Exploring Information Exchange between Thesium chinense and Its Host Prunella vulgaris through Joint Transcriptomic and Metabolomic Analysis.

BACKGROUND: Thesium chinense known as the "plant antibiotic" is a facultative root hemi-parasitic herb while Prunella vulgaris can serve as its host. However, the molecular mechanisms underlying the communication between T. chinense and its host remained largely unexplored. The aim of this study was to provide a comprehensive view of transferred metabolites and mobile mRNAs exchanged between T. chinense and P. vulgaris. RESULTS: The wide-target metabolomic and transcriptomic analysis identified 5 transferred metabolites (ethylsalicylate, eriodictyol-7-O-glucoside, aromadendrin-7-O-glucoside, pruvuloside B, 2-ethylpyrazine) and 50 mobile genes between T. chinense and P. vulgaris, as well as haustoria formation related 56 metabolites and 44 genes. There were 4 metabolites (ethylsalicylate, eriodictyol-7-O-glucoside, aromadendrin-7-O-glucoside and pruvuloside B) that are transferred from P. vulgaris to T. chinense, whereas 2-ethylpyrazine was transferred in the opposite direction. Furthermore, we inferred a regulatory network potentially involved in haustoria formation, where three metabolites (N,N'-Dimethylarginine/SDMA, NG,NG-Dimethyl-L-arginine, 2-Acetoxymethyl-anthraquinone) showed significant positive correlations with the majority of haustoria formation-related genes. CONCLUSIONS: These results suggested that there was an extensive exchange of information with P. vulgaris including transferred metabolites and mobile mRNAs, which might facilitate the haustoria formation and parasition of T. chinense.

PSTPIP2 ameliorates aristolochic acid nephropathy by suppressing interleukin-19-mediated neutrophil extracellular trap formation.

Aristolochic acid nephropathy (AAN) is a progressive kidney disease caused by herbal medicines. Proline-serine-threonine phosphatase-interacting protein 2 (PSTPIP2) and neutrophil extracellular traps (NETs) play important roles in kidney injury and immune defense, respectively, but the mechanism underlying AAN regulation by PSTPIP2 and NETs remains unclear. We found that renal tubular epithelial cell (RTEC) apoptosis, neutrophil infiltration, inflammatory factor, and NET production were increased in a mouse model of AAN, while PSTPIP2 expression was low. Conditional knock-in of Pstpip2 in mouse kidneys inhibited cell apoptosis, reduced neutrophil infiltration, suppressed the production of inflammatory factors and NETs, and ameliorated renal dysfunction. Conversely, downregulation of Pstpip2 expression promoted kidney injury. In vivo, the use of Ly6G-neutralizing antibody to remove neutrophils and peptidyl arginine deiminase 4 (PAD4) inhibitors to prevent NET formation reduced apoptosis, alleviating kidney injury. In vitro, damaged RTECs released interleukin-19 (IL-19) via the PSTPIP2/nuclear factor (NF)-κB pathway and induced NET formation via the IL-20Rß receptor. Concurrently, NETs promoted apoptosis of damaged RTECs. PSTPIP2 affected NET formation by regulating IL-19 expression via inhibition of NF-κB pathway activation in RTECs, inhibiting RTEC apoptosis, and reducing kidney damage. Our findings indicated that neutrophils and NETs play a key role in AAN and therapeutic targeting of PSTPIP2/NF-κB/IL-19/IL-20Rß might extend novel strategies to minimize Aristolochic acid I-mediated acute kidney injury and apoptosis.

Aristolochic acid nephropathy (or AAN for short) is a serious condition affecting the kidneys that is caused by certain traditional Chinese medicines containing a compound called aristolochic acid. This compound is known to have harmful effects on kidney tubular epithelial cells, causing increased inflammation and a form of controlled cell death called apoptosis, which can ultimately lead to organ failure. There is currently no effective treatment for AAN, highlighting the need for a deeper understanding of the mechanisms responsible. Previous studies have shown that immune cells called neutrophils infiltrate the kidneys and damage cells in the early stages of AAN. Neutrophils produce web-like structures called neutrophil extracellular traps, which have been identified as potentially contributing to the damage. A protein called PSTPIP2, which regulates inflammation, has also been shown to contribute to other types of kidney injury. To understand how these inflammatory factors might be involved in AAN, Du, Xu et al. genetically engineered mice to produce extra PSTPIP2 protein specifically in their kidneys. When given aristolochic acid, these mice displayed less kidney damage. Further studies of mouse kidney cells showed that PSTPIP2 protects the kidney by suppressing an inflammatory mechanism that leads to the production of neutrophil extracellular traps. By contrast, in models where PSTPIP2 levels were reduced, neutrophil extracellular traps were shown to cause both apoptosis and kidney injury. The findings of Du, Xu et al. show that neutrophil extracellular traps cause cell damage and apoptosis in a mouse model of AAN and that this action can be reduced by increasing the levels of the protein PSTPIP2. This sheds light on the inflammatory mechanisms behind the kidney damage caused by herbal medicines containing aristolochic acid. Additionally, it opens new avenues for studies aiming to find ways to treat AAN, suggesting that targeting PSTPIP2 could be a promising strategy.

Integrated Analysis of Transcriptome and Metabolome Reveals Molecular Mechanisms of Rice with Different Salinity Tolerances.

Rice is a crucial global food crop, but it lacks a natural tolerance to high salt levels, resulting in significant yield reductions. To gain a comprehensive understanding of the molecular mechanisms underlying rice's salt tolerance, further research is required. In this study, the transcriptomic and metabolomic differences between the salt-tolerant rice variety Lianjian5 (TLJIAN) and the salt-sensitive rice variety Huajing5 (HJING) were examined. Transcriptome analysis revealed 1518 differentially expressed genes (DEGs), including 46 previously reported salt-tolerance-related genes. Notably, most of the differentially expressed transcription factors, such as NAC, WRKY, MYB, and EREBP, were upregulated in the salt-tolerant rice. Metabolome analysis identified 42 differentially accumulated metabolites (DAMs) that were upregulated in TLJIAN, including flavonoids, pyrocatechol, lignans, lipids, and trehalose-6-phosphate, whereas the majority of organic acids were downregulated in TLJIAN. The interaction network of 29 differentially expressed transporter genes and 19 upregulated metabolites showed a positive correlation between the upregulated calcium/cation exchange protein genes (OsCCX2 and CCX5_Ath) and ABC transporter gene AB2E_Ath with multiple upregulated DAMs in the salt-tolerant rice variety. Similarly, in the interaction network of differentially expressed transcription factors and 19 upregulated metabolites in TLJIAN, 6 NACs, 13 AP2/ERFs, and the upregulated WRKY transcription factors were positively correlated with 3 flavonoids, 3 lignans, and the lipid oleamide. These results suggested that the combined effects of differentially expressed transcription factors, transporter genes, and DAMs contribute to the enhancement of salt tolerance in TLJIAN. Moreover, this study provides a valuable gene-metabolite network reference for understanding the salt tolerance mechanism in rice.

[Study on phosphate removal and recovery by activated alumina].

Activated alumina was studied for removing phosphate from water, and the recovery of adsorbed phosphate on activated aluminum oxide was also tested. Phosphate solution was prepared using distilled water, tap water and Luoshijiang River water, respectively. All the phosphate adsorption tests using activated alumina were proved to be well fitted with Langmuir isotherm and the respective maximum adsorption amount were 20.88, 32.15 and 29.85 mg x g(-1), respectively. The presence of electrolyte in water could be a positive factor for phosphate removal. As the pH value of phosphate solution became lower the Zeta potential of activated alumina increased, which could enhance the phosphate removal efficiency of activated alumina. The recovery tests indicated that NaOH (0.1 mol x L(-1)) solution could almost completely extract the phosphate adsorbed by activated alumina.

Removal of organic pollutants by surfactant modified zeolite: comparison between ionizable phenolic compounds and non-ionizable organic compounds.

The aim of this study was to examine the adsorption capability and mechanism of hexadecyltrimethylammonium modified zeolite, which was synthesized from coal fly ash, for the removal of ionizable phenolic compounds (phenol, p-chlorophenol and bisphenol A, with different pK(a)) and non-ionizable organic compounds (aniline, nitrobenzene, and naphthalene, with different hydrophobicity). The obtained zeolite was identified as type Na-P1 (Na(6)Al(6)Si(10)O(32)·12H(2)O, JCPDS code 39-0219), which is classified into the gismondine group with a pore size of 3.1 Å × 4.5 Å [100] and 2.8 Å × 4.8 Å [101]. The adsorption of the two kinds of organic compounds was due to loaded surfactant bilayer because modified zeolite showed great ability for the removal of organic chemicals while little adsorption by zeolite was observed. The isotherm data of ionizable compounds fitted well to the Langmuir model but those of non-ionizable chemicals followed a linear equation. Uptake of ionizable compounds depended greatly on pH, increasing at alkaline pH conditions. In contrary, adsorption of non-ionizable chemicals was essentially the same at all pH levels studied. The adsorption of both kinds of organic compounds correlated well to k(ow) value, suggesting that more hydrophobic organic contaminants are more easily retained by modified zeolite. Based on the different adsorption behavior, the uptake of non-ionizable pollutants was thought to be a single partitioning process into the surfactant bilayer. For ionizable compounds, however, interaction of the phenol group(s) with the positively charged "head" of surfactant additionally functions.