IL-17 is a proinflammatory cytokine produced by various immune cells. Polymorphonuclear neutrophils (PMNs) are the first line of defense in bacterial infection and express surface Toll-like receptor 9 (sTLR9). To study the relationship of sTLR9 and IL-17 in PMNs during bacterial infection, we infected mice with E. coli intraperitoneally to establish a septic peritonitis model for studying the PMNs response in peritoneal cavity. We found that PMNs and some of “giant cells” were massively accumulated in the peritoneal cavity of mice with fatal septic peritonitis induced by E. coli. Kinetically, the CD11b+ PMNs were increased from 20–40% at 18 hours to >80% at 72 hours after infection. After E. coli infection, sTLR9 expression on CD11b+ and CD11b− PMNs and macrophages in the PLCs were increased at early stage and deceased at late stage; IL-17 expression was also increased in CD11b+ PMNs, CD11b− PMNs, macrophages, and CD3+ T cells. Using experiments of in vitro blockage, qRT-PCR and cell sorting, we confirmed that PMNs in the PLCs did increase their IL-17 expression during E. coli infection. Interestingly, sTLR9−CD11b+Ly6G+ PMNs, not sTLR9+CD11b+Ly6G+ PMNs, were found to be able to increase their IL-17 expression. Together, the data may help understand novel roles of PMNs in septic peritonitis.

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Allogeneic tumors are eventually rejected by adaptive immune responses, however, little is known about how allogeneic tumors are eradicated at the early stage of tumor development. In present study, we found that NKG2DL low expressing cancer cells were developed into palpable allogeneic tumors in mice within a week after the inoculation, while NKG2DL high expressing cancer cells failed to. The NKG2DL high expressing cancer cells could increase NKG2D+ NK cells in the allogeneic mice after being inoculated for 3 days. Artificially up-regulating NKG2DL on cancer cells with low level expressed NKG2DL by a CpG ODN resulted in the retardation and rejection of the allogeneic tumors at the early stage. The contribution of up-regulated NKG2DL to the early rejection was further confirmed by the results that the development of allogeneic tumors from cancer cells transfected with NKG2DL genes was significantly inhibited in mice at the early stage. Overall, hopefully, the data may provide insights for combining the allogeneic NK cell adoptive transfer with the approaches of up-regulating NKG2DL to treat cancer patients.

Hepatocellular carcinoma (HCC) has a poor prognosis, while the diagnosis biomarkers or treatment targets for HCC are still lacking. Recently, mining strategies on public access databases has been successfully used to discover novel and sensitive biomarkers. In this study, bioinformatics analysis of the genomic and transcriptome data of HCC PBMC samples obtained from the Gene Expression Omnibus datasets. The analysis results showed that thrombospondin-1 (THBS-1) was dysregulated in HCC, and might be as biomarkers as it is a secretory protein and found to participate in liver dysfunction including HCC development. THBS-1 related micro RNAs are identified by bioinformatics analysis and tested as biomarkers as they are altered in many tumors and stable in circulation. The results showed that plasma THBS-1 and miR-194 were down-regulated in HCC patients and their correlations were positive. Whereas plasma level of miR-338-3p was significantly increased in the HCC patients and negatively correlated with THBS-1 and they showed a highly significant diagnostic value in discriminating HCC. In addition, THBS-1 and miR-338-3p combination displayed higher predictive power than them alone, and addition of miR-338-3p might enhance predictive power of AFP for HCC. Our data showed that THBS-1 and miR-338-3p displayed a highly significant diagnostic value in discriminating between HCC patients and control subjects. Addition of miR-338-3p might enhance the predictive potency of AFP for HCC.