Imaging Analysis of Ganglioneuroma and Quantitative Analysis of Paraspinal Ganglioneuroma.

BACKGROUND This study evaluated the imaging features of ganglioneuroma (GN) and assessed the diagnostic value of the enhancement rate (ER) of CT for GN. MATERIAL AND METHODS We retrospectively reviewed records of 49 patients with histopathologically confirmed GN who underwent preoperative contrast-enhanced CT or MRI between 2010 and 2018. The independent samples t test and chi-square test were used. Receiver operating characteristic (ROC) curves were generated to analyze the diagnostic sensitivity (SE) and specificity (SP). Positive predictive value (PPV) and negative predictive value (NPV) were calculated. RESULTS The CT values were 32.59±3.61 Hounsfield units (HU) for plain scans, 38.87±5.09 HU for the arterial phase, and 54.26±8.14 HU for the venous phase, and the incidence of calcification and cysts was 32.6% and 10.2%, respectively. There was no significant difference in CT results and clinical parameters between mediastinal ganglioneuroma (MGN) and retroperitoneal ganglioneuroma (RGN) (p>0.05). The area under the curves (AUCs) for the arterial enhancement rate (AER), venous enhancement rate (VER), and AER/VER combined index in diagnosing GN were 0.735, 0.980, and 0.990, respectively. The VER of 0.2819 exhibited the SE and SP at 92.9% and 92.9%, respectively, to characterize the GN, whereas the AER of 0.1779 had SE and SP of 52.4% and 90.5%, respectively. The SE and SP for the combined index were 88.1% and 100%, respectively. The GN showed hypointensity on T1WI, hyperintense, or slightly high signal on T2WI with the linear hypointensity, and hyperintense on DWI. CONCLUSIONS A hypodense mass was observed for GN on plain scan and presented delayed enhancement on contrast enhancement. VER or AER/VER combination is more accurate than AER for the diagnosis of paravertebral GN.

MicroRNA-155 promotes the pathogenesis of experimental colitis by repressing SHIP-1 expression.

AIM: To explore the mechanism by which microRNA-155 (miR-155) regulates the pathogenesis of experimental colitis. METHODS: A luciferase assay was performed to confirm the binding of miR-155 to the SHIP-1 3'-UTR. MiR-155 mimics, negative controls and SHIP-1 expression/knockdown vectors were established and then utilized in gain- and loss-of-function studies performed in raw264.7 cells and primary bone marrow-derived macrophages (BMDMs). Thereafter, dextran sulfate sodium (DSS)-induced colitis mouse model with or without antagomiR-155 treatment was established, and the levels of miR-155 and SHIP-1, as well as the pro-inflammatory capabilities, were measured by western blot, quantitative polymerase chain reaction, and immunohistochemistry. RESULTS: MiR-155 directly bound to the 3'-UTR of SHIP-1 mRNA and induced a significant decrease in SHIP-1 expression in both raw264.7 cells and primary BMDMs. MiR-155 markedly promoted cell proliferation and pro-inflammatory secretions including IL-6, TNF-α, IL-1ß, and IFN-γ, whereas these effects could be reversed by the restoration of SHIP-1 expression. In vivo studies showed that antagomiR-155 administration could alleviate DSS-induced intestinal inflammation in Balb/c mice. Moreover, significantly increased SHIP-1 expression, as well as decreased Akt activation and inflammatory response, were observed in the antagomiR-155-treated mice. CONCLUSION: MiR-155 promotes experimental colitis by repressing SHIP-1 expression. Thus, the inhibition of miR-155 might be a promising strategy for therapy.

MicroRNA-185 suppresses growth and invasion of colon cancer cells through inhibition of the hypoxia­inducible factor-2α pathway in vitro and in vivo.

MicroRNAs (miRs) are small non­coding RNAs with regulatory roles, which are involved in a broad spectrum of physiological and pathological processes, including cancer development and progression. However, the function of miR­185 in the development of human colon cancer has not yet been investigated. In this study, the association between miR­185 expression and the clinicopathological characteristics of patients with colon cancer was analyzed using quantitative polymerase chain reaction (qPCR). Using a gain­of­function approach, the effects of miR­185 overexpression on the expression of hypoxia­inducible factor­2α (HIF­2α), proliferating cell nuclear antigen (PCNA) and matrix metallopeptidase­2 (MMP­2) were investigated in SW620 colon cancer cells using qPCR and western blotting. Functional analysis of cellular proliferative activities, by MTT assay, and invasive potential, by Transwell assay, was conducted on SW620 cells expressing low levels of miR­185. miR­185 was found to be significantly downregulated in cancer tissues compared with adjacent non­cancerous tissues, and was negatively correlated with lymph node metastasis of colon cancer (P<0.001). miR­185 overexpression in vitro impeded cellular proliferation and invasive potential with reduced expression of HIF­2α, PCNA and MMP­2 in SW620 cells transfected with an miR­185 mimic. In addition, the tumor volumes in SW620 subcutaneous nude mouse models treated with miR­185 were significantly smaller than those of the control group. In conclusion, these findings indicate that miR­185 as a tumor suppressor may affect the development of colon cancer cells via inhibition of HIF­2α signaling, suggesting that miR­185 may serve as a potential therapeutic target in cancer treatment.

Recovery from TNBS-induced colitis leads to the resistance to recurrent colitis and an increased ratio of FOXP3 to CD3 mRNA.

OBJECTIVE: The aim of our study was to investigate the effects of the recovery from acute colitis on recurrent colitis with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. METHODS: Acute colitis was induced via an intrarectal injection of TNBS. For recurrent colitis, mice were intrarectally treated with a repeated TNBS 14 days after the first TNBS administration. And another two groups (control and recovery groups) were added to the analysis. Disease activity index (DAI), macroscopic and histological assessments, mRNA expression of interleukin (IL)-1ß, IL-6, tumor necrosis factor (TNF), IL-10, forkhead box P3 (FOXP3) and the ratio of FOXP3 to CD3 in the colonic tissues were evaluated. RESULTS: Mice developed colitis after treated with TNBS. After the last TNBS administration, DAI in the recurrent colitis group was lower than that in the acute colitis group. In the recurrent colitis group, the mice exhibited longer colon length, reduced histological damage and lower IL-1ß, IL-6, TNF, IL-10 mRNA expression in the colon compared with the acute colitis group. The ratio of FOXP3 to CD3 mRNA expression in the colon of recurrent colitis was higher than that in the acute colitis. There was a significant negative correlation between the ratio of FOXP3 to CD3 mRNA expression and DAI in the acute and recurrent colitis groups (r= -0.808, P<0.05). CONCLUSIONS: Mice that recovered from TNBS-induced acute colitis with intestinal epithelial disruption are resistant to recurrent colitis, which is associated with an increased ratio of FOXP3 to CD3 mRNA expression.

Expression of polymeric immunoglobulin receptor mRNA and protein in human paneth cells: Paneth cells participate in acquired immunity.

OBJECTIVE: Paneth cells are important effectors of intestinal innate immunity. It has been generally accepted that Paneth cells do not participate in the synthesis of polymeric immunoglobulin receptor (pIgR) or the secretion of immunoglobulin A (IgA) in the small intestine. However, we have previously shown that pIgR is specifically localized in Paneth cells of the rat small intestine. We therefore investigated the possibility that pIgR is also localized in human Paneth cells. METHODS: Double-labeled fluorescent immunohistochemistry and double-labeled fluorescent in situ hybridization were used to determine RNA and protein expression in normal human small intestine. RESULTS: Both pIgR mRNA and protein were colocalized with lysozyme in normal human Paneth cells. Furthermore, IgA was colocalized with lysozyme in the secretory granules of human Paneth cells. CONCLUSIONS: This is the first study to demonstrate that pIgR and IgA are colocalized in the secretory granules of human Paneth cells. These findings suggest that, in addition to their well-recognized role in innate immunity, Paneth cells are involved in IgA-mediated acquired immunity in the gastrointestinal tract. Furthermore, these results add to accumulating evidence that Paneth cells participate in intestinal inflammation.

Immunocytochemical localization of secretory component in Paneth cell secretory granules-rat Paneth cells participate in acquired immunity.

With the marker of Paneth cells-lysozyme, secretory component (SC) immunoreactivity was demonstrated exclusively in Paneth cells of rat small intestine. The other types of epithelial cells (columnar, goblet, endocrine) were negative. On electron microscopic level, many SC-positive colloidal gold particles were found in rough endoplasmic reticulum, Golgi complexes, basal membrane and secretory granules of Paneth cells. These results suggest that SC is not a component of ingested immune complex, but a membrane receptor on Paneth cell. It may function as receptor for polymeric IgA and mediate its transport across the mucosal epithelium. Thus, Paneth cells are responsible for SC synthesis and participate in IgA-mediated acquired immunity in rat small intestine.