Spleen contributes to restraint stress induced hepatocellular carcinoma progression

Abstract

The spleen is the largest secondary immune organ and plays a critical role in the progression of tumor. Psychological stress promotes tumor progression through inhibiting antitumor immune. However, the role of spleen in tumor progression induced by stress is unclear. Here, we showed that restraint stress promoted tumor growth, increased the percentage of CD11b+Gr-1+ MDSC while decreased the percentages of CD3-NK1.1+ NK and CD3+NK1.1+ NKT in the tumor tissues. Restraint stress decreased the percentages of CD3+CD4+ T lymphocytes and CD3+CD8+ T lymphocytes while increased the percentage of CD11b+Gr-1+ MDSC in the blood of tumor-bearing mice. Restraint stress increased the percentages of CD3+CD4+ T lymphocytes, CD3+CD8+ T lymphocytes, CD4+PD1+ T lymphocytes and CD8+PD1+ T lymphocytes while decreased the percentage of CD11b+Gr-1+ MDSC in the spleen of tumor-bearing mice. Interestingly, splenectomy inhibited tumor growth and attenuated the changes of CD3+CD4+ T lymphocytes, CD3+CD8+ T lymphocytes, and CD11b+Gr-1+ MDSC in blood induced by chronic restraint stress. Finally, splenectomy blocked the increases of CD11b+Gr-1+ MDSC but did not attenuate the decreases of CD3-NK1.1+ NK and CD3+NK1.1+ NKT in tumor tissue induced by chronic stress. Together, these data indicate that chronic restraint stress promotes hepatocellular carcinoma growth and suppresses the antitumor immunity of tumor-bearing mice. Splenectomy could inhibit tumor growth and partly block the decrease of antitumor immune activity induced by stress.