Intestinal homeostasis is a dynamic balance involving the interaction between the host intestinal mucosa, immune barrier, intestinal microecology, nutrients, and metabolites. Once homeostasis is out of balance, it will increase the risk of intestinal diseases and is also closely associated with some systemic diseases. Probiotics (Escherichia coli Nissle 1917, Akkermansia muciniphila, Clostridium butyricum, lactic acid bacteria and Bifidobacterium spp.), maintaining the gut homeostasis through direct interaction with the intestine, can also exist as a specific agent to prevent, alleviate, or cure intestinal-related diseases. With genetic engineering technology advancing, probiotics can also show targeted therapeutic properties. The aims of this review are to summarize the roles of potential native and engineered probiotics in oncology, inflammatory bowel disease, and obesity, discussing the therapeutic applications of these probiotics.

/pdf/native-and-engineered-probiotics-promising-agents-against-2dh5j1vf.pdf

Native and Engineered Probiotics: Promising Agents against Related Systemic and Intestinal Diseases

The development of drug delivery vehicles is in significant demand in the context of precision medicine. With the development of synthetic biology, the use of genetically engineered bacteria as drug delivery vectors has attracted more and more attention. Herein, we reviewed the research advances in bioengineered bacteria as drug carriers, with emphasis on the synthetic biology strategies for modifying these bacteria, including the targeted realization method of engineered bacteria, the designing scheme of genetic circuits, and the release pathways of therapeutic compounds. Based on this, the essential components, design principles, and health concerns of engineering bacteria as drug carriers and the development prospects in this field have been discussed. 

Engineered Bacteria as Drug Delivery Vehicles: Principles and Prospects

Engineering Escherichia coli Nissle 1917 as a microbial chassis for therapeutic and industrial applications.

Toxicological and bioremediation profiling of nonessential heavy metals (mercury, chromium, cadmium, aluminium) and their impact on human health: A review

The objective of the present study was to review the existing epidemiological and laboratory findings supporting the role of toxic metal exposure in non-alcoholic fatty liver disease (NAFLD). The existing epidemiological studies demonstrate that cadmium (Cd), lead (Pb), arsenic (As), and mercury (Hg) exposure was associated both with an increased risk of NAFLD and altered biochemical markers of liver injury. Laboratory studies demonstrated that metal exposure induces hepatic lipid accumulation resulting from activation of lipogenesis and inhibition of fatty acid β-oxidation due to up-regulation of sterol regulatory element-binding protein 1 (SREBP-1), carbohydrate response element binding protein (ChREBP), peroxisome proliferator-activated receptor γ (PPARγ), and down-regulation of PPARα. Other metabolic pathways involved in this effect may include activation of reactive oxygen species (ROS)/extracellular signal-regulated kinase (ERK) and inhibition of AMP-activated protein kinase (AMPK) signaling. The mechanisms of hepatocyte damage during development of metal-induced hepatic steatosis were shown to involve oxidative stress, endoplasmic reticulum stress, pyroptosis, ferroptosis, and dysregulation of autophagy. Induction of inflammatory response contributing to progression of NAFLD to non-alcoholic steatohepatitis (NASH) upon toxic metal exposure was shown to be mediated by up-regulation of nuclear factor κB (NF-κB) and activation of NRLP3 inflammasome. Moreover, epigenetic effects of the metals, as well as their effect on gut microbiota and gut wall integrity were also shown to mediate their role in NAFLD development. Despite being demonstrated for Cd, Pb, and As, the contribution of these mechanisms into Hg-induced NAFLD is yet to be estimated. Therefore, further studies are required to clarify the intimate mechanisms underlying the relationship between heavy metal and metalloid exposure and NAFLD/NASH to reveal the potential targets for treatment and prevention of metal-induced NAFLD. 

Dissecting the role of cadmium, lead, arsenic, and mercury in non-alcoholic fatty liver disease and non-alcoholic steatohepatitis.

Oleanolic acid inhibits mercury chloride induced-liver ferroptosis by regulating ROS/iron overload.

Jingmen tick virus (JMTV) is a novel tick‐borne virus first identified from Jingmen city, Hubei Province of China in 2010. It has been proved that JMTV can cause human diseases and is widely distributed both inside and outside of China. However, the survival mode and transmission characteristics of JMTV still need further research, particularly in terms of transovarial transmission. In this study, an investigation was conducted to explore the presence of JMTV from engorged female ticks to their offspring. All engorged female adult ticks were collected from domestic cattle and allowed to lay eggs in appropriate humidity and temperature conditions. Maternal ticks, eggs and larvae were screened for JMTV RNA through real‐time polymerase chain reaction (RT‐PCR) and nested PCR methods. The results revealed the positive rate of 10.53% (10/95) in engorged ticks, 9.09% (2/22) in eggs and 8% (4/50) in larvae pools, respectively. Phylogenetic analysis confirmed that sequences from eggs and larvae had closer relationship with those isolates from maternal engorged ticks with more than 99.7% homology and JMTV manifested with evolutional conservatism. Our study has identified for the first time that JMTV could be transmitted from mother generation to offspring of Haemaphysalis Longicornis. Nonetheless, the efficiency of transovarial transmission in JMTV and the significance of ticks as amplification hosts still need to be further illustrated.

Molecular evidence for potential transovarial transmission of Jingmen tick virus in Haemaphysalis longicornis fed on cattle from Yunnan Province, China

https://doi.org/10.1016/j.psj.2023.102724

Placenta-specific 8 facilitates the infection of duck hepatitis A virus type 1 by inhibiting the TLR7 MyD88-dependent signaling pathway

The innate immune system provides a defense against invading pathogens by inducing various interferon (IFN)-stimulated genes (ISGs). We recently reported that tripartite motif protein 25 (TRIM25), an important ISG, was highly upregulated in duck embryo hepatocyte cells (DEFs) after infection with duck viral hepatitis A virus type 1 (DHAV-1). However, the mechanism of upregulation of TRIM25 remains unknown. Here we reported that interleukin-22 (IL-22), whose expression was highly facilitated in DEFs and various organs of 1-day-old ducklings after DHAV-1 infection, highly enhanced the IFN-λ-induced production of TRIM25. The treatment with IL-22 neutralizing antibody or the overexpression of IL-22 highly suppressed or facilitated TRIM25 expression, respectively. The phosphorylation of signal transducer and activator of transcription 3 (STAT3) was crucial for the process of IL-22 enhancing IFN-λ-induced TRIM25 production, which was suppressed by WP1066, a novel inhibitor of STAT3 phosphorylation. The overexpression of TRIM25 in DEFs resulted in a high production of IFNs and reduced DHAV-1 replication, whereas the attenuated expression of IFNs and facilitated replication of DHAV-1 were observed in the RNAi group, implying that TRIM25 defended the organism against DHAV-1 propagation by inducing the production of IFNs. In summary, we reported that IL-22 activated the phosphorylation of STAT3 to enhance the IFN-λ-mediated TRIM25 expression and provide a defense against DHAV-1 by inducing IFN production. 

/pdf/interleukin-22-facilitates-the-interferon-l-mediated-22env676.pdf

Interleukin-22 facilitates the interferon-λ-mediated production of tripartite motif protein 25 to inhibit replication of duck viral hepatitis A virus type 1

Corrigendum to Hao et al. 2023. Placenta-specific 8 facilitates the infection of duck hepatitis A virus type 1 by inhibiting the TLR7 MyD88-dependent signaling pathway. Poult. Sci. 102:102724.

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