflammatory Cytokine Milieu is Prominent in Premalignant Oral Lesions, but Subsides when Lesions Progress to Squamous Cell Carcinoma. J Clin Cell Immunol 5:230. doi:10.4172/2155-9899.1000230
Copyright: © 2014 Woodford D, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

While head and neck squamous cell carcinomas (HNSCC) are associated with profound immune suppression, less is known about the immunological milieu of premalignant oral lesions. The present study shows dynamic shifts in the immune milieu within premalignant oral lesions and when they have progressed to HNSCC. Specifically, this study showed that the premalignant lesion environment consists of inflammatory mediators and IL-17, but this inflammatory phenotype declines when premalignant oral lesions have progressed to HNSCC. The cytokine profiles of human tissues did not correspond with plasma cytokine profiles. A murine carcinogen-induced premalignant lesion model that progresses to HNSCC was used to examine cytokine profiles released from tissues as well as regional lymph nodes. As in human tissues, murine premalignant lesions and regional lymph nodes released high levels of inflammatory cytokines and, very prominently, IL-17. Also similar to human tissues, release of inflammatory cytokines declined in HNSCC tissues of mice and in the regional lymph nodes of mice with HNSCC. Studies focusing on IL-17 showed that mediators from premalignant lesions stimulated normal spleen cells to produce increased levels of IL-17, while mediators from HNSCC were less stimulatory toward IL-17 production. IL-17 production by Th17-skewed CD4+ cells was strongly inhibited by normal oral epithelium as well as HNSCC. In contrast, premalignant lesion-derived mediators further increased IL-17 production by Th17-skewed cells. The stimulation of IL-17 production by premalignant lesions was dependent on IL-23, which premalignant lesions released in higher amounts than control tissues or HNSCC. HNSCC tissues instead produced increased levels of TGF-β compared to premalignant lesions, and skewed normal spleen cells toward the Treg phenotype. This skewing was blocked by supplementation with IL-23. These studies suggest IL-23 to be a significant contributor to the inflammatory IL-17 phenotype in premalignant oral lesions and suggest the decline in IL-23 in HNSCC leads to a decline in Th17 cells.

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