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Liu et al. Th17 activation by H. pylori and triglyceride

RESULTS correlation between H. pylori infection and metabolic
factors including plasma glucose, cholesterol, low
The effects of metabolic milieu on H. pylori- density lipoprotein, high density lipoprotein and TG
induced IL-17A expression [Table 2]. Taken together, the data demonstrated that
Since obesity was suggested to play an important H. pylori infection and lipid metabolic disorders could
role in H. felis-induced GC by stimulating Th17 synergistically increase IL-17A expression.
response in mice, we determined the effects of H.
[19]
pylori infection and lipid metabolic disorders on Th17- H. pylori infection contributes to Th17
related cytokines in human GC. Our results showed differentiation and response
that IL-17A was 5-fold higher in H. pylori-infected than IL-6 and leptin have been reported to promote Th17
[19,26]
uninfected patients [Figure 1A], while approximately differentiation and play roles in tumor progression.
Consistently, our results showed that the levels of
1.8-fold increase in IL-17A levels was seen in patients IL-6 and leptin expression were increased 20 and 6
with high TG (> 1.7 mmol/L) comparing to those with folds, respectively, in H. pylori-infected vs. uninfected
normal TG [Figure 1B]. However, abnormal TG could tumors [Figure 2A and B]. This data suggested that
not alone induce IL-17A expression as evidenced in H. pylori infection promoted the expression of factors
H. pylori-negative patients [Figure 1C]. H. pylori could that regulate Th17 differentiation.
increase IL-17A expression by 3.2 folds in patients
with normal plasma TG, but could further increase GM-CSF is an additional cytokine released by Th17
IL-17A expression (5.5 folds) in the milieu of high cells, and importantly, has been strongly linked to
TG content [Figure 1C]. However, the contingency pathogenicity of Th17 cells in other disease states. [27]
analysis showed that there was no significant Thus, we next examined whether GM-CSF was

Figure 1: IL-17A expression in H. pylori-associated GC was enhanced in abnormal lipid milieu. (A) H. pylori induced IL-17A expression.
RNA was extracted from GC specimens. The levels of IL-17A were quantitated with RT-qPCR and compared between HP (+) and HP (-)
groups; (B) the effect of high TG content on H. pylori-induced IL-17A expression. The GC patients were divided into groups with high TG (>
1.7 mmol/L) and normal TG (≤ 1.7 mmol/L). IL-17A levels were compared between these two groups; (C) the synergistic effects of H. pylori
and aberrant lipid metabolism on IL-17A induction. Regression analysis was employed. ***P < 0.001, HP (+) vs. HP (-); *P < 0.05, high TG
vs. normal TG. H. pylori: Helicobacter pylori; GC: gastric cancer; IL: interleukin; RT-qPCR: reverse transcription quantitative polymerase
chain reaction; TG: triglyceride
Journal of Cancer Metastasis and Treatment ¦ Volume 3 ¦ August 29, 2017 171