Yersinia pestis is a Gram-negative bacterium that causes plague. After Y. pestis overcomes the skin barrier, it encounters antigen-presenting cells, such as Langerhans and dendritic cells. They transport the bacteria from the skin to the lymph nodes. However, the molecular mechanisms involved in bacterial transmission are unclear. Langerhans cells express Langerin (CD207), a calcium-dependent (C-type) lectin. Furthermore, Y. pestis possesses exposed core oligosaccharides. In this study, we show that Y. pestis invades Langerhans cells and Langerin-expressing transfectants. However, when the bacterial core oligosaccharides are shielded or truncated, Y. pestis propensity to invade Langerhans- and Langerin-expressing cells decreases. Moreover, the interaction of Y. pestis with Langerin-expressing transfectants is inhibited by purified Langerin, a DC-SIGN-like molecule, an anti-CD207 antibody, purified core oligosaccharides and several oligosaccharides. Furthermore, covering core oligosaccharides reduces the mortality associated with murine infection by adversely affecting the transmission of Y. pestis to lymph nodes. These results demonstrate that direct interaction of core oligosaccharides with Langerin facilitates the invasion of Langerhans cells by Y. pestis. Therefore, Langerin-mediated binding of Y. pestis to antigen-presenting cells may promote its dissemination and infection.

Yersinia pestis, a Gram-negative bacterium and the etiologic agent of plague, has evolved from Yersinia pseudotuberculosis, a cause of a mild enteric disease. However, the molecular and biological mechanisms of how Y. pseudotuberculosis evolved to such a remarkably virulent pathogen, Y. pestis, are not clear. The ability to initiate a rapid bacterial dissemination is a characteristic hallmark of Y. pestis infection. A distinguishing characteristic between the two Yersinia species is that Y. pseudotuberculosis strains possess an O-antigen of lipopolysaccharide (LPS) while Y. pestis has lost the O-antigen during evolution and therefore exposes its core LPS. In this study, we showed that Y. pestis utilizes its core LPS to interact with SIGNR1 (CD209b), a C-type lectin receptor on antigen presenting cells (APCs), leading to bacterial dissemination to lymph nodes, spleen and liver, and the initiation of a systemic infection. We therefore propose that the loss of O-antigen represents a critical step in the evolution of Y. pseudotuberculosis into Y. pestis in terms of hijacking APCs, promoting bacterial dissemination and causing the plague.

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Background & AimsThe natural course of chronic hepatitis B virus (HBV) infection is characterized by different immune responses, ranging from immune tolerant (IT) to immune activated (IA) stages. In our study, we investigated the natural killer (NK) cells activity in patients at different immunological stages of chronic HBV infection.MethodsBlood samples obtained from 57 HBeAg positive patients with chronic hepatitis B (CHB), including 15 patients in the immune tolerant (IT) stage, 42 patients in the immune activated (IA) stage, and 18 healthy individuals (HI). The analyses included flow cytometry to detect NK cells, the determination of cytokine levels as well as of surface receptor expression and cytotoxicity.ResultsNK cells in peripheral blood were significantly lower in patients in the IA stage of CHB compared to HI (p<0.05). Patients in the IA stage of CHB had lower levels of NK cells activating receptor NKp30 and NKG2D expression, cytokine interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) production, as compared to patients in the IT stage and HI, respectively (p<0.05). Cytotoxicity of NK cells was lower in patients in the IA stage of CHB compared to patients in the IT stage and HI, respectively (p<0.05). The level of IFN-γ but not level of TNF-α and cytotoxicity of NK cells was inversely correlated with serum HBV load in patients with CHB. Peripheral NK cells activity did not correlate with ALT level.ConclusionNK cells activity was lower in CHB patients, especially in those in the IA stage.

Imazethapyr (IM) is a widely used chiral herbicide that inhibits the synthesis of branched-chain amino acids (BCAAs). IM is thought to exert its toxic effects on amino acid synthesis mainly through inhibition of acetolactate synthase activity, but little is known about the potential effects of IM on other key biochemical pathways. Here, we exposed the model plant Arabidospsis thaliana to trace S- and R-IM enantiomer concentrations and examined IM toxicity effects on the root proteome using iTRAQ. Conventional analyses of root carbohydrates, organic acids, and enzyme activities were also performed. We discovered several previously unknown key biochemical pathways targeted by IM in Arabidospsis. 1,322 and 987 proteins were differentially expressed in response to R- and S-IM treatments, respectively. Bioinformatics and physiological analyses suggested that IM reduced the BCAA tissue content not only by strongly suppressing BCAA synthesis but also by increasing BCAA catabolism. IM also affected sugar and starch metabolism, changed the composition of root cell walls, increased citrate production and exudation, and affected the microbial community structure of the rhizosphere. The present study shed new light on the multiple toxicity mechanisms of a selective herbicide on a model plant.

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Cover crops are key determinants of the ecological stability and sustainability of continuous cropping soils. However, their agro-ecological role in differentially reshaping the microbiome structure and functioning under a degraded agroecosystem remains poorly investigated. Therefore, structural and metabolic changes in soil bacterial community composition in response to diverse plant species were assessed. Winter catch leafy vegetables crops were introduced as cover plants in a cucumber-fallow period. The results indicate that cover crop diversification promoted beneficial changes in soil chemical and biological attributes, which increased crop yields in a cucumber double-cropping system. Illumina high-throughput sequencing of 16S rRNA genes indicated that the bacterial community composition and diversity changed through changes in the soil properties. Principal component analysis (PCA) coupled with non-metric multidimensional scaling (NMDS) analysis reveals that the cover planting shaped the soil microbiome more than the fallow planting (FC). Among different cropping systems, spinach–cucumber (SC) and non-heading Chinese cabbage–cucumber (NCCC) planting systems greatly induced higher soil nutrient function, biological activity, and bacterial diversity, thus resulting in higher cucumber yield. Quantitative analysis of linear discriminant analysis effect size (LEfSe) indicated that Proteobacteria, Actinobacteria, Bacteroidetes, and Acidobacteria were the potentially functional and active soil microbial taxa. Rhizospheres of NCCC, leaf lettuce–cucumber (LLC), coriander–cucumber (CC), and SC planting systems created hotspots for metabolic capabilities of abundant functional genes, compared to FC. In addition, the predictive metabolic characteristics (metabolism and detoxification) associated with host–plant symbiosis could be an important ecological signal that provides direct evidence of mediation of soil structure stability. Interestingly, the plant density of non–heading Chinese cabbage and spinach species was capable of reducing the adverse effect of arsenic (As) accumulation by increasing the function of the arsenate reductase pathway. Redundancy analysis (RDA) indicated that the relative abundance of the core microbiome can be directly and indirectly influenced by certain environmental determinants. These short-term findings stress the importance of studying cover cropping systems as an efficient biological tool to protect the ecological environment. Therefore, we can speculate that leafy crop diversification is socially acceptable, economically justifiable, and ecologically adaptable to meet the urgent demand for intensive cropping systems to promote positive feedback between crop–soil sustainable intensification.

Under natural conditions, plants are exposed to various abiotic and biotic stresses that trigger rapid changes in the production and removal of reactive oxygen species (ROS) such as hydrogen peroxide (H2O2). The ascorbate-glutathione pathway has been recognized to be a key player in H2O2 metabolism, in which reduced glutathione (GSH) regenerates ascorbate by reducing dehydroascorbate (DHA), either chemically or via DHA reductase (DHAR), an enzyme belonging to the glutathione S-transferase (GST) superfamily. Thus, DHAR has been considered to be important in maintaining the ascorbate pool and its redox state. Although some GSTs and peroxiredoxins may contribute to GSH oxidation, analysis of Arabidopsis dhar mutants has identified the key role of DHAR in coupling H2O2 to GSH oxidation. The reaction of DHAR has been proposed to proceed by a ping-pong mechanism, in which binding of DHA to the free reduced form of the enzyme is followed by binding of GSH. Information from crystal structures has shed light on the formation of sulfenic acid at the catalytic cysteine of DHAR that occurs with the reduction of DHA. In this review, we discuss the molecular properties of DHAR and its importance in coupling the ascorbate and glutathione pools with H2O2 metabolism, together with its functions in plant defense, growth, and development.