Escherichia coli O157:H7 senses microbiota-produced riboflavin to increase its virulence in the gut.

Riboflavin is produced by most commensal bacteria in the human colon, where enterohemorrhagic Escherichia coli (EHEC) colonizes and causes diseases. Sensing environmental signals to site-specifically express the type-III secretion system (T3SS), which injects effectors into host cells leading to intestinal colonization and disease, is key to the pathogenesis of EHEC. Here, we reveal that EHEC O157:H7, a dominant EHEC serotype frequently associated with severe diseases, acquired a previously uncharacterized two-component regulatory system rbfSR, which senses microbiota-produced riboflavin to directly activate the expression of LEE genes encoding the T3SS in the colon. rbfSR is present in O157:H7 and O145:H28 but absent from other EHEC serotypes. The binding site of RbfR through which it regulates LEE gene expression was identified and is conserved in all EHEC serotypes and Citrobacter rodentium, a surrogate for EHEC in mice. Introducing rbfSR into C. rodentium enabled bacteria to sense microbiota-produced riboflavin in the mouse colon to increase the expression of LEE genes, causing increased disease severity in mice. Phylogenic analysis showed that the O55:H7 ancestor of O157:H7 obtained rbfSR which has been kept in O157:H7 since then. Thus, acquiring rbfSR represents an essential step in the evolution of the highly pathogenic O157:H7. The expression of LEE genes and cell attachment ability of other EHEC serotypes in the presence of riboflavin significantly increased when rbfSR was introduced into them, indicating that those serotypes are ready to use RbfSR to increase their pathogenicity. This may present a potential public health issue as horizontal gene transfer is frequent in enteric bacteria.

Fluoride disrupts intestinal epithelial tight junction integrity through intracellular calcium-mediated RhoA/ROCK signaling and myosin light chain kinase.

Fluoride is a common contaminant of groundwater and agricultural commodity, which poses challenges to animal and human health. A wealth of research has demonstrated its detrimental effects on intestinal mucosal integrity; however, the underlying mechanisms remain obscure. This study aimed to investigate the role of the cytoskeleton in fluoride-induced barrier dysfunction. After sodium fluoride (NaF) treatment of the cultured Caco-2 cells, both cytotoxicity and cytomorphological changes (internal vacuoles or massive ablation) were observed. NaF lowered transepithelial electrical resistance (TEER) and enhanced paracellular permeation of fluorescein isothiocyanate dextran 4 (FD-4), indicating Caco-2 monolayers hyperpermeability. In the meantime, NaF treatment altered both the expression and distribution of the tight junction protein ZO-1. Fluoride exposure increased myosin light chain II (MLC2) phosphorylation and triggered actin filament (F-actin) remodeling. While inhibition of myosin II by Blebbistatin blocked NaF-induced barrier failure and ZO-1 discontinuity, the corresponding agonist Ionomycin had effects comparable to those of fluoride, suggesting that MLC2 serves as an effector. Given the mechanisms upstream of p-MLC2 regulation, further studies demonstrated that NaF activated RhoA/ROCK signaling pathway and myosin light chain kinase (MLCK), strikingly increasing the expression of both. Pharmacological inhibitors (Rhosin, Y-27632 and ML-7) reversed NaF-induced barrier breakdown and stress fiber formation. The role of intracellular calcium ions ([Ca2+]i) in NaF effects on Rho/ROCK pathway and MLCK was investigated. We found that NaF elevated [Ca2+]i, whereas chelator BAPTA-AM attenuated increased RhoA and MLCK expression as well as ZO-1 rupture, thus, restoring barrier function. Collectively, abovementioned results suggest that NaF induces barrier impairment via Ca2+-dependent RhoA/ROCK pathway and MLCK, which in turn triggers MLC2 phosphorylation and rearrangement of ZO-1 and F-actin. These results provide potential therapeutic targets for fluoride-induced intestinal injury.

A Novel Role of the Two-Component System Response Regulator UvrY in Enterohemorrhagic Escherichia coli O157:H7 Pathogenicity Regulation.

Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is an important human pathogen causing severe diseases, such as hemorrhagic colitis and lethal hemolytic uremic syndrome. The signal-sensing capability of EHEC O157:H7 at specific host colonization sites via different two-component systems (TCSs) is closely related to its pathogenicity during infection. However, the types of systems involved and the regulatory mechanisms are not fully understood. Here, we investigated the function of the TCS BarA/UvrY regulator UvrY in the pathogenicity regulation of EHEC O157:H7. Our results showed that UvrY acts as a positive regulator of EHEC O157:H7 for cellular adherence and mouse colonization through the transcriptional activation of the locus for enterocyte effacement (LEE) pathogenic genes. Furthermore, this regulation is mediated by the LEE island master regulator, Ler. Our results highlight the significance of UvrY in EHEC O157:H7 pathogenicity and underline the unknown importance of BarA/UvrY in colonization establishment and intestinal adaptability during infection.

Sm0.5Sr0.5Co1-xNixO3-δ-A Novel Bifunctional Electrocatalyst for Oxygen Reduction/Evolution Reactions.

The development of non-precious metal catalysts with excellent bifunctional activities is significant for air-metal batteries. ABO3-type perovskite oxides can improve their catalytic activity and electronic conductivity by doping transition metal elements at B sites. Here, we develop a novel Sm0.5Sr0.5Co1-xNixO3-δ (SSCN) nanofiber-structured electrocatalyst. In 0.1 M KOH electrolyte solution, Sm0.5Sr0.5Co0.8Ni0.2O3-δ (SSCN82) with the optimal Co: Ni molar ratio exhibits good electrocatalytic activity for OER/ORR, affording a low onset potential of 1.39 V, a slight Tafel slope of 123.8 mV dec-1, and a current density of 6.01 mA cm-2 at 1.8 V, and the ORR reaction process was four-electron reaction pathway. Combining the morphological characteristic of SSCN nanofibers with the synergistic effect of cobalt and nickel with a suitable molar ratio is beneficial to improving the catalytic activity of SSCN perovskite oxides. SSCN82 exhibits good bi-functional catalytic performance and electrochemical double-layer capacitance.

[Effect of Notch1 on extracellular matrix deposition in the renal tubulointerstitium of diabetes].

The aim of the present study was to observe the effects of Notch1 and autophagy on extracellular matrix deposition in renal tubulointerstitium of diabetes and to explore the mechanism. The mice were randomly divided into normal control group (db/m mice) and diabetes group (db/db mice). After 12 weeks of feeding, the mice were sacrificed and the corresponding biochemical indexes were measured. Rat renal tubular epithelial cells NRK52E were cultured under normal glucose (NG) and high glucose (HG) respectively, and the expression of Notch1 and LC3 proteins were detected by Western blotting. Autophagosomes in NRK52E cells with overexpressed and knockdown Notch1 under NG and HG conditions were observed by confocal microscope, and the expression changes of Notch1, Collagen-I and III protein were detected by immunofluorescence. The results showed that the Notch1 and Collagen-III expressions were increased (P < 0.01) and the LC3 expression was decreased (P < 0.05) in db/db mice compared with db/m mice. In vitro, the Notch1 was increased (P < 0.01) and the LC3 expression was decreased significantly (P < 0.01) in NRK52E cells of HG group compared with NG group. There was no significant change of Notch1 and LC3 expression between the mannitol (MA) group and the NG group. Autophagy was decreased and extracellular matrix deposition was aggravated when Notch1 was overexpressed. In contrast, autophagy was increased and extracellular matrix deposition was relieved by knockdown of Notch1 under HG conditions. In conclusion, Notch1 protein expression was increased and autophagy was reduced in renal tissue of diabetes and renal tubular epithelial cells under HG. The extracellular matrix deposition in the renal tubulointerstitium was relieved by regulating autophagy after the knockdown of Notch1.

Attapulgite and processed oyster shell powder effectively reduce cadmium accumulation in grains of rice growing in a contaminated acidic paddy field.

Heavy-metal contamination is widespread in agricultural soils worldwide, especially paddy soils contaminated by Cd. Amendment-induced immobilization of heavy metals is an attractive and effective technique, provided that cost-effective materials are used. This field experiment compared three alkaline passivators (attapulgite, processed oyster shell powder, and mixed soil conditioner) at a rate of 2.25 t ha-1 for their effectiveness in decreasing Cd bioavailability in soils and accumulation in rice plants in a paddy field contaminated by Cd (0.38 Cd mg kg-1). The utilization of attapulgite and processed oyster shell powder decreased labile fractions but increased stable fractions of Cd in soils through ion exchange, precipitation and complexation. The addition of attapulgite decreased the concentration of bioavailable Cd in both bulk and rhizosphere soils, whereas the amendment of processed oyster shell powder decreased it only in bulk soil. The Cd accumulation in rice plants correlated significantly with acid-soluble and residual Cd fractions in the rhizosphere soil but not in the bulk soil. The addition of attapulgite and processed oyster shell powder decreased Cd accumulation in rice grains from 0.26 mg kg-1 to 0.14 and 0.19 mg kg-1, respectively, meeting the National Food Safety Standard (< 0.20 mg kg-1). However, the mixed soil conditioner did not decrease the Cd accumulation in rice shoots or grains. This study demonstrated that attapulgite and processed oyster shell powder were economic agents in reducing Cd accumulation in rice grains.

Association of polymorphisms in the HBG1-HBD intergenic region with HbF levels.

BACKGROUND: Increased levels of fetal hemoglobin (HbF) can improve the clinical course of the patients with sickle cell anemia (SCA) or ß-thalassemia. The HBG1-HBD intergenic region plays an important role in this process. However, very few studies investigated whether the variations in this region have an effect on HbF expression. METHODS: We retrieved all the SNP data in the HBG1-HBD intergenic region and defined the haplotype blocks, then performed cluster analysis and selected a tagSNP. A total of 500 normal individuals and 300 ß-thalassemia carriers were enrolled. After routine blood and hemoglobin capillary electrophoresis testing, ß-thalassemia mutations were detected using PCR-reverse dot blot. The genotypes of the rs4910736 (A > C) and rs10128556 (C > T) were determined using Sanger sequencing; the relationship between the two SNPs and the levels of HbF was analyzed. RESULTS: Two haplotype blocks were constructed. Block 1 included seven haplotypes divided into two groups M and N by 11 tagSNPs, among which rs4910736 was selected as a tagSNP, while block 2 included three haplotypes. We found that the haplotypes of block 1 were statistically associated with HbF levels, but the non-tagSNP rs10128556 was shown to be more strongly associated with HbF levels than rs4910736. CONCLUSION: This work proved that the haplotypes in the HBG1-HBD intergenic region and SNP rs10128556 are both statistically associated with HbF levels, revealing the association of polymorphisms in the HBG1-HBD intergenic region with HbF levels.

Notch1 regulates PTEN expression to exacerbate renal tubulointerstitial fibrosis in diabetic nephropathy by inhibiting autophagy via interactions with Hes1.

Diabetic nephropathy (DN) is a serious clinical microvascular complication of diabetes mellitus. DN is characterized by the accumulation of extracellular matrix, resulting in progressive fibrosis leading to the loss of renal function. Notch1 and phosphatase and tensin homolog deleted on chromosome ten (PTEN) signaling have been associated with fibrosis. Autophagy serves as an essential regulator of tubular cellular homeostasis. However, how these molecules control the balance between fibrosis and autophagy, the main homeostatic mechanism regulating fibrosis, is not well understood. This association was confirmed using Notch1-siRNA in vitro, which prevented the increase in Hes1 and restored PTEN expression. In contrast, transfection with pHAGE-Hes1 repressed PTEN promoter-driven luciferase activity, implying a direct relationship between Hes1 and PTEN. The expression of Notch1 and Hes1 was increased in diabetic db/db mice by western blotting; in contrast, the expression of PTEN was decreased. Importantly, the dysregulation of these signaling molecules was associated with an increase in extracellular matrix proteins (Collagen-I and III) and the inhibition of autophagy. Similar results were evident in response to high glucose concentrations in vitro in the NRK-52e cells. Therefore, the high glucose concentrations present in diabetes promote fibrosis through the Notch1 pathway via Hes1, while inhibiting the PTEN and autophagy. In conclusion, the inhibition of PTEN by Notch1/Hes1 in response to high glucose concentration inhibits autophagy, which is associated with the progression of fibrosis. Therefore, these signaling molecules may represent novel therapeutic targets in diabetic nephropathy.

[Results of thalassemia screening and genetic diagnosis for 13 738 pregnant women].

OBJECTIVE: To report on the result of thalassemia screening and genetic diagnosis for pregnant women from Guiyang region. METHODS: Prenatal screening for thalassemia was carried out based on erythrocyte parameters and hemoglobin electrophoresis. Single-tube multiplex GAP-PCR and PCR-reverse dot blot hybridization were performed on suspected cases to identify common alpha- and beta- thalassemia mutations, and direct sequencing was used for identifying rare mutations. RESULTS: Among 13 738 pregnant women, 1745 (12.70%) were suspected as thalassemia. In terms of native place, the provinces with highest screening-positive rates were Guangxi, Guangdong, Jiangxi and Guizhou. And the ethnic groups with highest screening-positive rates were Zhuang, Li, and Buyi. Among 801 women subjected to genetic testing, 457 (57.05%) were diagnosed with thalassemia. In total 9 genotypes of alpha- thalassemia were detected, with the most common genotypes being --SEA/alpha alpha (63.35%), - alpha3.7/alpha alpha (19.37%) and - alpha4.2/alpha alpha (8.90%). Eleven genotypes of beta- thalassemia were detected, with the most common genotypes being CD17/N (42.91%), CD41-42/N (32.46%) and IVS-II-654/N (11.94%). Two cases were detected with rare beta-thalassemia mutations (CD54-58/N and IVS-I-130/N). CONCLUSION: The screening-positive rate of thalassemia among pregnant women in Guiyang region is relatively high. The rates have shown substantial difference in terms of native place and ethnic group. Thalassemia-related mutations in Guizhou region have a diverse spectrum, which showed certain difference from those of other regions.

The Prevalence and Spectrum of α-Thalassemia in Guizhou Province of South China.

α-Thalassemia (α-thal) is one of the most prevalent genetic diseases in the world and is especially frequent in tropical and subtropical regions, including South China. The aim of this study was to investigate the prevalence and spectrum of α-thal in Guizhou Province as this information was unknown. A total of 40 α-thal carriers were determined in 1219 newborn umbilical cord blood samples by hemoglobin (Hb) electrophoresis combined with DNA analysis, which revealed that the carrier rate of α-thal in Guizhou Province was 3.28%. One thousand and forty-five individuals referred to our hospital were tested for α-thal mutations. Two hundred and twenty-four cases were determined as α-thal carriers or patients. A total of 11 genotypes and five different α-thal mutations were identified in these 224 cases. Of these mutations, more than 96.0% were deletions, including - -(SEA) (65.89%), -α(3.7) (rightward) (22.87%) and -α(4.2) (leftward) (7.74%). The other two nondeletional mutations, Hb Constant Spring (Hb CS, α(CS)α, HBA2: c.427T > C) and Hb Quong Sze [Hb QS, α(QS)α, HBA2: c.377T > C (or HBA1)] account for 2.71% and 0.78%, respectively. The results of this study will be useful in genetic counseling and prenatal diagnosis (PND) of α-thal in Guizhou Province.

[Analysis of ß -thalassemia mutations in Guizhou Province].

OBJECTIVE: To investigate the spectrum of ß -thalassemia mutations in Guizhou Province. METHODS: For 542 individuals suspected to have ß -thalassemia by decreased mean corpuscular volume (MCV) and corpuscle hemoglobin (MCH) by routine blood test and hemoglobin electrophoresis, reverse dot blot hybridization (RDB) was performed to detect 17 known ß -thalassemia mutations, including 8 common and 9 rare mutations. For cases where no mutation was identified, the entire human ß -globin gene was screened to find other rare mutations. The distribution and frequencies of detected ß -thalassemia mutations were then analyzed. RESULTS: A total of 460 individuals were diagnosed as ß -thalassemia by DNA analysis, which included 352 heterozygotes, 67 compound heterozygotes and 41 mutant homozygotes. A total of 12 ß -thalassemia mutations were detected in these individuals. The mutations have ranked from high to low frequency as: CD17 (40.74%), CD41-42 (33.69%), IVS-II-654 (13.76%), -28 (3.70%), ß E (3.35%), CD71-72(1.94%), CD43 (1.06%), IVS-I-1 (0.71%), CD27-28 (0.35%), -29(0.35%), CAP (0.18%), and CD121 (0.18%). The former six mutations have accounted for 97.18% of all. CD121 (GAA> TAA) detected from a heterozygote, as a dominant mutation, has been firstly found in the Chinese population. CONCLUSION: The spectrum of ß -thalassemia in Guizhou Province showed certain distinct characteristics, with CD17 being the most common mutation. The newly discovered mutation of CD121 has expanded the spectrum of ß -thalassemia in Chinese population. Our result may provide valuable information for the prevention and control of ß -thalassemia in Guizhou.

Arsenic species uptake and subcellular distribution in Vallisneria natans (Lour.) Hara as influenced by aquatic pH.

Vallisneria natans (Lour.) Hara, a widely distributed submerged aquatic plant, is a promising species for arsenic (As) removal from contaminated water. We investigated the effects of pH on the accumulation, subcellular distribution and detoxification of As in V. natans. The results showed that the optimum pH for submerged V. natans growth is close to 7.0. The accumulation of As in the plant increased with the increase of pH (p < 0.05). This may have been due to arsenic/phosphate transporters with a higher affinity for the more highly electronegative AsO4 (3-) than for HAsO4 (2-) and H2AsO4 (-). After As(V) was accumulated by plants, more than 80 % was reduced to As(III), but As reduction decreased with increased pH. The majority of accumulated As and reduced As(III) (47 %-66 %) was found in the vacuoles. Higher As concentrations in vacuoles could be considered as an important mechanism for As detoxification in submerged plants.

Exploring metal(loid)s dynamics and bacterial community shifts in contaminated paddy soil: Impact of MgO-laden biochar under different water conditions.

In this study, a soil incubation experiment was conducted to explore the influence MgO-treated corn straw biochar (MCB) on the bioavailability and chemical forms of cadmium (Cd), lead (Pb), and arsenic (As), alongside the impact on the bacterial community within paddy soil subjected to both flooded and non-flooded conditions. Raw corn straw biochar (CB) served as the unmodified biochar control, aiding in the understanding of the biochar's role within the composite. The results showed that even at a minimal concentration of 0.5 %, MCB exhibited higher effectiveness in reducing the bioavailability of Pb and Cd compared to 1 % CB. In non-flooded conditions, 0.5 % MCB reduced the bioavailable Pb and Cd by 99.7 % and 87.4 %, respectively, while NaH2PO4-extracted As displayed a 14.5 % increase. With increasing MCB concentrations (from 0.5 % to 1.5 %), soil pH, DOC, EC, available phosphorus, and bioavailable As increased, while bioavailable Pb and Cd exhibited declining tendencies. Flooding did not notably alter MCB's role in reducing Pb and Cd bioavailability, yet it systematically amplified As release. Heavy metal fractions extracted by acetic acid increased in the MCB groups under flooding conditions, especially for As. The inclusion of 0.5 % MCB did not noticeably affect bacterial diversity, whereas higher doses led to reduced diversity and substantial changes in community composition. Specifically, the groups with MCB showed an increase in the Bacteroidetes and Proteobacteria phyla, accompanied by a decrease in Acidobacteria. These alterations were primarily attributed to the increased pH and EC resulting from MgO hydrolysis. Consequently, for Pb/Cd stabilization and soil bacterial diversity, a low dosage of MgO-treated biochar is recommended. However, caution is advised when employing MgO-treated biochar in soils with elevated arsenic levels, particularly under flooded conditions.

Nucleoside-diphosphate kinase of uropathogenic Escherichia coli inhibits caspase-1-dependent pyroptosis facilitating urinary tract infection.

Uropathogenic Escherichia coli (UPEC) is the most common causative agent of urinary tract infection (UTI). UPEC invades bladder epithelial cells (BECs) via fusiform vesicles, escapes into the cytosol, and establishes biofilm-like intracellular bacterial communities (IBCs). Nucleoside-diphosphate kinase (NDK) is secreted by pathogenic bacteria to enhance virulence. However, whether NDK is involved in UPEC pathogenesis remains unclear. Here, we find that the lack of ndk impairs the colonization of UPEC CFT073 in mouse bladders and kidneys owing to the impaired ability of UPEC to form IBCs. Furthermore, we demonstrate that NDK inhibits caspase-1-dependent pyroptosis by consuming extracellular ATP, preventing superficial BEC exfoliation, and promoting IBC formation. UPEC utilizes the reactive oxygen species (ROS) sensor OxyR to indirectly activate the regulator integration host factor, which then directly activates ndk expression in response to intracellular ROS. Here, we reveal a signaling transduction pathway that UPEC employs to inhibit superficial BEC exfoliation, thus facilitating acute UTI.

Lagging pollution of polycyclic aromatic hydrocarbons in the rebuilt e-waste site: From the perspective of characteristics, sources, and risk assessment.

Little information is known regarding how the lagged pollution of polycyclic aromatic hydrocarbon (PAH) influenced the environment and human health after an e-waste dismantling site was rebuilt. This study investigated the characteristics, sources, and risk assessment of PAHs in a rebuilt e-waste site and its surrounding farmland by analyzing the samples of soil, dust, water, and vegetable. Concentrations of PAHs in soil, vegetable and water in the rebuilt site were relatively higher than in its surrounding farmland. The concentrations in surface soils, soil columns, dust, vegetables, and water varied from 55.4 to 3990 ng g-1, 1.65 to 5060 ng g-1, 2190 to 2420 ng g-1, 2670 to 10,300 ng g-1, and 46.8 to 110 µg L-1 in the e-waste site, respectively. On the farmland, PAH concentrations in surface soils, vegetables, and water ranged from 41.5 to 2760 ng g-1, 506 to 7640 ng g-1, and 56.6 to 89.2 µg L-1, respectively. A higher proportion of high-molecular-weight PAHs (HMW-PAHs) appeared in all multimedia compared with low-molecular-weight PAHs (LMW-PAHs). Diagnostic ratio together with positive matrix factorization (PMF) revealed that vehicle emission was the primary source in this area, and the activity of e-waste disposal was another important source in the rebuilt e-waste site. Based on the deterministic health risks, people working in the reconstructed e-waste site were exposed to low risks, whereas the residents living near the surrounding farmland were exposed to low risk. Sensitivity analyses indicated that exposure frequency and PAH concentrations were the main factors that influenced exposure risk. This study provides valuable insight into the comprehension of the lagging pollution effects of PAH on the environment and human health after the e-waste site was rebuilt.

Salmonella enterica serovar Typhimurium remodels mitochondrial dynamics of macrophages via the T3SS effector SipA to promote intracellular proliferation.

Mitochondrial dynamics are critical in cellular energy production, metabolism, apoptosis, and immune responses. Pathogenic bacteria have evolved sophisticated mechanisms to manipulate host cells' mitochondrial functions, facilitating their proliferation and dissemination. Salmonella enterica serovar Typhimurium (S. Tm), an intracellular foodborne pathogen, causes diarrhea and exploits host macrophages for survival and replication. However, S. Tm-associated mitochondrial dynamics during macrophage infection remain poorly understood. In this study, we showed that within macrophages, S. Tm remodeled mitochondrial fragmentation to facilitate intracellular proliferation mediated by Salmonella invasion protein A (SipA), a type III secretion system effector encoded by Salmonella pathogenicity island 1. SipA directly targeted mitochondria via its N-terminal mitochondrial targeting sequence, preventing excessive fragmentation and the associated increase in mitochondrial reactive oxygen species, loss of mitochondrial membrane potential, and release of mitochondrial DNA and cytochrome c into the cytosol. Macrophage replication assays and animal experiments showed that mitochondria and SipA interact to facilitate intracellular replication and pathogenicity of S. Tm. Furthermore, we showed that SipA delayed mitochondrial fragmentation by indirectly inhibiting the recruitment of cytosolic dynamin-related protein 1, which mediates mitochondrial fragmentation. This study revealed a novel mechanism through which S. Tm manipulates host mitochondrial dynamics, providing insights into the molecular interplay that facilitates S. Tm adaptation within host macrophages.

Two-component system RstAB promotes the pathogenicity of adherent-invasive Escherichia coli in response to acidic conditions within macrophages.

Adherent-invasive Escherichia coli (AIEC) strain LF82, isolated from patients with Crohn's disease, invades gut epithelial cells, and replicates in macrophages contributing to chronic inflammation. In this study, we found that RstAB contributing to the colonization of LF82 in a mouse model of chronic colitis by promoting bacterial replication in macrophages. By comparing the transcriptomes of rstAB mutant- and wild-type when infected macrophages, 83 significant differentially expressed genes in LF82 were identified. And we identified two possible RstA target genes (csgD and asr) among the differentially expressed genes. The electrophoretic mobility shift assay and quantitative real-time PCR confirmed that RstA binds to the promoters of csgD and asr and activates their expression. csgD deletion attenuated LF82 intracellular biofilm formation, and asr deletion reduced acid tolerance compared with the wild-type. Acidic pH was shown by quantitative real-time PCR to be the signal sensed by RstAB to activate the expression of csgD and asr. We uncovered a signal transduction pathway whereby LF82, in response to the acidic environment within macrophages, activates transcription of the csgD to promote biofilm formation, and activates transcription of the asr to promote acid tolerance, promoting its replication within macrophages and colonization of the intestine. This finding deepens our understanding of the LF82 replication regulation mechanism in macrophages and offers new perspectives for further studies on AIEC virulence mechanisms.

Competitive adsorption of lead and cadmium on soil aggregate at micro-interfaces: Multi-surface modeling and spectroscopic studies.

Aggregates are the basic structural units of soils and play a crucial role in metal migration and transformation. Combined contamination of lead (Pb) and cadmium (Cd) is common in site soils, and the two metals may compete for the same adsorption sites and affect their environmental behavior. Herein, the adsorption behavior of Pb and Cd on aggregates of two soils and contributions of soil components in single and competitive systems were studied by combining cultivation experiments, batch adsorption, multi-surface models (MSMs), and spectroscopic techniques. The results demonstrated that < 2 µm size aggregate was the dominant sink for Pb and Cd competitive adsorption in both soils. Compared with Pb, the adsorption capacity and behavior of Cd were affected greatly under competition. MSMs prediction revealed that soil organic matter (SOM) contributed the most to Cd and Pb adsorption on aggregates (> 68.4%), but the dominant competitive effect occurred on different sites for Cd adsorption (primarily on SOM) and Pb adsorption (primarily on clay minerals). Further, 2 mM Pb coexistence caused 5.9 - 9.8% of soil Cd conversion to unstable species (Cd(OH)2). Thus, the competitive effect of Pb on Cd adsorption cannot be ignored in soils with high content of SOM and fine aggregates.

Lowered oral bioaccessibility of cadmium and selenium and associated health risk by co-digestion of rice and vegetables.

Since foods are not ingested individually, co-digestion, in accordance with human daily diet conditions, should be stressed when assessing elements bioaccessibility and associated health risks. The oral bioaccessibility of cadmium (Cd) and selenium (Se) in 11 types of crops (rice, maize, pakchoi, eggplant, red pepper, towel gourd, kidney bean, soybean, cowpea, sweet potato, and taro) were determined, and the effects of co-digestion of 7 types of rice and vegetables on the bioaccessibility of Cd and Se were evaluated and validated with in vitro PBET method. The underlying mechanism was revealed by observing the surface morphological characteristics of digested substrates, and the exposure risk of Cd and Se were assessed. The results showed that the average bioaccessibility of Cd and Se in 11 types of crops varied from 58.7 % to 39.1 % and 48.4 % to 62.6 % from the gastric phase (GP) to the intestinal phase (IP). Interestingly, co-digestion of rice and vegetables reduced the bioaccessibility of Cd and Se to varying degrees compared to theoretical values. Great reduction in the bioaccessibility of Cd and Se in the GP (16.9-36.4 % and 9.9-23.2 %) than that in the IP (0.2-6.62 % and 0.23-12.3 %) were detected, which was attributed to the rice-vegetable aggregates formed during co-digestion. Rice-vegetable aggregates inhibited the release of Cd and Se, which was more pronounced in the GP than in the IP. Consequently, co-digestion of rice and vegetables reduced the oral exposure to Cd by 35.8 % and to Se by 19.6 %. The areas with higher non-carcinogenic risk of Cd and Se in the study region were reduced by 17 % and 10 %, respectively. Therefore, the role of co-digestion in assessing Cd and Se bioaccessibility and associated health risk cannot be neglected. This study has significant implications for investigating elements bioaccessibility and optimizing associated health risk assessment from a novel perspective.

Tracking cadmium pollution from source to receptor: A health-risk focused transfer continuum approach.

Cadmium (Cd) exposure poses a substantial risk to human health. Despite this, the multi-stage process through which Cd is released to the environment before being taken up and impacting human receptors has rarely been investigated. Here we utilized an integrated model involving Cd emissions, atmospheric transport, deposition, uptake by rice, receptor ingestion and metabolic processing in quantifying the critical emission sources and human health risks of Cd. Atmospheric Cd emissions in the study area in southeastern China were estimated at 147 kg (2016), with >53 % of emissions from non-ferrous metals (NFM) smelting activities. Atmospheric Cd depositions caused elevated Cd content in soil and rice, accounting for 3-79 % and 50-85 % of, respectively, soil and rice Cd. Cumulative frequency analysis showed that an estimated 1.3 % of predicted urine Cd through the consumption of Cd-contaminated rice and exceeded existing safety standards (1 µg g-1), thus highlighting the risks posed to health from high levels of Cd pollution. Applying stricter industrial emission standards to the NFM sector in particular and effective soil management practices could substantially reduce exposure to Cd pollution. The results contribute to understanding of the Cd transfer process and draw attention to the relative health benefits of interventions aimed at mitigating Cd levels and exposure risks at different stages along the Cd transfer continuum from source to receptor.