Retracted: Taxol-Resistant Gene 1 (Txr1) Mediates Oxaliplatin Resistance by Inducing Autophagy in Human Nasopharyngeal Carcinoma Cells.

An editorial decision has been made to retract this manuscript due to breach of publishing guidelines, following the identification of non-original and manipulated figures. Reference: Hua-ming Chi, Jing-dong Du, Jie Cheng, Hua-dong Mao: Taxol-Resistant Gene 1 (Txr1) Mediates Oxaliplatin Resistance by Inducing Autophagy in Human Nasopharyngeal Carcinoma Cells. Med Sci Monit 2019; 25:475-483. 10.12659/MSM.913180.

Interleukin-27 Suppresses T Helper-17 Inflammation in Allergic Rhinitis.

BACKGROUND: T helper 17 (Th17) cells and the related cytokines, interleukin (IL)- 17 and IL-23, were proved to play pivotal roles during the development of allergic rhinitis (AR). IL-27, an anti-inflammatory cytokine, has been reported to promote the production of IL-12R and induce Th1 cell responses. However, its effect on Th17 responses was not fully understood. OBJECTIVE: We conducted the present research to explore the role of IL-27 in the regulation of Th17 responses in AR. METHODS: Thirty confirmed AR patients and 20 controls were recruited for the study. The mRNA expression and protein levels of IL-27 were analyzed employing quantitative PCR (qPCR) and enzyme-linked immunosorbent assay (ELISA), respectively, and their correlations with Th17 cytokines were analyzed. We utilized ELISA and qPCR to analyze the effect of IL-27 on the differentiation of Th17 cells and the production of IL-17 and IL-23 from peripheral blood mononuclear cells (PBMCs). RESULTS: We found that the IL-27 levels in AR were downregulated and negatively related to IL-17 and IL-23 levels. The recombinant IL-27 inhibited the mRNA expression of RORγt and the protein expression of IL-17 and IL-23 in PBMCs through MEK, NF-κB, and JNK pathways. CONCLUSION: Our data demonstrated that IL-27 suppressed Th17 responses through MEK, NF-κB, and JNK pathways.

Interleukin-27 inhibits helper T cell type-2 response in allergic rhinitis.

OBJECTIVE: Interleukin-27 (IL-27) is a recently identified cytokine which plays both pro-inflammatory and anti-inflammatory effect in different diseases. However, its function in the pathogenesis of allergic rhinitis (AR) was not clear so far. METHODS: Quantitative PCR (qPCR) and enzyme-linked immunosorbent assay (ELISA) were performed to detect the expression of interleukin 27 (IL-27) and Th2 cytokines (IL-4, IL-5, IL-13) from 22 patients diagnosed with AR and 20 normal controls. Purified peripheral blood mononuclear cells (PBMCs) were prepared for in vitro experiment. RESULTS: Serum mRNA and protein levels of IL-27 were down-regulated in AR patients compared with normal controls. The expression of IL-27 showed negative correlation with Th2 cytokines. In vitro study showed that IL-27 significantly inhibited Th2 cytokines expression from PBMCs. CONCLUSION: Our results suggested that decreased IL-27 expression in AR were correlated with Th2 response. IL-27 may be used as potential target in the future treatment of AR.

Taxol-Resistant Gene 1 (Txr1) Mediates Oxaliplatin Resistance by Inducing Autophagy in Human Nasopharyngeal Carcinoma Cells.

BACKGROUND Oxaliplatin (L-OHP) is an important chemotherapy regimen for nasopharyngeal carcinoma (NPC), but can fail due to drug resistance. In this study, the role of Txr1 (taxol-resistant gene 1) in oxaliplatin resistance was investigated. MATERIAL AND METHODS Cell viability assay was carried out using the CellTiter-Glo Luminescent Cell Viability Assay Kit. CNE1 and CNE2 cells were cultured continuously with gradually increasing concentrations of L-OHP for 6 months to establish drug-resistant cell lines. Autophagy was detected by electron microscopy. Txr1 expression in NPC cells was detected via Western blotting and real-time quantitative PCR (qRT-PCR). RESULTS In L-OHP-resistant CNE1/L-OHP and CNE2/L-OHP cells, mRNA and protein expression of Txr1 increased compared to the parental cells, and downregulation of Txr1 re-sensitized drug-resistant cells to L-OHP. Moreover, we found that Txr1-mediated L-OHP resistance was associated with increased autophagy. Txr1-overexpression cells developed L-OHP resistance and a high level of autophagy. Inhibiting autophagy using 2 different methods - inhibition of autophagy-related gene expression and autophagy inhibitor - attenuated L-OHP resistance of NPC cells. CONCLUSIONS We conclude that the detection of Txr1 might become a good indicator to evaluate the treatment and prognosis of nasopharyngeal carcinoma. Our data suggest that further investigation of Txr1 in the setting of L-OHP resistance is warranted.

Osteopontin induced vascular endothelial growth factor production in dispersed nasal polyp cells through the phosphatidylinositol 3-kinase-protein kinase B and the extracellular signal-regulated kinase 1/2 pathways.

BACKGROUND: Osteopontin (OPN) is involved in cell survival, migration, and angiogenesis. The role of OPN in inducing angiogenesis in tumor has been confirmed. In this study, we investigated the expression of OPN in patients with chronic rhinosinusitis (CRS) with nasal polyp (NP) and the relationship of OPN with vascular endothelial growth factor (VEGF) production. METHODS: We enrolled 45 subjects with CRS (25 with CRS with NPs [CRSwNP] and 20 subjects with CRS without NPs [CRSsNP]), and with 14 normal controls to determine the expression of OPN and VEGF. The distribution, messenger RNA (mRNA), and protein levels of OPN and VEGF were examined by immunohistochemistry, quantitative polymerase chain reaction, and enzyme-linked immunosorbent assay, respectively. The effect of OPN on the VEGF production was tested in dispersed NP cells (DNPC) and the involved signaling pathways were examined by Western blot. RESULTS: In NP tissue of the subjects with CRSwNP, the epithelial cells, interstitial cells, glandular cells, and endothelial cells were positive for OPN and VEGF staining, whereas OPN and VEGF immunoactivity in specimens of subjects with CRSsNP and in normal controls was significantly reduced. We found that the immunostainings, the mRNA expression, and the protein levels of OPN and VEGF were significantly increased in NPs compared with normal controls. OPN induced VEGF production by DNPCs in a time- and dose-dependent manner through phosphatidylinositol 3-kinase- protein kinase B and the extracellular signal-regulated kinase 1/2 pathway. Moreover, VEGF also induced OPN production, which formed a positive feedback between OPN and VEGF. CONCLUSION: Our findings demonstrated that OPN and VEGF were overproduced in NPs and that OPN induced VEGF production, which indicated that OPN-VEGF axis might contribute to angiogenesis in NPs.

Bacteriology and antibiotic sensitivity of tonsillar diseases in Chinese children.

Although many bacteriology studies on tonsillar diseases have been completed, only a few studies investigated bacteriology of tonsillar diseases in recent years, especially in Asian children population. The aim of our study is to elucidate the bacterial flora and antibiotic sensitivity of tonsillar diseases in Chinese children. A three-center study was performed on 2994 children with or without tonsillar diseases. We compared and analyzed differences of bacterial pathogens among recurrent tonsillitis, tonsillar hypertrophy and controls. We found that on the surface of tonsil, Staphylococcus aureus, Haemophilus influenzae and Streptococcus pneumoniae were noted in the order given in the recurrent tonsillitis (RT) group. In the tonsillar hypertrophy (TH) and control group, H. influenzae, S. aureus and S. pneumoniae were noted in the order given. For the core of tonsil, H. influenzae, S. aureus and ß-hemolytic streptococcus were noted in the order given in both RT and TH group. S. aureus and H. influenzae were the most prevalent types of bacteria present in cultures containing two strains in the RT and TH group, respectively. We also observed some differences in the types of bacteria in the surface and core between the recurrent tonsillitis and tonsillar hypertrophy groups. Our study provides recent bacteria distribution and antibiotic sensitivity for tonsillar diseases in Chinese children and will be helpful in the treatment of these diseases.

Role of IL-31 in regulation of Th2 cytokine levels in patients with nasal polyps.

Interleukin-31 (IL-31) is reported to be involved in Th2 cell-mediated diseases. However, the regulatory effect of IL-31 in the pathogenesis of nasal polyps (NPs) has not been understood. This study is aimed to determine whether IL-31 production is associated with Th2 cytokine levels and clinical severity in patients with NPs. Thirty patients with NPs and fifteen normal controls were included, and IL-31 production was determined by immunohistochemistry and enzyme-linked immunosorbent assay, respectively. The relationship between IL-31 expression and clinical severity was also evaluated. Besides, the effect of IL-31 on Th2 cytokine expression by polyp epithelial cells was investigated. We observed significantly enhanced IL-31 mRNA and protein level expression in NPs compared with normal control. IL-31+ cells were found to be positively correlated with clinical severity of NPs. Furthermore, we provided the direct evidence that IL-31 up-regulates Th2 cytokines expressed by polyp epithelial cells. Our results demonstrate that enhanced Th2 cytokine levels was correlated with IL-31 expression in NPs and provide a possible explanation for IL-31's regulatory role in the pathogenesis of NPs.

Expression and Regulation of Interleukin-37 in Pathogenesis of Nasal Polyps.

Interleukin-37 (IL-37) belongs to IL-1 family and is recently identified as a natural suppressor of innate inflammatory and immune responses. Its role in digestive system was well characterized, however, little is known about its function in respiratory diseases. This study is aimed to investigate the expression and regulation of IL-37 in patients with nasal polyps (NPs). Twenty-five patients with NPs and sixteen normal controls were included, and IL-37 production was determined by immunohistochemistry and enzyme-linked immuno sorbent assay, respectively. The relationship between IL-37 expression and Th1/Th2 cytokines was also evaluated. Besides, the effect of IL-37 on dispersed nasal polyp cells (DNPCs) was investigated. We observed significantly decreased IL-37 mRNA and protein levels expression in NPs compared with normal control. IL-37 was found negatively with Th2 cytokines and had no relation with Th1 cytokines. Furthermore, we provided the first evidence that IL-37 down-regulates Th2 cytokine expressed by DNPCs. Our results demonstrate that enhanced Th2 cytokine levels was related to decreased IL-37 expression in NPs, and provide a possible explanation for IL-37's regulatory role in the pathogenesis of NPs.