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.
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 β-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.
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.
BackgroundOxaliplatin (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/MethodsCell 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).ResultsIn 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.ConclusionsWe 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.
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