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Due to their low viscosity, high mobility, and high element contents, supercritical fluids are important agents in the cycling of elements. However, the chemical composition of supercritical fluids in natural rocks is poorly understood. Here, we investigate well-preserved primary multiphase fluid inclusions (MFIs) from an ultrahigh-pressure (UHP) metamorphic vein of the Bixiling eclogite in Dabieshan, China, thus providing direct evidence for the components of supercritical fluid occurring in a natural system. Via the 3D modeling of MFIs by Raman scanning, we quantitatively determined the major composition of the fluid trapped in the MFIs. Combined with the peak-metamorphic pressure–temperature conditions and the cooccurrence of coesite, rutile, and garnet, we suggest that the trapped fluids in the MFIs represent supercritical fluids in a deep subduction zone. The strong mobility of the supercritical fluids with respect to carbon and sulfur suggests that such fluids have profound effects on global carbon and sulfur cycling.

Arc magmas are enriched in sulfur relative to mid-ocean ridge basalts, commonly attributed to slab-derived sulfur inputs during subduction. However, the contribution of slab fluids remains debated because sulfur concentrations in sub-arc fluids have not been directly measured. Here we quantify sulfur in slab-derived fluids preserved as multiphase fluid inclusions composed of H 2 O, calcite, and chalcopyrite in omphacite from ultrahigh-pressure eclogites in the Sumdo orogenic belt. Three-dimensional Raman spectroscopy reveals high sulfur concentrations averaging ~6 wt.%. Mass-balance calculations indicate that such fluids can efficiently enrich the mantle wedge and supply up to ~70% of the sulfur emitted by arc volcanism. We further suggest that chalcopyrite formed through post-entrapment reduction of oxidized sulfur species by host omphacite, followed by precipitation with co-entrapped copper and iron. Our findings identify sub-arc depths as a critical window for slab sulfur release and provide key constraints on deep sulfur cycling and copper mobilization in arc systems. Three-dimensional Raman modelling of multiphase inclusions in Sumdo eclogites reveals sulfur rich slab-derived fluids at sub-arc depths, providing direct constraints on deep sulfur cycling and copper mobilization in subduction zones.

Enterococcus faecium HDRsEf1 (HDRsEf1) was identified to reduce the incidence of diarrhea in weaned piglets, but the mechanism has not been elucidated yet. Based on the fact that gut microbiota plays a crucial role in regulating inflammatory responses, the effects of HDRsEf1 on microbiota across the intestinal tract in weaned piglets were investigated. Microbiota from the luminal contents and the mucosa of the ileum, cecum, and colon of HDRsEf1-treated piglets were explored by 16S rRNA sequencing and qPCR. It was demonstrated that microbiota in different gut niches responded specifically to HDRsEf1, with major alterations occurring in the ileum and cecum. The total bacterial load of microbiota in ileal luminal contents and the relative abundance of Escherichia-Shigella in the ileal mucosa was significantly down-regulated by HDRsEf1 administration, while the relative abundance of butyrate-producing bacteria (including Clostridiaceae-1, Rumencoccidae, and Erysipelotrichaceae) in cecal luminal contents was significantly up-regulated. Moreover, the utilization of HDRsEf1 improved intestinal morphological development and reduced the inflammatory response, which were negatively correlated with the relative abundance of Escherichia-Shigella in the ileal mucosa and butyrate-producing bacteria in cecal luminal contents, respectively. Collectively, this study suggests that the administration of HDRsEf1 alters gut microbiota, thereby alleviating inflammation and improving intestinal morphological development in weaned piglets.

The gut microbiota is known to regulate the immune system and thereby influence susceptibility to infection. In this study, we observed that the administration of Enterococcus faecium HDRsEf1 (HDRsEf1) led to an improvement in the development of the immune system. This was evidenced by an increase in both the spleen index and the area of spleen white pulp. Specifically, the proportion of T helper (Th) 1 cells and the production of IFN-γ and IL-12 were significantly increased in the spleens of mice treated with HDRsEf1. In agreement with the in vivo results, we found that Th1-related cytokines, including IFN-γ and IL-12p70, were strongly induced in splenocytes treated with HDRsEf1. In addition, Th1 cell activation and high-level secretion of IL-12p70 were also confirmed by coculture of CD4+ T cells with bone marrow-derived dendritic cells treated with HDRsEf1. Moreover, the employment of HDRsEf1 was identified to augment resilience against systemic infection provoked by S. Typhimurium and stimulate the expression of the genes for TNFα and iNOS in the initial stage of infection, signifying that reinforced Th1 cells and IL-12 might activate macrophages for antibacterial safeguards. In summary, our study suggests that HDRsEf1 could act as an effective immunobiotic functional agent, promoting systemic Th1 immunological responses and priming defenses against infection.

Cecropins are peptide antibiotics used as drugs and feed additives. Cecropin B can inhibit the expression of CYP3A29, but the underlying mechanisms remain unclear. The present study was designed to determine the mechanisms responsible for the effects of cecropin B on CYP3A29 expression, focusing on the Toll-like receptors (TLRs) and NF-κB pathways. Our results indicated that the CYP3A29 expression was inhibited by cecropin B, which was regulated by pregnane X receptor (PXR) in a time- and dose-dependent manner. Cecropin B-induced NF-κB activation played a pivotal role in the suppression of CYP3A29 through disrupting the association of the PXR/retinoid X receptor alpha (RXR-α) complex with DNA sequences. NF-κB p65 directly interacted with the DNA-binding domain of PXR, suppressed its expression, and inhibited its transactivation, leading to the downregulation of the PXR-regulated CYP3A29 expression. Furthermore, cecropin B activated pig liver cells by interacting with TLRs 2 and 4, which modulated NF-κB-mediated signaling pathways. In conclusion, cecropin B inhibited the expression of CYP3A29 in a TLR/NF-κB/PXR-dependent manner, which should be considered in future development of cecropins and other antimicrobial peptides.

The gut microbiota is known to regulate the immune system and thereby influence susceptibility to infection. In this study, we observed that the administration of Enterococcus faecium HDRsEf1 (HDRsEf1) led to an improvement in the development of the immune system. This was evidenced by an increase in both the spleen index and the area of spleen white pulp. Specifically, the proportion of T helper (Th) 1 cells and the production of IFN-γ and IL-12 were significantly increased in the spleens of mice treated with HDRsEf1. In agreement with the in vivo results, we found that Th1-related cytokines, including IFN-γ and IL-12p70, were strongly induced in splenocytes treated with HDRsEf1. In addition, Th1 cell activation and high-level secretion of IL-12p70 were also confirmed by coculture of CD4+ T cells with bone marrow-derived dendritic cells treated with HDRsEf1. Moreover, the employment of HDRsEf1 was identified to augment resilience against systemic infection provoked by S. Typhimurium and stimulate the expression of the genes for TNFα and iNOS in the initial stage of infection, signifying that reinforced Th1 cells and IL-12 might activate macrophages for antibacterial safeguards. In summary, our study suggests that HDRsEf1 could act as an effective immunobiotic functional agent, promoting systemic Th1 immunological responses and priming defenses against infection.

The gut microbiota is known to regulate the immune system and thereby influence susceptibility to infection. In this study, we observed that the administration of Enterococcus faecium HDRsEf1 (HDRsEf1) led to an improvement in the development of the immune system. This was evidenced by an increase in both the spleen index and the area of spleen white pulp. Specifically, the proportion of T helper (Th) 1 cells and the production of IFN-γ and IL-12 were significantly increased in the spleens of mice treated with HDRsEf1. In agreement with the in vivo results, we found that Th1-related cytokines, including IFN-γ and IL-12p70, were strongly induced in splenocytes treated with HDRsEf1. In addition, Th1 cell activation and high-level secretion of IL-12p70 were also confirmed by coculture of CD4[sup.+] T cells with bone marrow-derived dendritic cells treated with HDRsEf1. Moreover, the employment of HDRsEf1 was identified to augment resilience against systemic infection provoked by S. Typhimurium and stimulate the expression of the genes for TNFα and iNOS in the initial stage of infection, signifying that reinforced Th1 cells and IL-12 might activate macrophages for antibacterial safeguards. In summary, our study suggests that HDRsEf1 could act as an effective immunobiotic functional agent, promoting systemic Th1 immunological responses and priming defenses against infection.

Cecropins are peptide antibiotics used as drugs and feed additives. Cecropin B can inhibit the expression of CYP3A29, but the underlying mechanisms remain unclear. The present study was designed to determine the mechanisms responsible for the effects of cecropin B on CYP3A29 expression, focusing on the Toll-like receptors (TLRs) and NF-κB pathways. Our results indicated that the CYP3A29 expression was inhibited by cecropin B, which was regulated by pregnane X receptor (PXR) in a time- and dose-dependent manner. Cecropin B-induced NF-κB activation played a pivotal role in the suppression of CYP3A29 through disrupting the association of the PXR/retinoid X receptor alpha (RXR-α) complex with DNA sequences. NF-κB p65 directly interacted with the DNA-binding domain of PXR, suppressed its expression, and inhibited its transactivation, leading to the downregulation of the PXR-regulated CYP3A29 expression. Furthermore, cecropin B activated pig liver cells by interacting with TLRs 2 and 4, which modulated NF-κB-mediated signaling pathways. In conclusion, cecropin B inhibited the expression of CYP3A29 in a TLR/NF-κB/PXR-dependent manner, which should be considered in future development of cecropins and other antimicrobial peptides.