Search Results (580)

The stem-boring herbivore Aeolesthes induta severely threatens tea (Camellia sinensis) production, yet the systemic defense mechanisms of tea plants remain largely elusive. The unique age-dependent infestation pattern of A. induta—with minimal damage to young tea plants but infestation rates reaching 20% in 30-year-old trees and nearly 100% in ancient tea trees—necessitated field sampling from naturally infested old tea plantations rather than controlled laboratory conditions. By integrating rhizosphere microbiomics, transcriptomics, and multi-omics modeling, this study characterized the defensive regulatory networks of 30-year-old Shuixian tea cultivars under A. induta infestation. Rhizosphere microbiome analysis revealed that herbivore attack significantly reshaped the microbial community structure, reducing bacterial diversity and simplifying co-occurrence network complexity. Transcriptomic and metabolomic profiling demonstrated a precise source–sink defense allocation between host tissues. In leaves acting as the photosynthetic source, metabolic reprogramming was dominated by the systematic accumulation of soluble sugars and sugar acids for systemic energy reallocation. Concurrently, the roots acting as the metabolic sink vigorously activated the jasmonic acid (JA) signaling cascade and upregulated genes enriched in phenylpropanoid biosynthesis and alpha-linolenic acid metabolism. This molecular activation drove the substantial de novo synthesis of defensive phenolic acids, while downregulating growth-related flavonoids. Integrated network modeling further highlighted the phenylpropanoid pathway as the central regulatory node coupling transcript–metabolite fluctuations. This study constructs an integrated soil microbiome–root–leaf defense network, providing novel mechanistic insights into plant–borer interactions and a valuable foundation for future insect-resistant breeding programs in the tea industry. Full article

Uropathogenic Escherichia coli (UPEC) remains the principal driver of urinary tract infections (UTIs), utilizing sophisticated immunoevasive strategies that consistently outmaneuver host defenses and conventional clinical management. This review synthesizes current evidence highlighting the development of recurrent UTIs (rUTIs). Particular emphasis is given to the transition of UPEC into intracellular bacterial communities (IBCs) and quiescent intracellular reservoirs (QIRs)—survival phenomena primarily characterized across specialized mammalian and cellular models. By highlighting the translational evidence gaps surrounding these intracellular sanctuaries, and the challenge of directly extrapolating these model-derived dynamics to human recurrent UTIs (rUTIs), alongside the role of extra-urinary niches, we provide a comprehensive view of the mechanisms driving recurrence. A critical assessment of the UPEC virulence arsenal, involving molecular mechanisms that regulate fimbrial phase variation resulting in evading host immune surveillance, to specialized adhesins, like FimH, which tightly bind uroplakin receptors, triggering host actin rearrangements via rho-GTPase signaling and facilitating bacterial internalization, is also addressed. Additionally, we integrate the roles of cytotoxic necrotizing factor-1 (CNF1) and hemolysin A (HlyA) in promoting cytosolic escape, host cell survival, and long-term persistence. Finally, this review presents a multidisciplinary framework evaluating next-generation non-antibiotic strategies, including bacteriophage therapy, vaccines, phytotherapy, probiotics, and estrogen therapy. By critically assessing their efficacy and clinical maturity across a spectrum of preclinical models and human trials, we evaluate the potential to navigate translational limitations to effectively disrupt the infection cycle. Full article

Insects lack adaptive immunity and rely exclusively on innate immune system for pathogen defense. However, the specific role of BmToll9-2, a key Toll receptor in the silkworm (Bombyx mori), in mediating immune responses, particularly against bacterial challenges in the larval fat body, remains incompletely understood. To address this gap, this study employed a combination of molecular approaches, including RNA interference (RNAi) targeting BmToll9-2, bacterial challenges with heat-inactivated Escherichia coli (Gram-negative) and Staphylococcus aureus (Gram-positive), and quantitative real-time PCR (qPCR) to assess the transcriptional changes of BmToll9-2 and immune-related genes in the fat body, a key immune tissue. Quantitative analysis showed that after BmToll9-2 RNAi, bacterial challenges significantly upregulated BmToll9-2 expression in the fat body at 12 h post-challenge, whereas BmToll9-2 silencing alone notably downregulated most downstream signaling genes of the Toll pathway by 53.07–83.14%, as well as 11 immune effector genes, including antimicrobial peptide genes, by 64.48–93.40%. Importantly, feeding bacteria post-RNAi reversed these downregulations: E. coli induced a stronger upregulation of both signaling and effector genes compared to S. aureus. This study provides transcriptional evidence that BmToll9-2 may act as a positive regulator of the Toll pathway signaling and antimicrobial peptides in silkworm larval fat body, facilitating robust and rapid immune signaling. This study deepens our understanding of Lepidopteran innate immunity by elucidating key molecular mechanisms, thereby providing a solid foundation for refining RNAi-based pest control strategies. Full article

Long-term excessive nitrogen application in arid cotton fields increases nitrate leaching risk during fallow and disrupts rhizosphere microecology. To clarify the cross-growth-stage regulatory effects of the biostimulant γ-polyglutamic acid (γ-PGA) combined with chemical fertilizer on rhizosphere microbial communities, we compared chemical fertilizer alone (NK) and γ-PGA plus chemical fertilizer (GT) using rhizosphere soils collected at boll-setting (August) and fallow (October), with physicochemical measurements and metagenomic sequencing technology. At boll-setting, GT lowered pH by 0.74 units compared with NK and increased NH₄⁺-N, NO₃⁻-N, and TN by 339.3%, 491.4%, and 23.0%, respectively. By fallow, GT increased TOC by 70.6% and maintained NH₄⁺-N at 18.38 mg/kg, while NK accumulated 66.85 mg/kg NO₃⁻-N. GT buffered post-harvest fungal community disturbance (Shannon: GT 4.06 vs. NK 2.80) and shifted bacterial communities toward oligotrophic taxa and archaea toward ammonium-preferring taxa. A metagenomic LEfSe analysis showed that GT was enriched in functional genes related to [Q]: Secondary metabolite biosynthesis, transport and catabolism, [T]: Signal transduction mechanisms, and [V]: Defense mechanisms, indicating a shift from resource acquisition to conservative maintenance. Mantel tests revealed that microbial functional profiles showed the strongest association with NH₄⁺-N (r = 0.828 in August, r = 0.883 in October, p < 0.001). Thus, γ-PGA with chemical fertilizer stabilizes fallow rhizosphere microbial communities, reduces nutrient leaching, and promotes carbon–nitrogen co-retention. Full article

Extraintestinal pathogenic Escherichia coli (ExPEC) is among the bacterial pathogens associated with infections of the female and male reproductive tracts, where it may contribute to inflammatory processes and impaired reproductive function. In this context, neutrophils constitute a critical component of host defense through the release of neutrophil extracellular traps (NETs), web-like structures composed of decondensed chromatin, histones, and antimicrobial proteins that capture and eliminate invading microorganisms. However, the interaction between E. coli and NETs is highly dynamic, as the bacterium has evolved immune-evasion mechanisms that facilitate persistence within the host. This raises a critical paradox: NETs may shift from an antimicrobial defense mechanism to a microenvironmental factor that inadvertently favors bacterial persistence and chronic inflammation. This review synthesizes current evidence on the colonization, virulence, and immune-evasion mechanisms of E. coli in the reproductive tract, with particular emphasis on the modulation of NETosis, biofilm formation, and their contribution to antimicrobial resistance. We further discuss the dual role of NETs as an innate immune defense mechanism and, conversely, as a potential contributor to tissue injury, oxidative stress, and chronic inflammation when dysregulated. Understanding the interplay among E. coli, extracellular traps, and antimicrobial resistance provides a valuable conceptual framework for the development of novel therapeutic approaches aimed at limiting bacterial persistence, preserving reproductive function, and addressing the growing global threat of antimicrobial resistance. Full article

Viral infections are a widely recognized cause of mortality. Recently it has been demonstrated that vitamin D plays an important immuno-modulatory role in both innate and adaptive immune responses against infections, by reducing excessive inflammation and enhancing defense mechanisms. Specifically, exacerbation of infections may cause sepsis, characterized by a dysregulated immune response with hyperinflammation and immune exhaustion. Vitamin D can modulate these processes through various mechanisms, such as enhancing antiviral protection, promoting anti-inflammatory responses, protecting endothelial barriers, and modulating T-cells. This has been demonstrated for various viral infections, including influenza viruses, respiratory syncytial virus, and severe acute respiratory syndrome coronavirus. Although vitamin D deficiency has been associated with increased susceptibility to viral infections and immune cells of infected patients are highly responsive to vitamin D, the clinical benefits of its supplementation to vitamin D-deficient infected individuals are uncertain and, most importantly, direct evidence linking vitamin D to viral sepsis specifically remains particularly limited, with most mechanistic inference extrapolated from non-septic viral infection and bacterial sepsis literature. Based on these assumptions, this review will outline the present understanding about vitamin D regulatory effects on immune system and the possible connection between its serum levels and viral infections, while also addressing controversial issues. Full article

Pseudomonas syringae pv. actinidiae (Psa) is the most destructive pathogen of kiwifruit, and the absence of curative measures makes the management of Psa-induced kiwifruit bacterial canker (KBC) particularly challenging. Elettaria cardamomum produces an essential oil (CAR) rich in bioactive compounds with demonstrated potential to act directly against Psa, but its mechanisms of action remain insufficiently explored. Here, we investigated CAR’s mode of action in plants with established mild KBC symptoms, and assessed its potential as a plant elicitor. In the in planta assay, CAR application (0.1% w/v, applied 7 days after inoculation) reduced KBC symptoms, with the strongest effect observed 14 days after treatment (DAT). However, CAR did not significantly affect oxidative stress biomarkers, antioxidant system, pigments and primary metabolism, or the expression of target genes related to systemic acquired resistance or salicylic acid and jasmonic acid pathways. For instance, Psa inoculation significantly upregulated PR1 (≈5.4-fold) and PR5 (≈4.3–5.5-fold), irrespective of CAR application. Complementary in vitro assays revealed a transient, phase-dependent antimicrobial activity of CAR: although the effect disappeared by 32 h in liquid-phase assay and no inhibition was observed under vapor-phase exposure, a strong reduction in Psa viable cells (79.7%) was observed after 8 h exposure in the liquid phase. This study demonstrates that CAR exerts a direct, albeit transient, antibacterial effect against Psa, conferring curative activity when applied to plants with mild KBC symptoms. Consequently, repeated applications may be required to maintain disease suppression, as CAR does not appear to induce a sustained preventive defense response in the host. Full article

Kiwifruit bacterial canker, caused by Pseudomonas syringae pv. actinidiae (Psa), severely restricts the sustainable development of the kiwifruit industry. Screening stable resistant germplasm and establishing efficient disease resistance evaluation methods are core prerequisites for breeding resistant cultivars. In this study, 86 Actinidia accessions were systematically assessed for Psa susceptibility over three consecutive years using the reported detached shoot inoculation assay. Seven representative accessions with contrasting resistance phenotypes, namely ‘Cuiyu’, ‘Chuhong’, ‘Jinmei’, ‘Hongyang’, ‘Cuixiang’, ‘Avfs08’, and ‘G3’, were selected to measure the activities of four defense-related enzymes post Psa inoculation to dissect the physiological mechanisms driving divergent Psa resistance in kiwifruit. Lesion lengths across years exhibited a significant positive correlation, demonstrating that this inoculation method delivers repeatable, genetically stable phenotypic data with limited environmental interference. Two accessions belonging to A. valvata and A. eriantha exhibited stable high resistance via synergistic biochemical defenses. By contrast, the widely grown cultivar ‘Hongyang’ was highly susceptible, while moderately resistant materials such as ‘Cuiyu’ and ‘Yannong 3’ were discovered within the inherently susceptible species A. chinensis. Highly resistant accessions rapidly induced coordinated increases in SOD and PAL activity at 24 h post inoculation to maintain ROS homeostasis and lignin biosynthesis, whereas susceptible accessions displayed chaotic, ineffective enzymatic stress responses. Temporal synergy of PAL and POD may act as the key defensive regulatory mode. This study uncovered substantial interspecific variation in Psa resistance across Actinidia germplasm, identified elite donors with stable resistance, and elucidated the physiological mechanisms of kiwifruit resistance to Psa. These findings provided a theoretical foundation and valuable germplasm for subsequent resistance gene mining and disease resistance breeding. Full article

Frequent outbreaks of bacterial and fungal diseases in aquaculture cause severe economic losses, making biological control using probiotics a crucial strategy. Bacillus velezensis synthesizes diverse antimicrobial secondary metabolites; however, its biocontrol potential is tightly regulated by environmental signals such as cultivation time. In this study, we investigated the effect of growing time on the antifungal activity of B. velezensis GHZJ-1, isolated from an aquatic environment. It was found that GHZJ-1 shows obvious antifungal activity against the aquatic pathogen Metschnikowia bicuspidata upon 48 h growth but no such activity for 24 h via the agar-diffusion method. We further compared the transcriptomes of GHZJ-1 cells collected at 24 h and 48 h through RNA-Seq. Our results revealed that compared with 24 h, 1821 genes were differentially expressed at 48 h, with 903 upregulated and 918 downregulated. Downregulated genes were enriched in primary metabolic pathways (e.g., ribosome assembly and carbon metabolism), whereas upregulated genes were enriched in secondary metabolite biosynthesis and transmembrane transport. Importantly, 35 upregulated genes directly associated with antimicrobial activity were identified, notably including the ones encoding core elements of a large polyketide synthase (e.g., pksN, log₂FC = 2.24), the petrobactin siderophore system (highest log₂FC = 3.39), and various antimicrobial peptide export systems. Furthermore, the degU gene was activated at 48 h. These data suggest that facing continuously increased environmental stress over time, GHZJ-1 undergoes global transcriptional reprogramming and resource reallocation, downregulating basal metabolism to construct a synergistic antagonistic system coupling chemical defense with nutritional competition. This study elucidates the time-dependent mechanism for antifungal activity in GHZJ-1, providing a molecular theoretical basis for its green biocontrol application in aquaculture diseases caused by fungi. Full article

Urinary tract infections (UTIs) caused by Klebsiella pneumoniae are an increasing challenge in pediatric practice due to the combined effects of biofilm formation, multidrug resistance (MDR), and limited therapeutic options for children. Biofilm development promotes bacterial persistence by impairing antibiotic penetration, enabling metabolic adaptation, promoting persister-cell formation, facilitating horizontal gene transfer (HGT), and inducing stress-induced mutagenesis, thereby reducing the effectiveness of conventional antimicrobial therapy. These mechanisms are further compounded by pediatric-specific challenges, including age-dependent pharmacokinetic variability, congenital urinary tract abnormalities, device-associated infections, and the limited availability of validated diagnostic tools for biofilm-associated infections. This narrative review integrates current knowledge of the molecular mechanisms underlying biofilm-mediated antimicrobial resistance with the unique diagnostic, pharmacological, and therapeutic challenges encountered in pediatric patients with K. pneumoniae UTIs. Emerging therapeutic strategies, such as optimized antibiotic combination therapy, bacteriophages, biofilm matrix-degrading enzymes, quorum-sensing inhibitors (QSIs), antimicrobial peptides (AMPs), and microbiome-directed approaches are critically evaluated with particular emphasis on their potential applicability in children. Although several anti-biofilm strategies have demonstrated encouraging results in experimental models, robust pediatric clinical evidence remains scarce. Current international guidelines continue to rely primarily on planktonic antimicrobial susceptibility testing without addressing biofilm-specific therapeutic considerations. In the absence of validated biofilm diagnostics, catheter stewardship and dosing optimization remain the most defensible clinical interventions available today. Broader translation of anti-biofilm strategies into pediatric practice will require dedicated pharmacokinetic studies, standardized biofilm diagnostics, and prospective clinical trials. Full article

Biotic stresses (pest feeding, pathogenic fungal/bacterial/viral infection) and diverse abiotic stresses (extreme temperature, drought, waterlogging, saline–alkali soil, heavy metal pollution, nutrient deficiency, UV-B, ozone) severely restrict crop growth and global agricultural yield. Lipids act as core membrane structural constituents and vital secondary signaling messengers, executing multi-layered adaptive balancing functions during cell-type interactive stress acclimation, rather than uniform whole-plant lipid responses. They sustain membrane structural integrity across distinct cell populations, serve as synthetic precursors of bioactive signaling molecules, and trigger cascaded transcriptional and metabolic reprogramming upon environmental stimuli to rebalance physiological status among different cell types. This review systematically summarizes cell-type interactive lipid-mediated plant defense and acclimation balance mechanisms across biotic and abiotic stress contexts. We elaborate the biological functions of fatty acids, phospholipids, galactolipids, sphingolipids and their derivatives (jasmonate, salicylic acid, phosphatidic acid, oxylipin) in stress signal transduction and antioxidant defense and strictly distinguish two categories of lipid changes under all stress types: active adaptive lipid remodeling and passive stress-induced lipid oxidative damage. Key contents include stress-triggered cell-type-specific membrane lipid remodeling, the hierarchical transcriptional regulatory network mediated by WRI1, LEC1, PHR, MADS and other transcription factors governing oil metabolism, as well as crosstalk between lipid metabolism and compartmentalized reactive oxygen species (reactive oxygen species (ROS)) signaling. We further compare conserved lipid-regulatory modules and species-specific divergent responses across model plants and economic oilseed crops, integrating state-of-the-art targeted/untargeted lipidomics, single-cell spatial lipidomics and multi-omics joint breeding strategies to improve multi-stress tolerance in oilseed crops. By consolidating global research progress up to 2025, including the two latest 2026 cross-species meta-analysis reviews, this review provides systematic theoretical support and operable multi-level technical frameworks for genetic engineering targeting conserved lipid pathways to breed stress-resilient high-oil crop germplasm, and highlights reliable lipid stress biomarker screening as a promising translational research direction. Full article

Yersinia enterocolitica is a psychrotrophic foodborne bacterium that can proliferate at refrigeration temperatures and is frequently associated with animal-source foods, raising concerns about food safety and public health. However, genomic data on Y. enterocolitica isolates from South Korea are limited, despite the increasing use of whole-genome sequencing (WGS) in bacterial surveillance. Herein, 91 Y. enterocolitica isolates recovered from chicken, pork, beef, and duck samples collected nationwide in 2024 were analyzed using WGS to elucidate their genomic diversity and genomic features. Phylogenomic analysis predicted all isolates as biotype 1A (sub-biotype 1Aa) and revealed substantial genetic diversity, comprising 27 sequence types and 43 core-genome types. Pan-genome analysis identified 11,230 gene clusters, revealing an open pan-genome in which accessory and unique gene clusters were assigned to predicted functional categories associated with metabolism, defense mechanisms, and stress responses. Although the canonical virulence plasmid pYV was absent, conserved chromosomal virulence-associated genes involved in adhesion (yapE), invasion (inv), secretion, and enterotoxicity (ystB) were detected. Antimicrobial resistance genes were predominantly intrinsic, particularly blaA and vat(F), whereas acquired resistance genes were identified sporadically. These findings provide a genomic baseline for biotype 1A Y. enterocolitica isolates recovered from animal-source foods in South Korea. The functional and public health significance of the detected virulence-associated loci requires further phenotypic investigation. Full article

Postpartum uterine diseases are among the most prevalent and economically important reproductive disorders affecting dairy cattle worldwide. These conditions, including metritis, clinical and subclinical endometritis, and pyometra, develop during the postpartum transition period when physiological, metabolic, endocrine, and immunological adaptations increase susceptibility to microbial invasion and persistent uterine inflammation. Although bacterial contamination of the postpartum uterus is nearly universal, healthy cows generally restore uterine homeostasis through coordinated immune responses, microbial regulation, and effective uterine involution. Failure of these defense mechanisms results in microbial dysbiosis, impaired endometrial repair, reduced fertility, and substantial economic loss. Major pathogens associated with postpartum uterine disease include Escherichia coli, Trueperella pyogenes, Fusobacterium necrophorum, Prevotella spp., and other anaerobic bacteria that interact synergistically to promote inflammation, tissue damage, and reproductive dysfunction. Advances in next-generation sequencing, metagenomics, and metatranscriptomics have transformed understanding of the postpartum uterine microbiota and host–microbe interactions involved in disease pathogenesis. This review synthesizes current evidence regarding uterine physiology, microbial ecology, immune regulation, virulence mechanisms, dysbiosis, diagnostic approaches, and emerging omics-based technologies relevant to postpartum uterine disease in dairy cattle. Particular emphasis is placed on the ecological and physiological interactions linking microbial succession, endocrine recovery, metabolic stress, and immune competence during the postpartum period. The review further discusses translational opportunities for precision diagnostics, microbiome-informed interventions, antimicrobial stewardship, and integrated herd management strategies to improve reproductive efficiency, animal welfare, and dairy herd sustainability. Full article

Gram-negative bacteria pose a significant threat to global health due to their high prevalence, multidrug resistance, and association with various infections. Zinc, an essential trace element, plays a dual role in host–microbe interactions, being crucial for both host immune function and bacterial metabolism. Maintaining optimal zinc homeostasis is essential for effective host defense and microbial survival. We comprehensively examine the multifaceted roles of zinc in host–microbe interactions, particularly focusing on its implications for the pathogenicity of Gram-negative bacteria and host immunity. As part of nutritional immunity, hosts have evolved zinc-mediated antimicrobial strategies that manipulate metal availability at the host–pathogen interface, including zinc limitation that restricts bacterial access to this essential nutrient and zinc intoxication that exposes invading bacteria to cytotoxic zinc concentrations. In Gram-negative bacteria, zinc homeostasis, maintained through zinc transporters and efflux systems, critically governs bacterial virulence, biofilm formation, and survival under host-imposed nutritional immunity. By integrating current advances, this review highlights zinc homeostasis as a central determinant of host–pathogen interactions and a promising target for combating multidrug-resistant Gram-negative infections. Understanding these complex zinc-mediated mechanisms provides new perspectives for developing metal-targeted therapeutic strategies. Full article

Water deficit represents a major environmental constraint that severely limits the growth and yield of common bean (Phaseolus vulgaris L.). Although inoculation with plant growth-promoting rhizobacteria (PGPR) has emerged as a promising strategy to mitigate drought-induced stress, the efficacy of specific strains, such as Priestia aryabhattai CMAA 1363, remains to be fully elucidated. This study evaluated the morpho-agronomic and biochemical responses of common bean to seed inoculation with P. aryabhattai CMAA 1363 under two contrasting irrigation regimes: 100% (well-watered) and 40% (water-restricted) of available water capacity (AWC) under greenhouse conditions. Water restriction significantly compromised plant performance, reducing plant and pod length, root dry biomass, and yield components (pod and grain counts, and total grain mass). Conversely, bacterial inoculation enhanced vegetative traits, increasing plant length by approximately 15% and root dry biomass by approximately 25% compared to non-inoculated controls. Notably, under severe water deficit (40% AWC), inoculated plants achieved a 20% increase in total grain mass per plant relative to their non-inoculated counterparts. Biochemical profiling indicated that inoculation effectively attenuated oxidative stress, as evidenced by lower malondialdehyde (MDA) accumulation and modulated superoxide dismutase (SOD) activity, while water-stressed plants adapted by accumulating total soluble sugars and increasing peroxidase (POD) activity. Overall, P. aryabhattai CMAA 1363 promotes vegetative development, preserves grain production under drought, and orchestrates antioxidant defense mechanisms, highlighting its potential as a sustainable bioinput to improve common bean resilience in water-limited agricultural systems. Full article