Abstract
Introduction
Since Vichow proposed the hypothesis that chronic inflammation was closely related to tumor in 1863, experimental, clinical and epidemiological studies have shown that inflammation plays an important role in tumor progression, immune response, tumor therapy and prognosis. In this study, 38B9 cells were injected into BALB/c mice to establish lymphoma-burdened mice model. The expression of IL-10, TNF- and IL-6 were observed in plasma and tissues to study the effects of tumor inflammatory factors on tumor environment.
Methods
Ten 9-week-old BALB/c mice were randomly divided into the control group and the tumor-burdened group. Each mouse in tumor-burdened group was injected with 2×106/200μl 38B9 cells, while the control group was injected with 200μl PBS buffer solution. The establishment of B-cell lymphoma tumor-burdened mice model was confirmed by magnetic resonance information (MRI). The peripheral blood samples were collected before injection, after tumorigenesis and when sacrificed. The tumor tissues were also collected. The level of IL-6, IL-10, TNF-α in the plasm were detected by enzyme-linked immuno sorbent assay (ELISA) and the relative value of mRNA in tissues were measured by quantitative real-time polymerase chain reaction (qRT-PCR).
Results
1.Compared with the control group, the levels of IL-6 and TNF-α in the tumor-burdened group were increased after injected 14 days (P <0.05). However, the level of IL-10 showed no significant difference (P >0.05). After injected 19 days, the levels of IL-6, IL-10 and TNF-α of tumor-burdened group were decreased (P<0.05).
2. The expression of IL-10 mRNA in tumor tissues was lower than the control group (P <0.05), while the expression of IL-6 mRNA in borderline tissues was higher than the control group (P<0.05). Compared with tumor tissue, the expression of IL-10 mRNA was increased in borderline tissue (P <0.05). The level of IL-6 and TNF-α showed no significant difference (P>0.05).
Conclusions
1. The level of IL-6, IL-10 and TNF-α in the tumor tissues and plasma were significantly higher after tumorigenesis.
2. The increased expression of inflammatory factors is related to tumor-induced inflammatory microenvironment.
No relevant conflicts of interest to declare.
Author notes
Asterisk with author names denotes non-ASH members.
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