The antioxidant activity and metabolomic analysis of the supernatant of Streptococcus alactolyticus strain FGM.

Strain-specific probiotics can present antioxidant activity and reduce damage caused by oxidation. Streptococcus alactolyticus strain FGM (S. alactolyticus strain FGM) isolated from the chicken cecum shows potential probiotic properties which have been previously demonstrated. However, the antioxidant properties of S. alactolyticus strain FGM remain unknown. In this view, cell-free supernatant (CFS), intact cells (IC) and intracellular extracts (CFE) of strain FGM and 3 strains of Lactobacillus (LAB) were prepared, and their scavenging capacities against DPPH, hydroxyl radicals and linoleic acid peroxidation inhibitory were compared in this study. The effects of strain FGM cell-free supernatant (FCFS) on NO production, activity of SOD and GSH-Px in RAW264.7 cells and LPS-induced RAW264.7 cells were analyzed. The metabolites in the supernatant were quantitated by N300 Quantitative Metabolome. It was shown that the physicochemical characteristics of CFS to scavenge DPPH, hydroxyl radicals, and linoleic acid peroxidation inhibitory were significantly stronger than that of IC and CFE in the strain FGM (P < 0.05), respectively 87.12% ± 1.62, 45.03% ± 1.27, 15.63% ± 1.34. FCFS had a promotional effect on RAW264.7 cells, and significantly elevated SOD and GSH-Px activities in RAW264.7 cells. 25 µL FCFS significantly promoted the proliferation of RAW264.7 cells induced by LPS, increased the activities of SOD and GSH-PX, and decreased the release of NO. Furthermore, among the differential metabolites of FCFS quantified by N300, 12 metabolites were significantly up-regulated, including lactic acid, indole lactic acid, linoleic acid, pyruvic acid etc., many of which are known with antioxidant properties. In conclusion, FCFS had good antioxidant properties and activity, which can be attributed to metabolites produced from strain FGM fermentation. It was further confirmed that S. alactolyticus strain FGM and its postbiotic have potential probiotic properties and bright application prospects in livestock and poultry breeding.

Correlation Between MicroRNA by Extracellular Vesicle Mediated and Antiviral Effects of Interferon Omega in Feline Peripheral Blood.

Feline interferon omega (IFN-ω) has been proven to have high antiviral activity; however, its in-depth antiviral effects remain unknown. Extracellular vesicles (EVs) have been demonstrated to participate in the regulation of the immune response pathway for the body through various active substances, especially through the microRNA (miRNA) carried by them. In this study, we isolated EVs from feline peripheral blood by differential centrifugation, and further found that the content of IFN-ω in EVs increased continuously within 24 h after IFN-ω treatment, and a large number of miRNAs were significantly downregulated in EVs within 12 h after IFN-ω treatment. These significantly differentially expressed miRNAs were important for regulating changes in antiviral cytokines. This study reveals for the first time the correlation between EVs-mediated miRNA in feline peripheral blood and IFN-ω on antiviral immune response, which may provide strong data support for the development of novel antiviral nanomedicine and the research of the antiviral effects of IFN-ω.

TFEB and TFE3 cooperate in regulating inorganic arsenic-induced autophagy-lysosome impairment and immuno-dysfunction in primary dendritic cells.

Arsenic (As) is a prevalent and hazardous environmental toxicant associated with cancer and various health problems, which has been shown suppressive effects on dendritic cells (DCs). Autophagy is essential for the innate and adaptive immune responses of DCs, and the transcription factors TFEB and TFE3 are key regulators of autophagic and lysosomal target genes. However, the detrimental alterations of the autophagy-lysosome pathway in As-exposed DCs and the possible coordinating roles of TFEB and TFE3 in the immune dysfunction of this cell are less understood. In this paper, we found that As exposure significantly impaired lysosomal number, lysosomal acidic environment, and lysosomal membrane permeabilization, which might lead to blocked autophagic flux in cultured DCs. Furthermore, our results confirmed that TFEB or TFE3 knockdown exacerbated the disorders of lysosome and the blockade of autophagic flux in As-exposed DCs, and also enhanced the inhibitory expression of co-stimulatory molecules Cd80 and Cd83; adhesion molecule Icam1; cytokines TNF-α, IL-1ß, and IL-6; chemokine receptor Ccr7; and antigen-presenting molecules MHC II and MHC I. By contrast, overexpression of TFEB or TFE3 partially alleviated the above-mentioned impairment of DCs by inorganic As exposure. In conclusion, these findings reveal a previously unappreciated inhibition of lysosome-mediated degradation and damage of lysosomal membrane integrity leading to dysregulated autophagy and impaired immune functions of DCs by arsenicals, and also suggest TFEB and TFE3 as potential therapeutic targets for ameliorating As toxicity.

Promotion of transcription factor EB-dependent autophagic process by curcumin alleviates arsenic-caused lung oxidative stress and inflammation in mice.

Arsenic is a human carcinogen widely distributed in the environment, and arsenic exposure from drinking water has received widespread attention as a global public health problem. Curcumin is a natural bioactive substance with high efficiency and low toxicity extracted from turmeric, which has a variety of biological properties such as antioxidation, anti-inflammation, anticancer, and immuno-modulatory activities. Curcumin is widely used in daily life as a food additive and dietary supplement. However, its protective effects in lung injuries by chronic arsenic exposure orally remain unexplored. In this study, curcumin treatment not only significantly accelerated arsenic elimination and improved lung tissue morphology, but also decreased arsenic-generated ROS by activating Nrf2 and its down-stream antioxidants. Further, curcumin alleviated inflammatory changes in mice exposed to arsenic for 6 and 12 weeks, as manifested by lung MPO levels, total protein and cellular levels in bronchoalveolar lavage fluid (BALF), serum IL-4 levels, and MAPK/NF-κB expression in lung tissue. Notably, our study also confirmed that curcumin could promote the expression and nuclear translocation of the transcription factor EB (TFEB), as well as activate TFEB-regulated autophagy in lung tissue of arsenic-treated mice, accompanied by inhibition of the AKT-mTOR signaling pathway. Overall, our study here suggests that natural bioactive compound curcumin could alleviate arsenic-induced pulmonary oxidative stress and inflammation in vivo, which is closely related to enhanced TFEB activity and induction of the autophagic process.

Cordyceps militaris Solid Medium Extract Alleviates Lipoteichoic Acid-Induced MH-S Inflammation by Inhibiting TLR2/NF-κB/NLRP3 Pathways.

The aim of this study was to investigate the inhibitory effects of Cordyceps militaris solid medium extract (CME) and cordycepin (COR) on LTA-induced inflammation in MH-S cells and their mechanisms of action. In this study, the establishment of an LTA-induced MH-S inflammation model was determined, the CCK-8 method was used to determine the safe concentration range for a drug for COR and CME, the optimal concentration of COR and CME to exert anti-inflammatory effects was further selected, and the expression of inflammatory factors of TNF-α, IL-1ß, IL-18, and IL-6 was detected using ELISA. The relative expression of TNF-α, IL-1ß, IL-18, IL-6, IL-10, TLR2 and MyD88 mRNA was detected using RT-PCR, and the IL-1ß, IL-18, TLR2, MyD88, NF-κB p-p65, NLRP3, pro-caspase-1, Caspase-1 and ASC protein expression in the cells were detected using Western blot; immunofluorescence assay detected the expression of Caspase-1 in MH-S cells. The results revealed that both CME and COR inhibited the levels of IL-1ß, IL-18, IL-6, and TNF-α in the supernatants of LTA-induced MH-S cells and the mRNA expression levels of IL-1ß, IL-18, IL-6, TNF-α, TLR2 and MyD88, down-regulated the LTA-induced IL-1ß, IL-18, TLR2 in MH-S cells, MyD88, NF-κB p-p65/p65, NLRP3, ASC, pro-caspase-1, and caspase-1 protein expression levels, and inhibited LTA-induced caspase-1 activation in MH-S cells. In conclusion, CME can play a therapeutic role in LTA-induced inflammation in MH-S cells via TLR2/NF-κB/NLRP3, and may serve as a potential drug for bacterial pneumonia caused by Gram-positive bacteria.

Clinical Values of Coagulation Factors X, XI, and XII in Cerebral Venous Sinus Thrombosis During Perinatal State.

Cerebral venous sinus thrombosis (CVST) has become a rare but potentially life-threatening condition in perinatal women. Early and rapid identification of CVST in pregnant women is a challenge for frontline clinical workers. In this study, 40 perinatal patients with CVST in our hospital were included in the five-year period, and 120 normal perinatal pregnant women in the obstetrics and gynecology department of our hospital were randomly enrolled in the five-year period as the control group, including 60 cases in pregnancy and puerperium. 5 mL of fasting venous blood was collected from puerperal CVST patients in the acute phase of onset (within 72 h of onset) and the recovery phase (fourth week of treatment). In the control group, 5 mL of fasting venous blood was collected. Coagulation factors X, XI, and XII, plasma D-Dimer were analyzed and compared. Coagulation factors X, XI, and XII in plasma of CVST patients were significantly increased compared with controls. Plasma coagulation factors X, XI, and XII and their combined detection (Union Model = 0.056 * FX: C + 0.046 * FXI: C + 0.081 * FXII: C) have diagnostic values for perinatal CVST. Plasma coagulation factors X, XI, and XII were significantly positively correlated with plasma D-dimer levels in perinatal CVST patients. Plasma coagulation factors X, XI, and XII have diagnostic values for perinatal CVST.

Genome Analysis and Safety Assessment of Achromobacter marplatensis Strain YKS2 Strain Isolated from the Rumen of Yaks in China.

Achromobacter marplatensis strain YKS2 isolated from the yak rumen has the feature of producing cellulose. This study aims to analyze the genome and safety of strain YKS2 in vivo, considering its future research and application prospects. The genome of strain YKS2 was sequenced and used for genomic in silico studies. The administration of strain YKS2 in three doses was carried out on mice for 3 days of oral and 7 days of clinical observation tests. The BW, FI, organ indices, gut microbiota, and histological appearances of organs and intestines, along with hematological parameters and serum biochemistry, were measured in mice. The chromosome size of strain YKS2 was 6,588,568 bp, with a GC content of 65.27%. The 6058 coding sequences of strain YKS2 without plasmid were predicted and annotated and have multiple functions. The mice in all groups were alive, with good mental states and functional activities. Compared with the control group, there was no significant difference in the three dose groups on BW, FI, hematological parameters (WBC, LYM, etc.), and serum biochemistry (ALB, ALT, etc.). No abnormalities were observed in the main visceral organs, intestinal tissue, and V/C value in groups. However, the IEL number of duodenum and gut microbiota diversity (Shannon's index) in the high-dose group was significantly higher than in the control group (p < 0.05). Besides, the low dose of strain YKS2 also significantly affected the bacterial abundance of Firmicutes, Actinobacteria, and desulphurizing Bacteroidetes at the phylum level. There was no significant effect at genus levels in groups. In conclusion, the study revealed the genome and potential functional genes of strain YKS2, which is beneficial to understanding the features of the A. marplatensis strain and proved strain YKS2 to be without acute toxicity to mice. However, a long-term feeding toxicity experiment in vivo should be performed to further ensure its potential application value strain in the animal industry.

Developing boron carbon nitride/boron carbon nitride-citric acid quantum dot metal-free photocatalyst and evaluating the degradation performance difference of photo-induced species for tetracycline via theoretical and experimental study.

For opening a way to synthesize novel metal-free catalysts and clarifying the photodegradation performance difference of photoactive species (such as ·O2-, h+), a series of metal-free photocatalysts have been synthesized by using different existing forms of the same materials (boron carbon nitride (BCN) and boron carbon nitride-citric acid quantum dot (BCQD)) as precursors via calcinating their mixture at 350 °C. BCQD has good fluorescence and up-conversion fluorescence performance. BCN/BCQD-350 has the highest removal efficiency (90%, including adsorption 60% and photodegradation 30%) for tetracycline (TC) among all samples under visible light irradiation. TC adsorption by BCN/BCQD-350 conforms to pseudo-second-order kinetic and Langmuir isotherm models. TC photodegradation by BCN/BCQD-350 conforms to type II heterojunction mechanism. Photoactive species capture experiments suggest that·O2- makes a higher contribution for TC photodegradation, followed by h+, ·OH, 1O2 and e-. From LC-MS results, TC photodegradation is initiated by the dehydration step. TC dehydration activated by ·O2- has the lowest barrier (43.4 kcal/mol) than that (50.1 kcal/mol) activated by h+, that (64.8 kcal/mol) without the activation by photoactive species. TC removal rate of BCN/BCQD-350 (0.01563 min-1) is higher than that of g-C3N4, P25 (TiO2), BNPA, BCNPA, etc. Furthermore, BCN/BCQD-350 can also photodegrade TC under infrared light irradiation (λ > 800 nm).

Molecular Characteristics, Functional Definitions, and Regulatory Mechanisms for Cross-Presentation Mediated by the Major Histocompatibility Complex: A Comprehensive Review.

The major histocompatibility complexes of vertebrates play a key role in the immune response. Antigen-presenting cells are loaded on MHC I molecules, which mainly present endogenous antigens; when MHC I presents exogenous antigens, this is called cross-presentation. The discovery of cross-presentation provides an important theoretical basis for the study of exogenous antigens. Cross-presentation is a complex process in which MHC I molecules present antigens to the cell surface to activate CD8+ T lymphocytes. The process of cross-representation includes many components, and this article briefly outlines the origins and development of MHC molecules, gene structures, functions, and their classical presentation pathways. The cross-presentation pathways of MHC I molecules, the cell lines that support cross-presentation, and the mechanisms of MHC I molecular transporting are all reviewed. After more than 40 years of research, the specific mechanism of cross-presentation is still unclear. In this paper, we summarize cross-presentation and anticipate the research and development prospects for cross-presentation.

Research on carbon emission measurement and low-carbon path of regional industry.

As industry is the world's leading carbon emitter, promoting industrial carbon reduction is of key significance to carbon peak and carbon neutrality. Using a data-driven method, based on the collection and processing of relevant data from statistical yearbooks and others, we analyze the efficiency and amount of carbon emission of each industrial sector after processing multi-dimensional data by the improved IPCC EF method of calculating carbon emissions. In addition, we adopt the LMDI decomposition method for data modeling to measure the contribution of energy efficiency, industrial structure, GDP per capita, and population size to carbon emission changes, to identify targets for industrial carbon reduction, and to propose a targeted optimization path for carbon emission. We show how the method is implemented by taking the statistics of Anhui Province from 2010 to 2019 as an example and advises on an optimization path for carbon emission in Anhui Province. This study is of both theoretical and practical significance as it provides theoretical and methodological support for the low-carbon development of the regional industry, and provides a reference for other countries and regions to explore the path of low-carbon and environment-friendly green transformation and upgrading.

Functional Analysis and Proteomics Profiling of Extracellular Vesicles From Swine Plasma Infected by African Swine Fever Virus.

African swine fever (ASF) has brought excellent barriers to swine production in China and the world. Studies have shown that extracellular vesicles mediate the RNA and protein spread of pathogenic microorganisms and RNA and proteins. After infection by pathogenic microorganisms causes significant differences in the proteins contained within extracellular vesicles. Based on the above studies, the extracellular vesicles were extracted from ASF virus (ASFV)-infected swine plasma. And qPCR, western blot, and confocal experiment were carried out. The research shows that extracted extracellular vesicles significantly promote the replication of ASFV in susceptible and non-susceptible cells Proteomics analysis of the extracellular vesicle proteins revealed that ASFV infection could cause significant differences in the protein profile. This study demonstrates that extracellular vesicles play a critical role in ASFV replication and transmission and cause significant differences in the protein profile encapsulated in extracellular vesicles.

Arsenic Induces Continuous Inflammation and Regulates Th1/Th2/Th17/Treg Balance in Liver and Kidney In Vivo.

Numerous studies on arsenic-induced hepatonephric toxicity including cancer have been reported. Given that chronic inflammatory response and immune imbalance are associated with oncogenesis, we investigated whether arsenic could influence the hepatic and nephritic expression of inflammatory factors and the differentiation of T cells. Mice were exposed to NaAsO2 (0, 25, and 50 mg/L) for 1 and 3 months. Our data showed the destruction of the structure and inflammatory infiltration in the liver. The arsenic markedly increased the activity of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). The myeloperoxidase (MPO) activities increased in the liver at 25 and 50 mg/L arsenic for 3 months as well as in the kidney at both 1 and 3 months. An increased expression of inflammatory indicators (IL-1ß, IL-12, and TNF-α) at 25 and 50 mg/L arsenic for 1 and 3 months in the liver and kidney, as well as IL-1ß in the liver for 3 months and in the kidney at 50 mg/L for 1 and 3 months were demonstrated in our experiments. Besides, a definite tendency toward Th1/Th17 cytokines in the liver while Th2/Th17 cytokines in kidney was also observed by arsenic. Moreover, arsenic enhanced the expression of MAPK/Nrf2/NF-κB signaling molecules. In conclusion, the results of the study suggested that arsenic induces continuous immune-inflammatory responses in the liver and kidney.

Coupling band structure and oxidation-reduction potential to expound photodegradation performance difference of biochar-derived dissolved black carbon for organic pollutants under light irradiation.

Herein, the photodegradation performances difference of rice straw biochar-derived dissolved black carbon (DBC) for Tetracycline and Methylene Blue under visible light irradiation have been investigated. Tetracycline is easier degraded (degradation rate: 68%), followed by Methylene Blue (degradation rate: 14%). Singlet oxygen (1O2), superoxide radicals (O2-), holes (h+) and triplet DBC (3DBC*) are all make contribution for Tetracycline degradation by DBC, whereas just singlet oxygen (1O2), superoxide radicals (O2-) and 3DBC* are involved in the MB degradation by DBC. Singlet oxygen (1O2) maybe from the fulvic acid-like structure of DBC, while band structure of DBC can explain why superoxide radicals (O2-) and holes (h+) can be formed, whereas hydroxyl radicals (OH) cannot be formed. The oxidation-reduction potential results of Tetracycline and Methylene Blue suggests that Tetracycline is easier to be oxidized than Methylene Blue as well as Methylene Blue is easier to be reduced than Tetracycline. Furthermore, experimental and theoretical results support that DBC has good interaction with Tetracycline, but the interaction between DBC and Methylene Blue is very weak. This likely explain why holes (h+) is not detected for Methylene Blue degradation by DBC since Methylene Blue has not too much chance to meet holes (h+). TC photodegradation intermediates are less toxic than Tetracycline based on QSAR method. Two possible photodegradation path of Tetracycline by DBC are proposed according to HPLC-MS results.

Corrigendum: Foot-and-Mouth Disease Virus Capsid Protein VP1 Antagonizes TPL2-Mediated Activation of the IRF3/IFN-ß Signaling Pathway to Facilitate the Virus Replication.

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Curcumin functions as an anti-inflammatory and antioxidant agent on arsenic-induced hepatic and kidney injury by inhibiting MAPKs/NF-κB and activating Nrf2 pathways.

Chronic arsenic exposure has been associated with various toxic effects, especially to the organs of liver and kidney. As a plant polyphenol, curcumin is the most vital bioactive ingredient of turmeric and has a wide range of pharmacological activities. In the present study, we investigated the potential roles of curcumin against arsenic-induced liver and kidney dysfunctions in mice. Curcumin treatment (200 mg/kg) not only decreased the deposition of arsenic in liver and kidney, but also relieved the hepatic and nephritic biochemical indexes (Glutamic oxaloacetic transaminase [AST], Alanine aminotransferase [ALT], albumin, and creatinine) altered by arsenic at doses of 10 and 25 mg/L via drinking water. What's more, curcumin exerted influences on the activities of myeloperoxidase and on the secretion of inflammatory cytokines in liver and kidney tissues. In addition, the levels of mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B (NF-κB) phosphorylation were declining while NRF2-signaling targets were increasing in mice liver and kidney by curcumin administration. In conclusion, our results here suggest that curcumin could exert both anti-inflammatory and antioxidant functions on arsenic-induced hepatic and kidney injury by inhibiting MAPKs/NF-κB and activating Nrf2 pathways cooperatively.

Differential effects of arsenic species on Nrf2 and Bach1 nuclear localization in cultured hepatocytes.

Arsenic is a ubiquitous metalloid element present in both inorganic and organic forms in the environment. The liver is considered to be a primary organ of arsenic biotransformation and methylation, as well as the main target of arsenic toxicity. Studies have confirmed that Chang human hepatocytes have an efficient arsenic methylating capacity. Our previous studies have proven that arsenite activates nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in hepatocytes. This study aimed to explore the activation of the Nrf2 pathway upon treatment of arsenic in various forms, including inorganic and organic arsenic. Our results showed that inorganic arsenic-both As2O3 and Na2HAsO4 significantly induced the expression of Nrf2 protein and mRNA, enhanced the transcription activity of Nrf2, and induced the expression of downstream target genes. These results confirmed the inorganic arsenic-induced Nrf2 pathway activation in hepatocytes. Although all arsenic chemicals used in the study induced Nrf2 protein accumulation, the organic arsenic C2H7AsO2 did not affect the expression of Nrf2 downstream genes which were elevated by inorganic arsenic exposures. Through qRT-PCR and Nrf2 luciferase reporter assays, we further confirmed that C2H7AsO2 neither increased Nrf2 mRNA level nor activated the Nrf2 transcription activity. Mechanistically, our results confirmed inorganic arsenic-induced both the nuclear import of Nrf2 and export of Bach1 (BTB and CNC homology 1), which is an Nrf2 transcriptional repressor, while organic arsenic only induced Nrf2 translocation. The unique pattern of Nrf2 regulation by organic arsenic underlines the critical role of Nrf2 and Bach1 in the arsenic toxicology.

Transition to sustainable transport: understanding the antecedents of consumer's intention to adopt electric vehicles from the emotional research perspective.

Electric vehicles (EVs) are recognized as one of the effective measures to realize sustainable transport. Therefore, many countries have issued related policy initiatives and measures to promote EVs. However, consumer's cognition and acceptance of EVs is not ideal, which affects the early diffusion speed of EVs on the market. This research attempts to explore how consumer's driving experience affects EVs adoption intention from the perspective of consumer's emotional response (satisfaction and trust) by using stimulus-organism-response framework. Based on the analysis of 692 sample data collected through questionnaire survey, we found that consumer's driving experience has a significant and positive impact on EVs adoption intention. Meanwhile, driving experience also significantly and positively affects consumer's satisfaction while has no significant effect on trust. Furthermore, satisfaction has a significantly positive effect on trust, and satisfaction and trust are both significantly and positively associated with EVs adoption intention. The results further uncovered that satisfaction not only plays a mediating role between driving experience and adoption intention but also plays a multiple mediating role between driving experience and adoption intention together with trust. On this basis, relevant recommendations have been made to promote the development of EVs from the perspective of government and enterprise.

Foot-and-Mouth Disease Virus Structural Protein VP1 Destroys the Stability of TPL2 Trimer by Degradation TPL2 to Evade Host Antiviral Immunity.

Tumor progression locus 2 (TPL2) is a serine/threonine kinase that belongs to the mitogen-activated protein 3 kinase (MAP3K) family, and it plays an important role in pathogen infection. The trimer complex of TPL2, p105, and ABIN2 is essential for maintenance of TPL2 steady-state levels and host cell response to pathogens. Foot-and-mouth disease virus (FMDV) is a positive-strand RNA virus of the family Picornaviridae that encodes proteins capable of antagonizing host immune responses to achieve infection. The VP1 protein of FMDV is a multifunctional protein that can bind host cells and induce an immune response as well as cell apoptosis. However, the role and mechanisms of TPL2 in FMDV infection remain unknown. Here, we determined that FMDV infection could inhibit TPL2, p105, and ABIN2 at the transcription and protein levels, while VP1 could only inhibit TPL2, p105 and ABIN2 at protein level. TPL2 inhibited the replication of FMDV in vivo and in vitro, the 268 to 283 amino-acid region in the TPL2 kinase domain was essential for interaction with VP1. Moreover, VP1 promoted K48-linked polyubiquitination of TPL2 and degraded TPL2 by the proteasome pathway. However, VP1-induced degradation of p105 and ABIN2 was independent of proteasome, autophagy, lysosome, and caspase-dependent pathways. Further studies showed that VP1 destroyed the stability of the TPL2-p105-ABIN2 complex. Taken together, these results revealed that VP1 antagonized TPL2-meditated antivirus activity by degrading TPL2 and destroying its complex. These findings may contribute to understand FMDV-host interactions and improve development of a novel vaccine to prevent FMDV infection.Importance Virus-host interactions are critical for virus infection. This study was the first to demonstrate the antiviral effect of host TPL2 during FMDV replication by increasing production of interferons and antiviral cytokines. Both FMDV and VP1 protein can reduce host TPL2, ABIN2 and p105 to destroy TPL2-p105-ABIN2 trimer complex. VP1 interacted with TPL2 and degrade TPL2 via proteasome pathway to repress TPL2-mediated antivirus activity. This study provided new insights into FMDV immune evasion mechanisms, elucidating new informations regarding FMDV counteraction of host antivirus activity.

Foot-and-mouth disease virus degrades Rab27a to suppress the exosome-mediated antiviral immune response.

Foot-and-mouth disease (FMD) is a highly contagious infection caused by foot-and-mouth disease virus (FMDV). Exosomes are extracellular vesicles that mediate antiviral immune responses in host cells and could be used by pathogens to evade host cell immune responses. Whether FMDV affects exosome secretion or whether exosomes derived from FMDV-infected cells mediate host cell antiviral immune responses is not yet clarified. In this study, the exosomes were identified and extracted from FMDV-infected PK-15 cells, and it was found that FMDV inhibits exosome secretion. Further investigation revealed that FMDV suppresses exosomes by degrading Rab27a via the autophagy-lysosome pathway. Also, microRNA (miRNA) differential analysis was performed in exosomes, which revealed that miRNA-136 was highly differentially expressed in exosomes and may be the key miRNA that inhibits the proliferation of FMDV. In summary, these results showed that host cells take advantage of exosomes to mediate their antiviral immune response, while FMDV evades exosome-mediated immune responses by degrading the exosome molecular switch, Rab27a.

Inhibition of orf virus replication in goat skin fibroblast cells by the HSPA1B protein, as demonstrated by iTRAQ-based quantitative proteome analysis.

Orf virus (ORFV) infects sheep and goat tissues, resulting in severe proliferative lesions. To analyze cellular protein expression in ORFV-infected goat skin fibroblast (GSF) cells, we used two-dimensional liquid chromatography-tandem mass spectrometry coupled with isobaric tags for relative and absolute quantification (iTRAQ). The proteomics approach was used along with quantitative reverse transcription polymerase chain reaction (RT-qPCR) to detect differentially expressed proteins in ORFV-infected GSF cells and mock-infected GSF cells. A total of 282 differentially expressed proteins were identified. It was found that 222 host proteins were upregulated and 60 were downregulated following viral infection. We confirmed that these proteins were differentially expressed and found that heat shock 70-kDa protein 1B (HSPA1B) was differentially expressed and localized in the cytoplasm. It was also noted that HSPA1B caused inhibition of viral proliferation, in the middle and late stages of viral infection. The differentially expressed proteins were associated with the biological processes of viral binding, cell structure, signal transduction, cell adhesion, and cell proliferation.