Search Results (873)

Soil salinization impacts over one billion hectares, threatening global food security. Here, a salt-tolerant bacterial strain, Pseudomonas fluorescens G3, was isolated from the rhizosphere of maize (Jinongyu-719) growing in saline–alkali soils in Gansu Province, China. This strain demonstrated the ability to secrete indole-3-acetic acid (IAA), 1-aminocyclopropane-1-carboxylic acid (ACC) deaminase, and extracellular polysaccharides. It also exhibited notable phosphate-solubilizing activity and robust siderophore production capabilities. Under salt stress conditions (200 mM NaCl), the P. fluorescens G3 strain significantly improved maize’s growth parameters, namely its plant height, root length, and dry weight. Further, it enhanced antioxidant enzyme activity while reducing the accumulation of malondialdehyde (MDA), mitigating stress-induced oxidative damage. In P. fluorescens G3-inoculated plants, leaf and root Na⁺ contents decreased by 34.90% and 33.91%, while their K⁺ contents increased by 40.20% and 33.47%, respectively. Inoculation with P. fluorescens G3 enhanced taxonomic richness (ACE, Chao1) and evenness (Shannon, Simpson) in the rhizosphere bacterial community, leading to a significantly greater relative abundance of several bacterial genera: Pseudomonas, Methylophaga, Enhygromyxa, Desulfuromonas, and Devosia. These shifts in the microbial community composition suggest a potential restructuring of functional profiles, possibly enhancing processes beneficial to plant salt tolerance, such as ion homeostasis and stress mitigation: the biosynthesis of cofactors and secondary metabolites; bacterial secretion and two-component systems; porphyrin metabolism; flagellar assembly; biofilm formation; and bacterial chemotaxis. Redundancy analysis revealed positive correlations between microbial composition at both the phylum and genus levels and the activity of stress resistance enzymes after treatment with Pseudomonas fluorescens. This study provides important theoretical foundations and microbial resources for utilizing microbial community regulation in saline–alkali soil bioremediation. Full article

EmCRT is a calreticulin secreted by Echinococcus multilocularis during its infection in host, playing an important role in evading host immune attack as a survival strategy. Our previous study has demonstrated that recombinant EmCRT (rEmCRT) was able to bind to C1q and lectin to interfere with host classical and lectin complement activation pathway, respectively. However, the C1q-binding site on EmCRT and the associated immune evasion mechanism remain unknown. In this study, the C1q-binding site on EmCRT was determined through molecular docking analysis and fragment expression to be localized to the S-domain (EmCRT-S) between Lys¹⁴⁰ at the N-domain and Gln²⁹² at the P-domain. The recombinant EmCRT-S protein (rEmCRT-S) was subsequently expressed in bacteria. Functional analysis confirmed that rEmCRT-S was able to bind to human C1q and inhibit C1q-initiated complement activation at the similar level to the full-length rEmCRT, resulting in the reduction in C4b/C3b deposition and antibody-sensitized sheep red blood cell hemolysis. Furthermore, rEmCRT-S binding to C1q suppressed THP-1-derived macrophage chemotaxis and ROS generation. Given that the identified functional domain EmCRT-S provides similar complement regulatory functions to the full-length EmCRT, this domain is a more feasible and practical target for vaccine development against E. multilocularis infection or for inflammatory and autoimmune diseases. Full article

Background/Objectives: Viral respiratory tract infections (VRTIs) in patients with diabetes mellitus (DM) are characterized by a severity gap rather than an infection gap. This review synthesizes evidence from the 2023–2026 respiratory seasons to provide a post-pandemic framework for managing the synergistic metabolic and viral threats in this population. Materials and Methods: A scoping review of literature from PubMed, Scopus, and Embase (2023–2026) was conducted, focusing on clinical outcomes and mechanistic interactions between DM and emerging respiratory pathogens. Results: Recent data identify human Metapneumovirus (hMPV) and adenovirus as significant threats to diabetic hosts, with mortality risks equivalent to seasonal influenza (HR 1.00 for hMPV vs. influenza). The two-hit model combines a baseline of innate immune paralysis, characterized by impaired neutrophil chemo-taxis and mechanical SP-D dysfunction, with a cellular signaling environment primed for cytokine overreaction by epigenetic metabolic memory. The stress hyperglycemia ratio (SHR) has emerged as a promising predictor of mortality compared to absolute glucose or HbA1c, with a proposed threshold of ≥1.14 identifying patients at 3.5-fold increased risk for mechanical ventilation. Precision management should consider the prudent suspension of SGLT2 inhibitors to mitigate euglycemic DKA risks and considering the early use of GLP-1 receptor agonists for their hypothesized pulmonary anti-inflammatory properties. Conclusions: Closing the mortality gap may require a shift from generic viral care to a precision model that treats metabolic susceptibility with high clinical priority alongside the treatment of the viral pathogen. Full article

This paper is concerned with a chemotaxis-competition system modeling the spatiotemporal evolution of two species that proliferate and compete according to Lotka–Volterra-type kinetics. We study the asymptotic behavior of solutions in the case of strong competition and show that they spatially segregate as the competition rate tends to infinity. Moreover, using a blow-up method, we obtain the uniform Hölder continuity of the solutions. Full article

N-glycosylation is a fundamental post-translational modification that contributes to protein folding, stability, and secretion in eukaryotes. The catalytic subunit STT3 of the oligosaccharyltransferase complex mediates the transfer of preassembled oligosaccharides to nascent polypeptides in the endoplasmic reticulum. Here, we identified and functionally characterized PsSTT3B, one of the STT3 paralogs in Phytophthora sojae (P. sojae). PsSTT3B plays an important role in the growth, development, and pathogenicity of P. sojae. CRISPR/Cas9-mediated deletion of PsSTT3B resulted in reduced vegetative growth, sporangia production, and zoospore production in P. sojae. PsSTT3B deletion mutants demonstrated significantly reduced virulence on soybean leaves and etiolated seedlings. Importantly, PsSTT3B deletion mutants also exhibited reduced zoospore germination and diminished chemotaxis toward soybean isoflavones. Moreover, deletion of PsSTT3B increased sensitivity to tunicamycin and dithiothreitol and influenced the ConA-binding glycoprotein profile. Our findings show that PsSTT3B is associated with asexual development, virulence, and sensitivity to ER stress-related conditions of P. sojae. Our study suggests that PsSTT3B represents a potential candidate gene for the prevention and control of P. sojae. Full article

Background: In an earlier murine model of myocardial infarction (MI), we showed that CD8 cells and myeloid dendritic cells (mDCs) infiltrate the infarcted myocardium within the first week. However, in humans, the spatial interplay between CD8⁺ T cells and dendritic cells in the spatial context of human myocardial infarction remains underexplored. Objective: In the present study, we applied spatial transcriptomics and functional assays to characterize immune–stromal dynamics in infarcted myocardium and peripheral blood. Methods & Results: Spatial transcriptomics analysis of infarcted human myocardium at days 2 and 6 post-MI, combined with peripheral blood flow cytometry and EPC colony-forming assays, was performed. Cell composition, pathway enrichment, and cell-to-cell communication analyses were conducted to map immune–stromal cells’ dynamics across time points. Spatial mapping identified dynamic shifts in immune, fibroblast, and endothelial populations, with fibroblasts and endothelial cells remaining abundant throughout. CD8⁺ T cells accumulated in ischemic regions while their circulating levels declined. Gene Ontology and pathway analyses of CD8A⁺ transcripts revealed enrichment of proinflammatory and NF-κB survival programs. ITGAX/CD33/THBD⁺ APCs progressively increased within infarct zones, activating antigen-presentation and leukocyte chemotaxis pathways. Early (day 2) APC–endothelial crosstalk showed the strongest predicted recruitment signals for CD8⁺ T cells, which diminished by day 6. Finally, EPC colony-forming capacity showed a tendency for reduction in MI patients and inversely correlated with coronary lesion burden, indicating impaired vascular repair potential. Conclusions: This integrative spatial and functional study demonstrates that APC-driven CD8⁺ recruitment and EPC dysfunction are key features of human MI. Immune–endothelial niches facilitate early cytotoxic T-cell infiltration, while progenitor depletion limits vascular regeneration. These findings provide mechanistic insight into immune–vascular imbalance during infarct healing and highlight potential therapeutic targets to modulate inflammation and restore vascular repair. Full article

Inflammatory-oxidative stress generated by immune cells plays an important role in aging and in age-related neurodegenerative disorders such as Alzheimer’s disease (AD). Triple-transgenic mice for AD (3xTg-AD) are a suitable model for mimicking this disease in an age-dependent manner. We previously showed that peritoneal leukocyte functions and their redox-inflammatory state are altered early in female 3xTg-AD mice, which exhibit premature aging compared to non-transgenic (NTg) animals. However, their characteristics at 9 months of age, when they present an early neuropathological state, and the sex differences are not known. Here, we analyzed several spleen and thymus leukocyte functions (chemotaxis, natural killer activity, and lymphoproliferation in response to mitogens), pro-inflammatory (IL-1B, TNF-alpha) and anti-inflammatory (IL-10) released cytokine concentrations, and redox parameters (glutathione concentrations and glutathione peroxidase, glutathione reductase, and xanthine oxidase activities) in male and female 3xTg-AD mice compared to age-matched controls. We also analyzed the effects of voluntary physical exercise on immune functions. Our results show that 9-month-old male and female 3xTg-AD mice have worse immune functions, redox state, and inflammation than NTg counterparts. Physical exercise improves immune function. Thus, accelerated aging reflected by peripheral immunosenescence and oxidation-inflammation in 3xTg-AD mice precedes hallmark neuropathology, and exercise can slow down AD progression. Full article

Gut microbiota dysbiosis is implicated in metabolic disorders, yet taxonomic and functional alterations in canine diabetes remain incompletely defined. Here, we performed shotgun metagenomic sequencing of fecal samples from 38 diabetic dogs and 37 healthy controls under controlled conditions (no recent antibiotic/probiotic exposure and stable commercial diets). Alpha-diversity indices did not differ between groups, whereas beta-diversity revealed significant separation of community structure at both genus and species levels (p < 0.05). Linear discriminant analysis effect size (LEfSe) identified enrichment of opportunistic-associated taxa in diabetic dogs, including Enterobacterales/Enterobacteriaceae (e.g., Escherichia coli, Klebsiella pneumoniae, Salmonella enterica) and Enterococcus faecalis. In contrast, healthy dogs were enriched for putatively beneficial taxa linked to bile acid and short-chain fatty acid (SCFA) metabolism, including Turicibacter spp. and Romboutsia spp. Functional profiling showed higher abundances of pathways related to carbohydrate/energy metabolism, membrane transport, and virulence/colonization in diabetic dogs; 17 KEGG level-3 pathways and 320 KOs differed at FDR < 0.05, with enriched modules including bacterial secretion systems, lipopolysaccharide biosynthesis, chemotaxis/flagellar assembly, and biofilm formation. Collectively, canine diabetes is associated with a remodeled gut microbiome characterized by expansion of opportunistic pathogens and elevated virulence and metabolic potential, supporting exploration of microbiota-targeted strategies as a complement to conventional management. Full article

Staphylococcus aureus (S. aureus) is the most prevalent pathogen associated with subclinical mastitis, which significantly impacts dairy farming worldwide. Fluctuations in reproductive hormones, such as bovine prolactin (bPRL) and 17β-estradiol (E2), are known to compromise the innate immune response (IIR) of the mammary gland (MG). In this study, we evaluated the effects of bPRL and E2 on the effector response of primary bovine macrophages, isolated from lactating Holstein cows, challenged with S. aureus. We demonstrated that physiological concentrations of bPRL (5 ng/mL) and E2 (50 pg/mL) induced differential changes in the expression of pro-inflammatory (TNF-α, IL-6, and IL-1β) and anti-inflammatory (IL-10) cytokines, chemokines (IL-8), antimicrobial peptides (BNBD10 and S100A7), and miRNAs (miR-451, miR-155, miR-7863, miR-146a, miR-21a, Let-7a-5p, miR-30b, and miR-23a) in S. aureus-challenged macrophages. Moreover, these hormones promoted global histone H3 acetylation and the epigenetic H3K9ac mark without affecting H3K9me2 levels. Hormonal treatment also modulated histone deacetylase (HDAC) activity. Furthermore, hormonal treatment altered macrophage chemotaxis and phagocytosis. In conclusion, bPRL and E2 modulate the effector functions of bovine macrophages during S. aureus infection. This process could be associated with the regulation of histone H3 modifications, such as H3K9ac, in IIR-related genes. Full article

Different rhizobial strains can lead to distinct symbiotic phenotypes in alfalfa, yet molecular differences at the mature nodule stage remain unclear. Here, we analyzed 21-day post-inoculation (dpi) nodules induced by strains WE2 and WWL2. We measured nitrogenase activity (acetylene reduction assay, ARA) and performed dual RNA-seq to compare gene expression in both the alfalfa host and the rhizobia. On the host side, WE2-induced nodules showed higher expression of mature nodule marker genes (ENOD93 and leghemoglobin (Lb) genes) and higher expression of genes encoding SWEET transporters and amino acid and peptide transporters. Host differentially expressed genes were enriched in pathways related to transmembrane transport, redox and heme-related functions, and processes linked to maintaining microaerobic conditions. On the rhizobial side, WE2 nodules showed higher expression of genes involved in microaerobic respiration and nitrogen fixation (e.g., nif/fix and key respiratory chain genes), whereas WWL2 nodules showed higher expression of genes linked to transport, chemotaxis/motility, and environmental information processing. Together, these host and rhizobia expression patterns suggest coordinated differences between host pathways related to resource supply and microaerobic conditions and rhizobial expression programs for respiration and nitrogen fixation. Based on these associations, we propose a working model and provide candidate genes and pathways for functional validation and inoculant screening. Full article

Yersinia enterocolitica is a foodborne pathogen that forms biofilms on surfaces, enhancing its survivability and increasing bacterial resistance, which poses a significant challenge to public health. Therefore, developing effective strategies to inhibit biofilm formation is crucial. Lipoic acid (LA) is a compound with antibiofilm properties. This study investigates the effects of LA on biofilm formation by Y. enterocolitica BNCC 108930 (a standard strain from the BeNa Culture Collection). Biofilm formation, maturation, removal, and cell viability were evaluated by crystal violet staining, extracellular polysaccharide assay, Methylthiazolyldiphenyl-tetrazolium bromide assays, motility, and quorum sensing (QS) assays. The results indicate that LA interferes with the early stages of biofilm formation by compromising cell membrane integrity and reducing cellular adhesion. Furthermore, 2.5 mg/mL of LA reduced biofilm biomass (with a 48 h treatment inhibition rate of 51.46 ± 1.29%) and extracellular polysaccharide production (with a relative inhibition rate of 30.09 ± 1.8%), while significantly reducing the metabolic activity of bacteria within the biofilm (inhibition rate over 85%) compared to the untreated group. Confocal laser scanning microscopy and field emission gun scanning electron microscopy confirm that LA induces a sparse biofilm structure, reduced aggregation, and decreased biofilm thickness to 21.33 ± 2.27 μm. Motility and QS assays demonstrate that LA affects flagellar motility and the secretion of N-acyl homoserine lactones. Transcriptome analysis revealed downregulation of genes involved in the QS system and biofilm formation (e.g., lsrA, lsrC, lsrD, lsrR, and oppA), as well as upregulation of genes related to bacterial chemotaxis and flagellar assembly (e.g., RS19655, RS15590, fliE, fliJ, fliP, fliA, and fliK). These alterations suggest that LA inhibits Y. enterocolitica biofilm formation by affecting intercellular communication and flagellar motility. This study highlights the antibiofilm properties of LA, providing a theoretical basis for potential applications in microbial and biofilm control. Full article

Background: Bone remodeling depends on the dynamic balance between osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Follistatin-like 1 (FSTL1) has been reported as an osteoclast-secreted protein that inhibits osteoclast differentiation, but its direct effects on osteoblast differentiation remain unclear. This study aimed to determine whether FSTL1 regulates osteoblast differentiation and mesenchymal stem cell migration and characterizes its role in osteoclast-osteoblast cellular cross-talk under in vitro conditions. Methods: Bone marrow-derived macrophages (BMMs) and stromal cells (BMSCs) from mice were used to induce osteoclast and osteoblast differentiation, respectively. Chemotaxis was assessed by Transwell migration, and osteoblast differentiation was evaluated in BMSC and MC3T3-E1 cells using staining, qRT-PCR, Western blotting, and proliferation assays. Results: FSTL1 significantly suppressed osteoclast differentiation and resorptive activity, confirmed by TRAP staining and pit assay, respectively. Expression of osteoclast markers such as NFATc1, TRAP, and DC-STAMP was reduced under FSTL1 treatment. In BMSCs, FSTL1 did not affect proliferation but significantly enhanced chemotaxis. Moreover, FSTL1 promoted osteogenic differentiation and mineralization, as demonstrated by increased ALP activity and Alizarin Red S staining. In MC3T3-E1 pre-osteoblasts, FSTL1 increased cell proliferation and mineralization by MTS and Alizarin Red staining. Key osteogenic markers, including Runx2 and osteocalcin, were also upregulated. Conclusions: Osteoclast-derived FSTL1 significantly suppresses osteoclastogenesis and promotes mesenchymal cell chemotaxis and osteogenic differentiation, indicating a role in regulating osteoclast–osteoblast cellular interactions in vitro. Targeting FSTL1 signaling may represent a promising therapeutic strategy for osteoporosis and other disorders of impaired bone remodeling. Full article

Rice volatiles play a crucial role in mediating resistance to the brown planthopper (Nilaparvata lugens Stål, Hemiptera: Delphacidae), a major pest of rice crops. In this study, we analyzed secondary metabolites from rice plants to identify compounds associated with insect behavior. A total of 31 volatile metabolites were detected, among which 16 differed significantly between 51 resistant or susceptible varieties. Fifteen volatiles were more abundant in susceptible plants, while one was enriched in resistant varieties. Electrophysiological (EAG) and Y-tube olfactometer assays revealed that both male and female adults exhibited positive chemotaxis toward five volatiles: Cyclohexanone, 2,2,6-trimethyl-; 3-Cyclohexen-1-one, 3,5,5-trimethyl-; (+)-Isomenthol; Benzoic acid, 2-hydroxy-, methyl ester; and 2-Methoxy-4-vinylphenol. In contrast, male adults were repelled by Benzaldehyde, 3-ethyl-, and 3-Buten-2-one, 4-(2,6,6-trimethyl-1-cyclohexen-1-yl)-. These results indicate that characteristic volatiles serve as functional cues for host selection and may act as phytochemical markers for assessing rice resistance. The findings provide new insights into plant–insect chemical interactions and suggest potential strategies for environmentally friendly pest management, including the use of attractant- or repellent-based approaches and breeding for optimized volatile profiles to control N. lugens. Full article

Dogs can develop chronic inflammatory diseases that induce progressive tissue damage and illness. Delphinidin is a component of maqui (Aristotelia chilensis) and has anti-inflammatory and antioxidant effects. This study evaluated the immunomodulatory effects of delphinidin chloride (DC) and delphinidin-3-glucoside (D3G) on neutrophils and peripheral blood mononuclear cells (PBMCs) in dogs. Leukocytes were isolated from 20 clinically healthy dogs and treated with DC and D3G at concentrations of 50, 100, and 150 µM. The cells were then stimulated with lipopolysaccharide (LPS), platelet-activating factor (PAF), or phorbol 12-myristate 13-acetate (PMA) to evaluate cell viability, reactive oxygen species (ROS) production, neutrophil extracellular trap (NET) formation, phagocytosis, chemotaxis, matrix metalloproteinase 9 (MMP-9) activity, and cytokine production. The results showed that both compounds preserved cell viability, significantly reducing ROS production and NET formation. DC significantly increased chemotaxis and D3G significantly reduced MMP-9 activity. Both compounds reduced the secretion of interleukin (IL) 1β (IL-1β) and tumor necrosis factor α (TNF-α) in neutrophils. In PBMCs, they decreased the production of IL-4 and IL-6 and modulated the production of interferon γ (IFN)-γ. In conclusion, delphinidin exerts selective anti-inflammatory activities in canine leukocytes, promoting inflammation resolution, suggesting its potential role as a nutraceutical for managing inflammatory pathologies in dogs. Full article

This paper analyses the self-organization and spatio-temporal pattern formation in bacterial and human populations using chemotaxis-based mathematical models. The pattern formation in the following three chemotaxis-type systems is investigated: the self-organization of suspensions of luminous Escherichia coli bacteria, the capital-induced labor migration in a spatial Solow model, and the movement of urban criminals forming crime hotspots. The three models are selected as representative examples of chemotaxis mechanisms that capture distinct modeling assumptions and applications. Nonlinear two-dimensional as well as one-dimensional-in-space reaction–diffusion–chemotaxis models were used to simulate the pattern formation in all three chemotactic systems within a restricted area—a circle. The models are formulated in dimensionless form, and the corresponding dimensional parameters are estimated through the comparison of simulation results with experimental and statistical data. The numerical simulation under the transient conditions was carried out using the finite difference technique. This study highlights substantial differences between bacterial motility and the geographical movement of humans; however, human populations’ movement toward an attractant can be regarded as analogous to the chemotactic behavior of biological cells, differing primarily in scale. Full article