Abstract
Abstract Introduction: Visceral adipose tissue is believed to be fuelling a state of chronic inflammation in obese patients, establishing an environment favourable for tumor growth. However, the exact immunological mechanisms remain unclear. Recent animal studies have pointed to an important role for visceral adipose tissue CD8+ T cells in both the establishment of and maintenance of adipose tissue inflammation in obese models. This novel study aimed to phenotypically characterize both CD4+ and CD8+ T cells in the omentum of esophageal adenocarcinoma (EAC) patients, as EAC has one of the strongest association with obesity and arises in a background of inflammation. Methods: Peripheral blood and visceral adipose tissue from the greater omentum were taken from 30 EAC patients at the commencement of resectional surgery. Peripheral blood mononuclear cells were isolated using density centrifugation and the stromal vascular fraction of the adipose tissue was obtained following collagenase digestion. T cell activation status and cytokine production were assessed by both surface and intracellular flow cytometry and serum cytokines were determined by ELISA. Results: The omentum was found to be a rich source of both CD4+ and CD8+ T cells, which display an activated inflammatory phenotype, expressing significantly higher (p<0.0001) CD69, CD107a, CD45RO and IFN-γ than T cells in the blood. Omental CD8+ T cells also expressed significantly higher (p<0.0001) IFN-γ than CD4+ T cells, suggesting that CD8+ T cells are an important source of this inflammatory cytokine within visceral fat. The highest circulating levels of the IFN-γ were detected in the serum of viscerally obese cancer patients. Conclusions: This novel study demonstrates that omental T cells may be key players in driving adipose tissue inflammation, potentially mediated by IFN-γ. The highest serum levels of IFN-γ were detected in viscerally obese cancer patients, suggesting that visceral adipose tissue may be the source of this inflammatory cytokine, thus providing an immunotherapeutic target to attenuate chronic inflammation associated with visceral obesity. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 791. doi:10.1158/1538-7445.AM2011-791
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