Expression of
IL-23, a heterodimeric
cytokine involved in the induction of Th17 cells, is increased in human
tumors. Although the endogenous
IL-23 expression has been reported to promote
tumor development and growth, the studies using local and systemic administration of
IL-23 have shown that its application at the excessive amount induces antitumor immune responses.
IL-23 is, today, considered the key driver of intestinal
inflammation and its role in inflammatory responses is tissue-specific. The aim of this study was to investigate the role of circulating levels of
IL-23 in patients with resected
colorectal cancer (CRC) before and after
chemotherapy, respect to healthy controls. Twenty-five patients were enrolled between June 2007 and January 2009, and followed through 2010. All patients underwent
chemotherapy, mostly FOLFOX4. Twenty-sex and age-matched healthy donors were recruited as controls.
IL-23 serum concentrations, measured by a quantitative
enzyme immunoassay technique, were significantly higher in patients with resected CRC (26.02 ± 28.63 pg/ml versus 7.1 ± 6.4 pg/ml, P < 0.001) and after
chemotherapy respect to controls (21.74 ± 23.82 pg/ml versus 7.17 ± 6.43 pg/ml, P < 0.001). An increase was documented also before
chemotherapy (26.02 ± 28.63 pg/ml versus 21.74 ± 23.82 pg/ml, P = 0.7) but not statistically significant. This work investigated, for the first time, the role of
IL-23 in CRC resection and
chemotherapy, showing no correlation with the severity of disease,
tumor removal, and chemotherapeutic treatment. However, other works are needed to better clarify if
IL-23 could be considered a key-molecule in human CRC and a target for
tumor treatment.