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BACKGROUND: Introducing new goat breeds or transferring adult goats from farms to slaughterhouses requires transportation, which can engender adverse effects, such as oxidative stress, pathological cell apoptosis and autophagy. Current evidence suggests that malondialdehyde (MDA) is a metabolite of lipid peroxidation during oxidative stress, while superoxide dismutase (SOD) and catalase (CAT) can alleviate injury caused by free radicals and reactive oxygen species (ROS). Meanwhile, Bcl-2, Bax, LC3B, PINK1 and Parkin are important proteins that participate in pathological cell apoptosis and autophagy. This study aimed to investigate the effects of transportation stress on oxidative stress indexes and expressions of Bcl-2, Bax, LC3B, PINK1 and Parkin in the small intestine of goats. Twelve healthy adult male goats from western Jiangxi province were randomly divided into control, 2 h transportation stress, and 6 h transportation stress groups (n = 4 per group). RESULTS: Our results showed that MDA in the small intestine significantly increased after transportation, while SOD and CAT activities decreased, with a significantly increased apoptosis rate of the small intestine cells. The jejunum and duodenum exhibited the highest apoptosis rate in the 2 h and 6 h transportation groups, respectively. The expression of apoptosis-related genes Bcl-2 and Bax and their corresponding proteins exhibited varying degrees of down-regulation or up-regulation, while Bcl-2 and Bax genes in the small intestine were upregulated in the 6 h transportation group. In addition, autophagosomes and autophagolysosomes were found in various parts of the small intestine by transmission electron microscopy, and autophagy-related genes LC3B, PINK1 and Parkin were significantly down-regulated in the 2 h group and up-regulated in the 6 h group. CONCLUSIONS: Our results indicate that the contents of MDA, SOD and CAT in the small intestine, the expression of pathologic apoptosis-related genes Bcl-2 and Bax, and autophagy-related genes LC3B, PINK1 and Parkin correlated with stress duration caused by transportation. Moreover, this study provides a foothold for further studies on the mechanism of transportation stress in goats and improving animal welfare.
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Apoptose , Cabras , Masculino , Animais , Proteína X Associada a bcl-2/farmacologia , Cabras/metabolismo , Estresse Oxidativo , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Autofagia , Antioxidantes/metabolismo , Superóxido Dismutase/metabolismo , Jejuno/metabolismo , Ubiquitina-Proteína Ligases/metabolismo , Ubiquitina-Proteína Ligases/farmacologia , Proteínas QuinasesRESUMO
Swine viruses are well known as a threat to the pig industry. Many signaling pathways and a number of proteins were discovered to participate in the immune responses to swine viruses. Noncoding RNAs (ncRNAs), comprising a different set of transcripts including housekeeping RNAs (for example, rRNAs and tRNAs) and regulatory RNAs (small RNAs and long non-coding RNAs), recently have been described as important regulators of viral infections regarding to swine. A growing number of studies have shown ncRNAs are an indispensable part in the responses to virus infection, involved not only in antiviral responses, but in many interactions between host and virus, some of which may benefit the certain types of swine virus. Here we review the relationship of noncoding RNA and viruses through several representative swine viruses. Further, we discuss the potential of using ncRNAs as antiviral biomarkers.
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Introduction: Ochratoxin A (OTA) is a widely distributed mycotoxin. Nano-selenium (Nano-Se) is an emerging form of selenium known for its superior bioavailability, remarkable catalytic efficiency, and robust adsorbing capacity. Despite these characteristics, its impact on the microbial community and metabolomics in the cecum of chickens exposed to OTA has been infrequently investigated. This research examined the microbiota and metabolomic alterations linked to OTA in chickens, with or without Nano-Se present. Methods: A cohort of 80 healthy chickens at the age of 1 day was randomly distributed into four groups of equal numbers, namely the Se cohort (1 mg/kg Nano-Se), the OTA cohort (50 µg/kg OTA), the OTA-Se cohort (50 µg/kg OTA + 1 mg/kg Nano-Se), and the control group. Each chicken group's caecal microbiome and metabolome were characterized using 16S rRNA sequencing and Liquid chromatography coupled with mass spectrometry (LC-MS) analyses. Results and discussion: Our results showed that the on day 21, the final body weight was significantly reduced in response to OTA treatments (p < 0.05), the average daily gain in the OTA group was found to be inferior to the other groups (p < 0.01). In addition, Nano-Se supplementation could reduce the jejunum and liver pathological injuries caused by OTA exposure. The 16S rRNA sequencing suggest that Nano-Se supplementation in OTA-exposed chickens mitigated gut microbiota imbalances by promoting beneficial microbiota and suppressing detrimental bacteria. Moreover, untargeted metabolomics revealed a significant difference in caecal metabolites by Nano-Se pretreatment. Collectively, the dataset outcomes highlighted that Nano-Se augmentation regulates intestinal microbiota and associated metabolite profiles, thus influencing critical metabolic pathways, and points to a possible food-additive product.
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Animal feed can easily be infected with molds during production and storage processes, and this can lead to the production of secondary metabolites, such as mycotoxins, which eventually threaten human and animal health. Furthermore, livestock production is also not free from viral infections. Under these conditions, the essential trace element, selenium (Se), can confer various biological benefits to humans and animals, especially due to its anticancer, antiviral, and antioxidant properties, as well as its ability to regulate immune responses. This article reviews the latest literature on the antagonistic effects of Se on mycotoxin toxicity and viral infections in animals. We outlined the systemic toxicity of mycotoxins and the primary mechanisms of mycotoxin-induced toxicity in this analysis. In addition, we pay close attention to how mycotoxins and viral infections in livestock interact. The use of Se supplementation against mycotoxin-induced toxicity and cattle viral infection was the topic of our final discussion. The coronavirus disease 2019 (COVID-19) pandemic, which is currently causing a health catastrophe, has altered our perspective on health concerns to one that is more holistic and increasingly embraces the One Health Concept, which acknowledges the interdependence of humans, animals, and the environment. In light of this, we have made an effort to present a thorough and wide-ranging background on the protective functions of selenium in successfully reducing mycotoxin toxicity and livestock viral infection. It concluded that mycotoxins could be systemically harmful and pose a severe risk to human and animal health. On the contrary, animal mycotoxins and viral illnesses have a close connection. Last but not least, these findings show that the interaction between Se status and host response to mycotoxins and cattle virus infection is crucial.
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It has been speculated that bats serve as reservoirs of a huge variety of emerging coronaviruses (CoVs) that have been responsible for severe havoc in human health systems as well as negatively affecting human economic and social systems. A prime example is the currently active severe acute respiratory syndrome (SARS)-CoV2, which presumably originated from bats, demonstrating that the risk of a new outbreak of bat coronavirus is always latent. Therefore, an in-depth investigation to better comprehend bat CoVs has become an important issue within the international community, a group that aims to attenuate the consequences of future outbreaks. In this review, we present a concise introduction to CoVs found in bats and discuss their distribution in Southeast Asia. We also discuss the unique adaptation features in bats that confer the ability to be a potential coronavirus reservoir. In addition, we review the bat coronavirus-linked diseases that have emerged in the last two decades. Finally, we propose key factors helpful in the prediction of a novel coronavirus outbreak and present the most recent methods used to forecast an evolving outbreak.
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Quirópteros/virologia , Coronavirus/classificação , SARS-CoV-2 , Animais , Sudeste Asiático , Saúde GlobalRESUMO
Transport stress causes a series of problems to goat production, such as tissue injury and immunity damage. As a pro-survival pathway, the heat shock response protects healthy cells of goat from stressors. To evaluate the effects of transport stress on heat shock protein (HSPs) expression on goat primary parenchymatous organs, a total of three batches of goats were treated in this study. For each batch, 12 healthy adult male goats were randomly and averagely divided into three groups: Control group (non-transported group), 2 hr transported group and 6 hr transported group. Real-time PCR results indicated that the mRNA expression level of heat shock protein 27 (HSP27) in all examined organs of 2 hr transport-treated goats were upregulated (p < .05) except lung, and heat shock protein 70 (HSP70; except spleen) and heat shock protein 90 (HSP90; except liver and lung) were also increased (p < .05). In 6 hr transported group, the transcription levels of HSP27 (except heart and kidney), HSP70 (except heart, liver and lymph nodes) and HSP90 (except heart and spleen) were all backed to the original levels or even reduced (p < .05). Enzyme-linked immunosorbent assay (ELISA) results showed that the protein levels of HSP27 (except lymph nodes), HSP70 (except spleen) and HSP90 (except liver and lung) were all increased after 2 hr transport (p < .05). After 6 hr transport, HSP27 only in kidney and HSP70 only in heart and liver were upregulated (p < .05), while HSP90 in all the examined organs except liver and lung were also maintained in relatively high levels (p < .05). Taken together, these results suggested that the expression of HSPs in goat primary parenchymatous organs may be regulated by transport stress time. Moreover, this study also provides some new data to advocate reducing transport stress of goats and improving animal welfare.
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Perfilação da Expressão Gênica/veterinária , Expressão Gênica , Cabras/genética , Proteínas de Choque Térmico HSP27/genética , Proteínas de Choque Térmico HSP70/genética , Proteínas de Choque Térmico HSP90/genética , Estresse Fisiológico , Criação de Animais Domésticos , Animais , Ensaio de Imunoadsorção Enzimática/veterinária , Cabras/metabolismo , Proteínas de Choque Térmico HSP27/metabolismo , Proteínas de Choque Térmico HSP70/metabolismo , Proteínas de Choque Térmico HSP90/metabolismo , Reação em Cadeia da Polimerase em Tempo Real/veterináriaRESUMO
Porcine circovirus-associated disease (PCVAD), which is induced by porcine circovirus type 2 (PCV2), is responsible for severe economic losses. Recently, the role of noncoding RNAs, and in particular microRNAs, in PCV2 infection has received great attention. However, the role of long noncoding RNA (lncRNA) in PCV2 infection is unclear. Here, for the first time, we describe the expression profiles of lncRNAs in an intestinal porcine epithelial cell line (IPEC-J2) after PCV2 infection, and analyze the features of differently expressed lncRNAs and their potential target genes. After strict filtering of approximately 150 million reads, we identified 13,520 lncRNAs, including 199 lncRNAs that were differentially expressed in non-infected and PCV2-infected cells. Furthermore, trans analysis found lncRNA-regulated target genes enriched for specific Gene Ontology terms (P < 0.05), such as DNA binding, RNA binding, and transcription factor activity, which are closely associated with PCV2 infection. In addition, we analyzed the predicted target genes of differentially expressed lncRNAs, including SOD2, TNFAIP3, and ARG1, all of which are involved in infectious diseases. Our study identifies many candidate lncRNAs involved in PCV2 infection and provides new insight into the mechanisms underlying the pathogenesis of PCVAD.