Search Results (3,235)

Calonectria ilicicola (anamorph: Cylindrocladium parasiticum) is a globally important soil-borne fungal pathogen, causing Cylindrocladium black rot (CBR) in peanuts (Arachis hypogaea) and red crown rot (RCR) in soybeans (Glycine max), two legume crops central to global food security. Under favorable conditions, these diseases can cause yield losses of 15–50%, with severe epidemics causing substantial economic damage. A defining feature of C. ilicicola is its production of melanized microsclerotia that persist in soil for up to seven years, complicating long-term disease management across major production regions worldwide. The recent spread of RCR into the U.S. Midwest highlights the adaptive potential of the pathogen and underscores the urgency of updated, integrated control strategies. This review synthesizes current knowledge on disease symptoms, pathogen biology, the life cycle, isolation techniques, and molecular diagnostics, with particular emphasis on recent genomic and multiomics advances. These approaches have identified key virulence-associated genes and core pathogenicity factors, providing new insights into host–pathogen interactions and enabling more targeted resistance breeding through marker-assisted selection and the use of wild germplasm. We critically evaluate integrated disease management strategies, including host resistance, chemical and biological control, cultural practices, and physical interventions, highlighting their complementarities and limitations. By integrating classical pathology with emerging molecular and ecological innovations, this review provides a comprehensive background for developing more effective and sustainable management approaches for CBR and RCR. Full article

Staphylococcus aureus is a key pathogen in bovine mastitis, and antibiotic therapy is challenged by resistance and residue concerns. Milk-derived extracellular vesicles emerge as promising natural antimicrobials. This study aimed to evaluate the antimicrobial activity and explore potential associated mechanisms of milk-derived extracellular vesicles against S. aureus. Milk-derived EV-enriched fractions (mEVs) from healthy (HmEVs) and mastitic (MmEVs) bovine milk suppressed S. aureus growth in vitro and were associated with oxidative imbalance, with MmEVs showing stronger inhibition. In addition, MmEVs significantly reduced biofilm biomass, extracellular matrix production, and the expression of key biofilm-associated genes (sarA, icaB, fnbA, clfB, cidA). Small RNA sequencing revealed distinct miRNA profiles between HmEVs and MmEVs; in particular, MmEVs were enriched in miRNAs predicted to target the S. aureus biofilm-associated gene clfB. Although we did not directly demonstrate uptake of mEV-derived miRNAs by bacteria or their regulation of bacterial gene expression in this study, our small RNA sequencing data together with subsequent bioinformatic predictions suggest that vesicular miRNAs should be regarded as candidate contributors, rather than demonstrated mediators, of the observed antibacterial and antibiofilm effects. Taken together, these findings indicate the potential of mEVs as residue-free adjuncts for controlling bovine mastitis, while recognizing that the present conclusions are mainly derived from in vitro experiments with S. aureus and bioinformatic analyses. Therefore, functional validation of candidate miRNAs, in vivo studies, and evaluation of activity against other mastitis-associated pathogens are still required to clarify the underlying mechanisms, therapeutic potential, and spectrum of activity of mEVs. Full article

ROS derived from NADPH oxidase, particularly NOX2, are central to antimicrobial defense, coupling direct pathogen killing with redox signaling that shapes inflammation. This narrative review integrates recent advances on NOX2 structure, assembly, and spatiotemporal control in phagocytes, and outlines how ROS interact with NF-κB, MAPK, and Nrf2 networks to coordinate microbicidal activity and immune modulation. We summarize evidence that both ROS deficiency, as in chronic granulomatous disease, and uncontrolled excess, as in sepsis and severe COVID-19, drive clinically significant pathology, emphasizing the need for precise redox balance. Emerging therapeutic strategies include selective NOX2 inhibitors that limit pathological oxidative bursts, redox-modulating peptides that disrupt upstream activation cues, and Nrf2 activators that enhance endogenous antioxidant capacity, with attention to dosing challenges that preserve host defense while mitigating tissue injury. Key gaps remain in biomarker standardization, real-time in vivo ROS monitoring, and translation from animal models to patients, motivating personalized, combination approaches to redox medicine in infectious diseases. Full article

The aim of this study was to determine fungal diversity and composition in an area of high host diversity and identify the organisms involved in the appearance of symptoms in Pinus needles. Asymptomatic and symptomatic live needle samples were obtained from different Pinus spp. in an arboretum with confirmed presence of brown spot needle blight. The samples were analysed using high-throughput sequencing of fungal ITS2rDNA. Ascomycota dominated all samples, with Lophodermium as the most abundant genus, although it showed lower representation in symptomatic needles. Other genera with recognised pathogenic potential, including Lecanosticta, Pestalotiopsis, Cyclaneusma, Rhizosphaera, Neophysalospora, and Cenangium, were also detected, whereas the Dothistroma genus was absent despite its presence in the region. Alpha diversity was higher in asymptomatic needles, with a significant difference only for the Shannon index, while Bray–Curtis dissimilarity revealed significant shifts in community composition between needle types. Functional guilds were dominated by pathotroph–saprotroph trophic mode, and the functional guild ‘plant pathogen’ was the most abundant across samples. These findings identify fungal genera associated with symptomatic and asymptomatic needles and provide guidance for future targeted isolation and detailed morphological and molecular identification using more resolutive techniques, enabling a deeper understanding of pathogenic community presence and their potential synergistic interactions. Full article

Background: Asthma and atherosclerosis frequently coexist in clinical populations and share convergent immunometabolic pathways amplified by gut microbial dysbiosis. We propose the gut–lung–vascular axis as a unifying mechanistic framework connecting epithelial and endothelial inflammation providing a foundation for understanding shared inflammatory mechanisms beyond tissue-specific disease boundaries. Methods: A targeted narrative review systematically appraised clinical, experimental and multi-omics studies published over the last five years to delineate microbiota-driven pathways relevant to asthma and atherosclerosis. Particular emphasis was placed on specific microbial taxa, metabolite profiles and immunometabolic networks that connect gut dysbiosis with respiratory and cardiovascular dysfunction. Results: Across human and experimental cohorts, dysbiosis marked by depletion of short-chain fatty acids (SCFAs) producing taxa (Faecalibacterium, Roseburia, Bacteroides) and enrichment of pathobionts (Proteobacteria, Haemophilus, Moraxella, Streptococcus) promotes epithelial and endothelial barrier dysfunction, amplifying Th2/Th17-skewed inflammation and endothelial injury. Key metabolites, including SCFAs, trimethylamine N-oxide (TMAO), secondary bile acids (BA), indole/tryptophan derivatives and lipopolysaccharides (LPS), serve as molecular connectors linking gut, airway and vascular inflammation. Microbial signatures and metabolomic patterns hold emerging diagnostic and therapeutic potential, and several drug classes (e.g., statins, corticosteroids, proton-pump inhibitors (PPIs)) further modulate host–microbiota interactions. Conclusions: Shared microbial taxa and metabolite signatures in asthma and atherosclerosis support microbiota-mediated immune dysregulation along the gut–lung–vascular axis as a common pathogenic framework. Microbial and metabolite profiling may enable improved risk stratification and precise, microbiota-targeted therapies. Integrating microbiome-informed diagnostics and personalized interventions could help reduce systemic inflammation and the burden of these overlapping inflammatory diseases. Full article

Root rot disease severely threatens tropical fruit production, leading to plant mortality and reduced yields; however, the mechanisms of host defense responses and pathogen infection remain poorly understood. In this study, Fusarium acutatum was isolated from diseased Annona squamosa roots and identified through morphological features and ITS phylogeny (99.8% identity). Infection triggered a marked activation of antioxidant defenses, with elevated POD, SOD, PAL, PPO, and CAT activities. Transcriptomic and TMT-based quantitative proteomic analyses identified 23,791 and 74,403 differentially expressed genes (DEGs) and 367 and 609 differentially expressed proteins (DEPs) in root at 5 and 10 days post inoculation, respectively, relative to the control. These DEGs and DEPs were consistently enriched in pathways involving redox regulation, protein synthesis and processing, ubiquitin-mediated proteolysis, phenylpropanoid and flavonoid metabolism, cell wall remodeling, plant–pathogen interaction and MAPK signaling. Integrated transcriptomic–proteomic correlation analysis showed clear positive associations between key defense-related genes and proteins, suggesting that phenylpropanoid metabolism and reactive oxygen species (ROS) scavenging play central roles in resistance. Key genes such as CHI2, CHS, and CYP were strongly induced and validated by qPCR, supporting coordinated activation of the defense systems. Furthermore, F. acutatum exhibited upregulation of 50 pathogenic-related proteins, including 4 cell wall-degrading enzymes (e.g., CBH1, pectate lyase), 5 metabolic regulation or signal transduction enzymes (e.g., gabD, TPI, and ENO) and 3 potential effectors, suggesting coordinated pathogen strategies for host colonization. Collectively, this study provides comprehensive multi-omics insight into the molecular mechanisms underlying A. squamosa defense against F. acutatum and offers candidate targets supported by omics evidence, serving as a theoretical reference for the management of root rot. Full article

Wheat dwarf virus (WDV) is a major constraint to global wheat production, causing severe yield losses and economic disruption. Understanding the molecular basis of wheat–WDV interactions is essential for developing resistant cultivars. Non-coding RNAs (ncRNAs), including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), are key regulators of gene expression and defence. This study identified ncRNAs involved in wheat responses to WDV, including host lncRNAs, miRNAs, and viral small interfering RNAs (siRNAs) targeting WDV genomic regions. High-throughput sequencing revealed extensive ncRNA reprogramming under WDV infection. A total of 437 differentially expressed lncRNAs (DElncRNAs) and 58 miRNAs (DEmiRNAs) were detected. Resistant genotypes displayed more DElncRNAs (204 in Svitava; 163 in Fengyou 3) than the susceptible Akteur (141). In Akteur, 66.7% of DElncRNAs were downregulated, whereas in Svitava, 56.9% were upregulated. Akteur also exhibited more DEmiRNAs (28) than resistant genotypes (15), with predominant downregulation. A co-expression network analysis revealed 391 significant DElncRNA–mRNA interactions mediated by 16 miRNAs. The lncRNA XLOC_058282 was linked to 298 transcripts in resistant genotypes, suggesting a central role in the host defence. Functional annotation showed enrichment in signalling, metabolic, and defence-related pathways. Small RNA profiling identified 1166 differentially expressed sRNAs targeting WDV, including conserved hotspots and 408 genotype-specific sites in Akteur versus Fengyou 3. Infected plants displayed longer sRNAs, a sense-strand bias, and a 5′ uridine preference, but lacked typical 21–24 nt phasing. These findings highlight the central roles of ncRNAs in orchestrating wheat antiviral defence and provide a molecular framework for breeding virus-resistant wheat. Full article

Background: Evidence on COVID-19 convalescent plasma (CCP) is mixed. We examined associations between CCP administration and in-hospital outcomes among patients hospitalized during early pandemic waves in Poland. Methods: We conducted a retrospective, single-center cohort study of adults hospitalized with COVID-19 between October 2020 and January 2021. Patients receiving CCP were compared with contemporaneous controls without CCP. Primary outcomes were in-hospital mortality and discharge alive. Requirement for invasive mechanical ventilation/intubation was summarized descriptively because timing of intubation was not reliably available. Group comparisons used χ²/Fisher’s exact tests and t-test/Mann–Whitney U tests as appropriate. Associations with mortality and discharge were evaluated using logistic regression: (i) a prespecified age-adjusted model and (ii) an exploratory prognostic model including in-hospital treatments and severity markers (systemic glucocorticoids, remdesivir, oxygen therapy, and antibiotic use), interpreted prognostically rather than causally. Results: The cohort included 224 patients (CCP, n = 92; controls, n = 132); outcome status was missing for eight controls. Baseline demographics, comorbidities, and admission laboratory values were broadly comparable between groups. Crude in-hospital mortality was 25% in the CCP group (23/92) versus 42% in controls (52/124; p = 0.010), and discharge alive occurred in 66% versus 50%, respectively (p = 0.022). Invasive mechanical ventilation/intubation was required in 12.0% of CCP recipients and 4.5% of controls (p = 0.071). In age-adjusted models, CCP was associated with lower odds of in-hospital death. In exploratory prognostic models incorporating systemic glucocorticoids, remdesivir, oxygen therapy, and antibiotic use, CCP remained associated with lower odds of death and higher odds of discharge alive. Conclusions: In this early-wave retrospective cohort, CCP administration was associated with lower in-hospital mortality and higher discharge rates. Exploratory analyses adjusted for concomitant in-hospital therapies and severity markers should be interpreted as prognostic associations rather than evidence of causal efficacy. Full article

Biofilms are more than just structural microbial communities. They are dynamic chemical ecosystems that synthesize a range of extracellular compounds involved in functions that extend beyond biofilm architecture. From quorum-sensing molecules like acyl-homoserine lactones (AHLs) to short-chain fatty acids (SCFAs), phenazines, indoles, and reactive sulfur species (RSS), biofilm-derived metabolites can impact the physiology and behavior of microorganisms living in the same ecosystem, including other bacteria and protozoa. It has recently been demonstrated that such molecules may also modulate competition between microbes, promote cooperation, and impact motility, differentiation, or virulence of free-living and parasitic protozoa. This review aims to discuss biofilm compounds that mediate interspecies or interkingdom interactions and their involvement in regulating gut and environmental microbiomes functions, and host–pathogen relationships with special emphasis on protozoan activity and the infection outcome. This review will also address how this chemical dialog can be explored to identify new therapeutic interventions against microbial infections and parasitic diseases. Full article

This review article discusses glucose metabolic alterations affecting immune cell responses to influenza virus infection. It highlights possible relationships between essential metabolic targets and influenza replication dynamics in immune cells. Thus, kinases as essential regulators of glucose metabolism as well as critical immune mediators during this infection such as interferons, tumor necrosis factor-alpha and transforming growth factor beta have been illustrated. Mechanistic highlights are provided for both the Warburg effect, where glycolysis shifts to lactate production during influenza infection, and the PFK1/PFKFB3 enzyme complex as the rate-determining regulator of glycolysis whose activity increases during the course of influenza infection. The mechanisms of mammalian target of rapamycin (mTOR) signaling as a promotor of glycolysis and a regulator of inflammatory cytokine production are discussed across various immune cell types during infection. We conclude that modulation of the metabolic changes associated with immune responses plays an important role in disease progression, and that targeting metabolic checkpoints or kinases may offer promising avenues for future immunotherapy approaches for the treatment of influenza virus infection. We also emphasize the need for further research to develop a comprehensive biological model that clarifies host outcomes and the complex nature of immune-metabolic regulation and crosstalk. Full article

The Coronaviridae family represents a broad group of RNA-containing viruses that infect humans and animals. This family belongs to the order Nidovirales and is divided into four main genera: α-CoV, β-CoV, γ-CoV and δ-CoV. It is particularly noteworthy that representatives of β-CoV have caused serious epidemics in humans, such as the outbreaks of SARS-CoV, MERS-CoV, and COVID-19 caused by SARS-CoV-2. Although the clinical manifestations of CoVs can range from mild cold-like symptoms to severe respiratory diseases, they share common features in their structure, modes of transmission, and natural reservoirs. Identifying natural reservoirs, as well as establishing intermediate hosts, is crucial for understanding the mechanisms of interspecies transmission of CoVs. These processes are often mediated by molecular interactions between viral spike (S) proteins and cellular receptors of different species, which contribute to zoonotic outbreaks. Thus, the interaction of various species and the study of these processes of viral spread, cross-species transmission, and pathogen evolution play a key role in ensuring global biological safety. Therefore, we conducted this review to summarize the data from existing studies focused on the taxonomy of CoVs, their main types, natural reservoirs, intermediate hosts, pathways of interspecies transmission, and the significance of the One Health concept as an interdisciplinary approach to monitoring, prevention and control of CoV infections at the intersection of human, animal, and environmental health. We examined databases such as PubMed, Science Direct, Web of Science, and Google Scholar to identify relevant scientific articles in English available for such a review. The aim of this work is to study the taxonomy and classification of coronaviruses, as well as to identify their natural reservoirs, intermediate hosts, and applicable control measures. A review of human and animal coronaviruses has revealed their evolutionary diversity, their main natural reservoirs, their intermediate hosts, and their interactions with cellular receptors. This information allows for a better understanding of the mechanisms by which the viruses are transmitted from animals to humans. The concept of One Health demonstrated the interconnections between human, animal and environmental factors. Full article

KSRP (KH-type splicing regulatory protein) has emerged as a pivotal regulator of gene expression at multiple levels, acting as a transcription and splicing factor in the nucleus, and mediating AU-rich element (ARE)-dependent mRNA decay, translational silencing, and microRNA (miRNA) maturation in the cytoplasm. We and others have shown that KSRP acts as a regulator of immune responses, e.g., by dampening the expression of proinflammatory cytokines such as TNF-α, IL-6, IL-8, but also of NOS2, and facilitating the maturation of regulatory miRNAs, including let-7a, miR-129, and miR-155. This review aims to present current knowledge on the regulation of KSRP activity as conferred by miRNAs, phosphorylation, ubiquitination, SUMOylation, and interactions with long non-coding RNAs to enable dynamic responses towards inflammatory stimuli, and the effects of KSRP on innate immune reactions. Here, KSRP acts as an inhibitor by attenuating RIG-I-mediated antiviral signaling, cytokine production, and phagocytosis. In vivo, KSRP deficiency reduced arthritis severity but heightened inflammatory responses in sepsis and enhanced pathogen clearance in invasive pulmonary aspergillosis. These findings position KSRP as a dual regulator that limits tissue damage while constraining antimicrobial immunity. As a perspective, modulation of KSRP activity by applying pharmacological inhibitors may provide strategies to either suppress hyperinflammation in autoimmunity and sepsis or enhance host defense in immunocompromised states. Full article

Rice blast, caused by Magnaporthe oryzae, is a devastating global disease. Its control through the deployment of host resistance genes relies on a detailed knowledge of the pathogen’s race structure and the corresponding avirulence (Avr) genes. To guide effective rice breeding for blast resistance, this study investigated the population dynamics of M. oryzae in Jilin Province from 2022 to 2024. The distribution frequencies of seven Avr genes were detected using PCR and Avr gene-specific primers, and the physiological race structure of 193 isolates was characterized using a set of Chinese differential cultivars, which contains seven cultivars. The results revealed a high prevalence and stability of specific Avr genes, with Avr-Pi9, Avr-Pias, Avr-Piz-t, and Avr-Pib all exhibiting detection frequencies exceeding 80%. In particular, Avr-Pib showed a high frequency (80.83%) and a very low disease incidence (0.64%) on the differential variety Sifeng 43 (which carries Pib), confirming its low mutation rate and the ongoing effectiveness of the corresponding resistance gene. Conversely, the significant decline in Avr-co39 suggests that its corresponding resistance gene should be avoided. Race diversity increased over the three-year period, characterized by a shift toward a more complex structure dominated by ZG1, ZA17, ZA43, and ZB31. Based on the gene-for-gene interactions and pathogen population structure, we recommend a breeding strategy that prioritizes the incorporation of the highly effective Pib, Pi54, and Pik genes, utilizing resistant donors like Sifeng 43. These results can help inform the design of sustainable management strategies adapted to the changing pathogen population. Full article

Chagas disease is caused by the protozoan Trypanosoma cruzi, and its current treatment is limited to the use of two nitroderivatives, benznidazole (Bz) and nifurtimox; however, their toxicity often leads to discontinuation, justifying the search for new therapeutic options. The biological activity of quinones has long shown efficacy towards pathogenic microorganisms. In our previous investigations, two naphthoquinones combining ortho- and para-quinoidal moieties exhibited remarkable trypanocidal activity and presented low toxicity to host cells. Here, these two active compounds were further assessed. On trypomastigotes and epimastigotes, brominated (NQ1) and chlorinated (NQ2) nor-beta-lapachone-derived 1,2,3-triazoles were more active than Bz, presenting IC₅₀/24 h values in the range of 0.8 to 3.1 µM. NQ1-treated epimastigotes showed a mitochondrial impairment and reactive oxygen species (ROS) production under electron microscopy and flow cytometry. The in vitro evaluation of both combinations of compounds with Bz indicated an additive interaction. In vivo, oral treatment with NQ1 reduced parasitemia in an acute model, with no evidence of toxicity. The treatment also led to a reduction in myocarditis, decreasing the PR interval in electrocardiographic analysis and reversing the sinus bradycardia caused by infection. These data suggest that T. cruzi mitochondrion are part of the NQ1 mechanism of action. In vivo, this compound presented moderate trypanocidal and promising anti-inflammatory activity. Its combination with Bz could enhance current therapeutic protocols and should be better explored in the future. Full article

Streptococcus suis is an important zoonotic pathogen responsible for severe infections in pigs and humans. Its capacity to survive within phagocytic cells is considered a key virulence mechanism that contributes to dissemination and persistence in host tissues. This study employed comparative proteomic profiling to investigate intracellular adaptation of S. suis serotypes 2 (SS2) and 14 (SS14) during infection of human U937 macrophages. Five isolates originating from humans and pigs were analyzed using gel electrophoresis with liquid chromatography–tandem mass spectrometry (GeLC–MS/MS), revealing 118 differentially expressed proteins grouped into 11 functional categories. Translation-related proteins represented the largest group (48%), including upregulated ribosomal subunits (30S: S2, S5, S7, S8, S12, S15; 50S: L1, L5, L18, L22, L24, L33, L35) and translation factors such as GidA/TrmFO and RimP. Enrichment of carbohydrate metabolism and DNA replication proteins, including phosphoenolpyruvate carboxylase (PEP), UDP-N-acetylglucosamine pyrophosphorylase (GlmU), and ATP-dependent DNA helicase RuvB, indicated metabolic reprogramming and stress adaptation under intracellular conditions. Stress-response proteins such as molecular chaperone DnaK were also induced, supporting their multifunctional, “moonlighting” roles in virulence and host interaction. Comparative analysis showed that SS2 expressed a broader range of adaptive proteins than SS14, consistent with its higher virulence potential. These findings reveal conserved intracellular responses centered on translation, energy metabolism, and stress tolerance, which enable S. suis to survive within human macrophages. Integration of these intracellular proteomic signatures with previous exoproteomic, peptidomic, and network-based studies highlights translational and metabolic proteins—particularly DnaK, enolase, elongation factor EF-Tu, and GlmU—as multifunctional candidates linking survival and immunogenicity. This work establishes a comparative proteomic foundation for understanding S. suis intracellular adaptation and highlights potential targets for future vaccine or therapeutic development against this zoonotic pathogen. Full article