Objective:To investigate the expression of Slug,EMMPRIN and E-cadherin in salivary adenoid cystic carcinoma (SACC)and its correlation with clinicopathological characteristics,and the correlation among themselves.Methods:Slug,EMMPRIN and E-cadherin expression in 1 1 5 SACC cases of SACC was examined by immunohistochemical staining.The results and clinicopatho-logical data were statistically analyzed.Results:High positive expression frequencies of Slug(76.5%)and EMMPRIN(69.6%)and low positive expression frequency of E-cadherin(51 .3%)were found in 1 1 5 SACC cases.The expression of Slug and EMMPRIN was positively associated with the histopathological types,clinical stages,perineural invasion,recurrence and distance metastasis(P <0.05).The expression of E-cadherin was negatively associated with the histopathological types,clinical stages,perineural invasion and distance metastasis(P <0.05).There was a significant correlation between Slug and EMMPRIN expression(P <0.05),negative correlation between EMMPRIN and E-cadherin expression(P <0.05)and between Slug and E-cadherin expression(P <0.05).Con-clusion:The expression of Slug,EMMPRIN and E-cadherin is closely correlated to the clinicopathological characteristics of SACC.

Objective To screen high-affinity aptamers binding to the surface lipopolysaccharide (LPS) of Pseudomonas aeruginosa (PA), and to analyze their inhibitory effects on macrophage polarization. Methods LPS of PA was ectracted and purified. High-affinity aptamers binding to the LPS of PA were screened by systematic evolution of ligands by exponential enrichment (SELEX). Enzyme-linked oligonucleotide assay (ELONA) and quantitative PCR (Q-PCR) were performed to investigate their influences on macrophage polarization. Results In this study, an aptamer PL-6 that could specifically bind to PA-LPS was screened suc-cessfully and found to be able to block the binding of PA-LPS to the corresponding receptor TLR4, inhibit mac-rophage M1 polarization and maintain macrophage homeostasis. Conclusion This study found a high-affinity aptamer binding to the LPS of PA, which might provide a new strategy for the prevention and treatment of sepsis caused by PA.

Objective: To study the mechanism of lncRNA-mtb in Mycobacterium tuberculosis (M.tuberculosis)-infected macrophages. Methods: A predicting software and Western blot assay were used to verify the non-coding nature of lncRNA-mtb. RT-qPCR was performed to detect lncRNA-mtb expression in macrophages infected by different Mycobacteria. Cytokine secretion was detected with ELISA after silencing the expression of lncRNA-mtb in macrophages with RNA interference (RNAi) technology. Western blot and RT-qPCR were performed to analyze whether the activation of macrophage inflammation could be induced by lncRNA-mtb during M. tuberculosis infection. Effects of lncRNA-mtb silencing on the bactericidal activity of M. tuberculosis-infected macrophages were evaluated. Results: Increased expression of lncRNA-mtb was observed in macrophages infected with M. tuberculosis H37Rv or H37Ra. After silencing the expression of lncRNA-mtb, IL-1β secretion in H37Rv infected-macrophages was significantly decreased. Further studies revealed that lncRNA-mtb might be involved in the activation of NLRP3 in M. tuberculosis-infected macrophages. The bactericidal activity of macrophages against H37Ra was impaired after silencing the expression of lncRNA-mtb. Conclusions Enhanced expression of lncRNA-mtb could be induced in macrophages infected with H37Rv or H37Ra. Moreover, lncRNA-mtb was involved in M. tuberculosis-induced inflammation in cells. Silencing lncRNA-mtb wolud attenuate the ability of macrophages to clear M. tuberculosis.