Transcriptome analysis of epithelioma papulosum cyprini cells after SVCV infection

BACKGROUND: Spring viraemia of carp virus (SVCV) has been identified as the causative agent of spring viraemia of carp (SVC) and it has caused significant losses in the cultured common carp (Cyprinus carpio) industry. The molecular mechanisms that underlie the pathogenesis of the disease remain poorly understood. In this study, deep RNA sequencing was used to analyse the transcriptome and gene expression profile of EPC cells at progressive times after SVCV infection. This study addressed the complexity of virus–cell interactions and added knowledge that may help to understand SVCV. RESULTS: A total of 33,849,764 clean data from 36,000,000 sequence reads, with a mean read length 100 bp, were obtained. These raw data were assembled into 88,772 contigs. Of these contigs, 19,642 and 25,966 had significant hits to the NR and Uniprot databases where they matched 17,642 and 13,351 unique protein accessions, respectively. At 24 h post SVCV infection (1.0 MOI), a total of 623 genes were differentially expressed in EPC cells compared to non-infected cells, including 288 up-regulated genes and 335 down-regulated genes. These regulated genes were primarily involved in pathways of apoptosis, oxidative stress and the interferon system, all of which may be involved in viral pathogenesis. In addition, 8 differentially expressed genes (DEGs) were validated by quantitative PCR. CONCLUSIONS: Our findings demonstrate previously unrecognised changes in gene transcription that are associated with SVCV infection in vitro, and many potential cascades identified in the study clearly warrant further experimental investigation. Our data provide new clues to the mechanism of viral susceptibility in EPC cells. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/1471-2164-15-935) contains supplementary material, which is available to authorized users

Prognostic role of iodine values for gastric cancer after neoadjuvant chemotherapy: a strong independent prognostic factor

PURPOSEWe aimed to systematically explore the value of iodine values calculated from dual-energy computed tomography (DECT) as potential prognostic factors for locally advanced gastric cancer (LAGC) patients undergoing neoadjuvant chemotherapy (NAC).METHODSEighty-five LAGC patients were examined using DECT before and after NAC and were divided into responders and non-responders based on the tumor regression grade (TRG). The iodine values including portal- and delayed-phase iodine uptake (IUp and IUd, mg/mL) and total iodine uptake (TIUp and TIUd, mg) were acquired. Correlations between the reduction ratios of iodine values and TRG were analyzed. The diagnostic performance of parameters for differentiating responders from non-responders was calculated. Kaplan–Meier method was used for survival analysis.RESULTSThe reduction ratios of total iodine uptake (%ΔTIUp and %ΔTIUd) were significantly correlated with TRG (P < .001). The ypN stage, %ΔTIUp, and %ΔTIUd were significant factors influencing progression-free survival (PFS) (P < .050). A value of %ΔTIUd ≤ 62.19% was associated with negative prognosis [relative risk (RR):2.103; P = 0.021], as was ypN stage (RR: 4.250; P = .003).CONCLUSIONIodine values (especially the TIU) are noninvasive quantitative parameters that are potentially helpful for evaluating the treatment response and survival prognosis of LAGC after NAC. %ΔTIUd represents a strong independent prognostic factor, increasing preoperative risk assessment performance

Region- or state-related differences in expression and activation of extracellular signal-regulated kinases (ERKs) in naïve and pain-experiencing rats

<p>Abstract</p> <p>Background</p> <p>Extracellular signal-regulated kinase (ERK), one member of the mitogen-activated protein kinase (MAPK) family, has been suggested to regulate a diverse array of cellular functions, including cell growth, differentiation, survival, as well as neuronal plasticity. Recent evidence indicates a role for ERKs in nociceptive processing in both dorsal root ganglion and spinal cord. However, little literature has been reported to examine the differential distribution and activation of ERK isoforms, ERK1 and ERK2, at different levels of pain-related pathways under both normal and pain states. In the present study, quantitative blot immunolabeling technique was used to determine the spatial and temporal expression of ERK1 and ERK2, as well as their activated forms, in the spinal cord, primary somatosensory cortex (SI area of cortex), and hippocampus under normal, transient pain and persistent pain states.</p> <p>Results</p> <p>In naïve rats, we detected regional differences in total expression of ERK1 and ERK2 across different areas. In the spinal cord, ERK1 was expressed more abundantly than ERK2, while in the SI area of cortex and hippocampus, there was a larger amount of ERK2 than ERK1. Moreover, phosphorylated ERK2 (pERK2), not phosphorylated ERK1 (pERK1), was normally expressed with a high level in the SI area and hippocampus, but both pERK1 and pERK2 were barely detectable in normal spinal cord. Intraplantar saline or bee venom injection, mimicking transient or persistent pain respectively, can equally initiate an intense and long-lasting activation of ERKs in all three areas examined. However, isoform-dependent differences existed among these areas, that is, pERK2 exhibited stronger response than pERK1 in the spinal cord, whereas ERK1 was more remarkably activated than ERK2 in the S1 area and hippocampus.</p> <p>Conclusion</p> <p>Taken these results together, we conclude that: (1) under normal state, while ERK immunoreactivity is broadly distributed in the rat central nervous system in general, the relative abundance of ERK1 and ERK2 differs greatly among specific regions; (2) under pain state, either ERK1 or ERK2 can be effectively phosphorylated with a long-term duration by both transient and persistent pain, but their response patterns differ from each other across distinct regions; (3) The long-lasting ERKs activation induced by bee venom injection is highly correlated with our previous behavioral, electrophysiological, morphological and pharmacological observations, lending further support to the functional importance of ERKs-mediated signaling pathways in the processing of negative consequences of pain associated with sensory, emotional and cognitive dimensions.</p

Bi-directional regulation of type I interferon signaling by heme oxygenase-1

Summary: Moderate activation of IFN-I contributes to the body’s immune response, but its abnormal expression, stimulated by oxidative stress or other factors causes pathological damage. Heme oxygenase-1 (HO-1), induced by stress stimuli in the body, exerts a central role in cellular protection. Here we showed that HO-1 could promote IFN-1 under Spring Viremia of Carp virus (SVCV) infection and concomitantly attenuate the replication of SVCV. Further characterization of truncated mutants of HO-1 confirmed that intact HO-1 was essential for its antiviral function via IFN-I. Importantly, HO-1 inhibited the IFN-I signal by degrading the IRF3/7 through the autophagy pathway when it was triggered by H2O2 treatment. The iron ion-binding site (His28) was critical for HO-1 to degrade IRF3/7. HO-1 degradation of IRF3/7 is conserved in fish and mammals. Collectively, HO-1 regulates IFN-I positively under viral infection and negatively under oxidative stress, elucidating a mechanism by which HO-1 regulates IFN-I signaling in bi-directions

Pathogenic Elizabethkingia miricola Infection in Cultured Black-Spotted Frogs, China, 2016

Multiregional outbreaks of meningitis-like disease caused by Elizabethkingia miricola were confirmed in black-spotted frog farms in China in 2016. Whole-genome sequencing revealed that this amphibian E. miricola strain is closely related to human clinical isolates. Our findings indicate that E. miricola can be epizootic and may pose a threat to humans

Dysbiosis of intestinal homeostasis contribute to Whitmania pigra edema disease

Abstract Whitmania pigra is widely used in traditional Chinese medicine. However, W. pigra is being threatened by an edema disease with unknown causes (WPE). In this study, a comprehensive exploration of virome, microbiome, and metabolome aberrations in the intestine of W. pigra was performed to address the aetiology of WPE. Virome analysis indicated that eukaryotic viruses did not contribute to WPE, whereas an expansion of Caudovirales was observed in WPE. Compared to the control, the microbial richness and diversity in diseased W. pigra decreased remarkably. Nine genera, including Aeromonas, Anaerotruncus, Vibrio, Proteocatella, Acinetobacter, and Brachyspira were overrepresented in WPE, whereas eleven genera, including Bifidobacterium, Phascolarctobacterium, Lactobacillus, Bacillus and AF12, were enriched in healthy individuals. Furthermore, certain metabolites, especially amino acids, short‐chain fatty acids, and bile acids, were found to be linked to intestinal microbiota alterations in WPE. An integration of the microbiome and metabolome in WPE found that dysbiosis of the gut microbiota or metabolites caused WPE. Notably, W. pigra accepted intestinal microbiota transplantation from WPE donors developed WPE clinical signs eventually, and the dysbiotic intestinal microbiota can be recharacterized in this recipient W. pigra. Strikingly, pathological features of metanephridium and uraemic toxin enrichment in the gut indicated a putative interconnection between the gut and metanephridium in WPE, which represents the prototype of the gut–kidney axis in mammals. These finding exemplify the conservation of “microecological Koch's postulates” from annelids to insects and other vertebrates, which provides a direction of prevention and treatment for WPE and opens a new insight into the pathogenesis of aquatic animal diseases from an ecological perspective