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Non‐alcoholic fatty liver disease (NAFLD) represents a growing global health concern that can lead to liver disease and cancer. It is characterized by an excessive accumulation of fat in the liver, unrelated to excessive alcohol consumption. Studies indicate that the gut microbiota‐host crosstalk may play a causal role in NAFLD pathogenesis, with epigenetic modification serving as a key mechanism for regulating this interaction. In this review, we explore how the interplay between gut microbiota and the host epigenome impacts the development of NAFLD. Specifically, we discuss how gut microbiota‐derived factors, such as lipopolysaccharides (LPS) and short‐chain fatty acids (SCFAs), can modulate the DNA methylation and histone acetylation of genes associated with NAFLD, subsequently affecting lipid metabolism and immune homeostasis. Although the current literature suggests a link between gut microbiota and NAFLD development, our understanding of the molecular mechanisms and signaling pathways underlying this crosstalk remains limited. Therefore, more comprehensive epigenomic and multi‐omic studies, including broader clinical and animal experiments, are needed to further explore the mechanisms linking the gut microbiota to NAFLD‐associated genes. These studies are anticipated to improve microbial markers based on epigenetic strategies and provide novel insights into the pathogenesis of NAFLD, ultimately addressing a significant unmet clinical need. [ABSTRACT FROM AUTHOR]

Aims: Liver damage has caused great illness in human beings. Bifidobacterium catenulatum LI10 has been determined with protective effect against D‐galactosamine‐induced liver damage. However, due to the sample limitation, the individual difference in its protective effect was not determined. The current study was designed to characterize the gut microbiota of LI10‐pretreated rats with lower levels of liver damage. Methods and Results: A series of experiments and bioinformatic analyses were carried out. Two rat cohorts with different levels of liver damage were determined, that is, Non‐Severe and Severe cohorts. Six out of the seven measured liver function variables were lower in the Non‐Severe cohort, while four cytokine variables also yielded differences between the two cohorts. The Non‐Severe and Severe cohorts were determined with distinct gut microbiota, among which ASV14_Parabacteroides and ASV7_Bacteroides were most associated with Non‐Severe and Severe cohorts, respectively. Five phylotypes were determined as structural gatekeepers in the microbiota network of Non‐Severe cohort, ASV135_Lachnospiraceae_NK4A136 of which contributed most to the stability of the network. Conclusions: The relevant findings suggest that some gut bacteria could benefit the protective effect of LI10 on lowering the severity of rat liver damage. Significance and Impact of the Study: The bacteria benefiting the protective effects of potential probiotics could be further investigated for future clinical application. [ABSTRACT FROM AUTHOR]

Liver injury has caused significant illness in humans worldwide. The dynamics of intestinal bacterial communities associated with natural recovery and therapy for CCl4-treated liver injury remain poorly understood. This study was designed to determine the recovery dynamics of intestinal bacterial communities in CCl4-treated mice with or without mesenchymal stem cell transplantation (i.e., MSC and CCl4 groups) at 48 h, 1 week (w), and 2 w. MSCs significantly improved the histopathology, survival rate, and intestinal structural integrity in the treated mice. The gut bacterial communities were determined with significant changes in both the MSC and CCl4 groups over time, with the greatest difference between the MSC and CCl4 groups at 48 h. The liver injury dysbiosis ratio experienced a decrease in the MSC groups and a rise in the CCl4 groups over time, suggesting the mice in the MSC group at 48 h and the CCl4 group at two weeks were at the least gut microbial dysbiosis status among the corresponding cohorts. Multiple OTUs and functional categories were associated with each of the bacterial communities in the MSC and CCl4 groups over time. Among these gut phylotypes, OTU1352_S24-7 was determined as the vital member in MSC-treated mice at 48 h, while OTU453_S24-7, OTU1213_Ruminococcaceae, and OTU841_Ruminococcus were determined as the vital phylotypes in CCl4-treated mice at two weeks. The relevant findings could assist the diagnosis of the microbial dysbiosis status of intestinal bacterial communities in the CCl4-treated cohorts with or without MSC transplantation. [ABSTRACT FROM AUTHOR]

Non-alcoholic fatty liver disease (NAFLD) represents a growing global health concern that can lead to liver disease and cancer. It is characterized by an excessive accumulation of fat in the liver, unrelated to excessive alcohol consumption. Studies indicate that the gut microbiota-host crosstalk may play a causal role in NAFLD pathogenesis, with epigenetic modification serving as a key mechanism for regulating this interaction. In this review, we explore how the interplay between gut microbiota and the host epigenome impacts the development of NAFLD. Specifically, we discuss how gut microbiota-derived factors, such as lipopolysaccharides (LPS) and short-chain fatty acids (SCFAs), can modulate the DNA methylation and histone acetylation of genes associated with NAFLD, subsequently affecting lipid metabolism and immune homeostasis. Although the current literature suggests a link between gut microbiota and NAFLD development, our understanding of the molecular mechanisms and signaling pathways underlying this crosstalk remains limited. Therefore, more comprehensive epigenomic and multi-omic studies, including broader clinical and animal experiments, are needed to further explore the mechanisms linking the gut microbiota to NAFLD-associated genes. These studies are anticipated to improve microbial markers based on epigenetic strategies and provide novel insights into the pathogenesis of NAFLD, ultimately addressing a significant unmet clinical need., Competing Interests: The authors have declared no conflicts of interest., (© 2023 The Authors. Engineering in Life Sciences published by Wiley‐VCH GmbH.)

Liver injury has caused significant illness in humans worldwide. The dynamics of intestinal bacterial communities associated with natural recovery and therapy for CCl 4 -treated liver injury remain poorly understood. This study was designed to determine the recovery dynamics of intestinal bacterial communities in CCl 4 -treated mice with or without mesenchymal stem cell transplantation (i.e., MSC and CCl 4 groups) at 48 h, 1 week (w), and 2 w. MSCs significantly improved the histopathology, survival rate, and intestinal structural integrity in the treated mice. The gut bacterial communities were determined with significant changes in both the MSC and CCl 4 groups over time, with the greatest difference between the MSC and CCl 4 groups at 48 h. The liver injury dysbiosis ratio experienced a decrease in the MSC groups and a rise in the CCl 4 groups over time, suggesting the mice in the MSC group at 48 h and the CCl 4 group at two weeks were at the least gut microbial dysbiosis status among the corresponding cohorts. Multiple OTUs and functional categories were associated with each of the bacterial communities in the MSC and CCl 4 groups over time. Among these gut phylotypes, OTU1352_ S24-7 was determined as the vital member in MSC-treated mice at 48 h, while OTU453_ S24-7 , OTU1213_Ruminococcaceae, and OTU841_ Ruminococcus were determined as the vital phylotypes in CCl 4 -treated mice at two weeks. The relevant findings could assist the diagnosis of the microbial dysbiosis status of intestinal bacterial communities in the CCl 4 -treated cohorts with or without MSC transplantation., Competing Interests: The authors declare no competing interests., (Copyright © 2020 Yanping Xu et al.)

Tail fan necrosis (TFN), a disorder commonly found in some populations of commercially fished and cultured lobsters, is thought to be initiated by injuries caused by handling and containment. The unsightly appearance of affected lobster tails significantly lowers their commercial value. Knowledge about TFN is limited. In this study we describe the morphological features of TFN and apply 6 common methods for evaluating the immune status of wild-caught Australasian red spiny lobsters Jasus edwardsii with and without TFN. The disease was more frequent in uropods than in telsons of the tail fan, and more extensive on the ventral versus the dorsal surfaces of the tail fan. Missing appendages (i.e. antenna, pereiopod or pleopod) were significantly more common and greater in number for individual lobsters affected with TFN versus those without, possibly as a result of handling in the fishery or as an indirect effect of the disease. Two immune parameters, total haemocyte count and phenoloxidase activity in the haemocyte lysate supernatant (HLS), were significantly compromised in lobsters with TFN. No differences were found in the other immune parameters, i.e. haemocyte viability, haemolymph bacterial count and the protein content of haemolymph plasma and HLS. The results are consistent with injury sustained during prior capture and handling that initiates TFN in these natural caught lobsters. These results raise some potential concerns about the fitness of lobsters in natural populations that are affected by TFN, and some potential solutions are proposed.