Search Results (3,946)

Background: Bicuspid aortic valve disease (BAVD) is the most frequent congenital heart disease, occurring either as an isolated lesion or in association with other congenital cardiovascular malformations, with variable patterns of progression and risk of valvular and vascular complications. Studies addressing pediatric bicuspid aortopathy are still in their infancy. This narrative review aims to provide a comprehensive perspective on the current scientific evidence regarding BAVD-associated aortopathy in pediatric patients, underscoring multiple challenges in initial diagnosis, long-term surveillance, and therapeutic decision-making, and focusing on the potential roles of circulating biomarkers and advanced multimodal imaging tools that may improve individualized risk stratification. Methods: Despite the narrative design of this review, a structured search of the current available literature was performed to identify studies addressing pediatric BAV, associated aortopathy, biomarkers, vascular remodeling, and multimodal imaging. Priority was given to pediatric cohorts, longitudinal studies, consensus documents, and contemporary guidelines. The search was conducted in the online databases PubMed/Medline and Web of Science for English-language original articles published in the last 10 years, up to May 2026. We used the following main terms: “Bicuspid Aortic Valve Disease” [MeSH], “Aorta” [MeSH], “Infant” [MeSH], “Child” [MeSH], “Adolescent” [MeSH], combined by Boolean operators with secondary keywords: “pathogenesis”, “mechanism”, “progression”, “multimodal imaging”, “echocardiography”, “cardiovascular magnetic resonance imaging”, “computed tomography”, “circulating biomarkers”. The retrieved studies were screened for eligibility using previously established inclusion and exclusion criteria. A total of 63 studies were included in the analysis for this narrative review. Results: Two main theories underpin the etiopathogenesis of aortopathy associated with the bicuspid aortic valve, positing that genetic factors predispose the aortic wall to remodeling in an abnormal hemodynamic environment. Embryological development and dysregulation of molecular and cellular structures are also intertwined during the formation and progression of the aortic valve with two semilunar cusps, resulting in consequent alterations in the aortic wall’s architectural organization. Advances in molecular studies have highlighted circulating biomarkers with potential utility in predicting aortopathy, as they are involved in extracellular matrix remodeling, endothelial dysfunction, and aortic valve calcification, including matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs), transforming growth factor-β (TGF-β), and microRNAs. In addition, multimodal imaging techniques have emerged as essential tools for assessing the morphology and function of cardiovascular structures, particularly aortic biomechanical properties and hemodynamic abnormalities, at the time of initial diagnosis and during regular monitoring. Taken together, blood biomarkers and imaging parameters of aortic remodeling and flow disturbances might gain increasing prognostic value in pediatric BAVD-associated aortopathy. However, larger longitudinal studies are required for clinical validation beyond research settings. Although guidelines on the management of BAVD are available for adults, they are not entirely applicable to children, who are undergoing continuous somatic growth that affects diagnostic possibilities and therapeutic options. Conclusions: Despite growing literature in the realm of BAVD and related conditions, the management of pediatric patients remains challenging in daily clinical practice, as adult guidelines cannot be completely applied to children. Given the heterogeneity and complexity of pathogenic mechanisms, clinical presentations, natural history, and outcomes, future research is warranted to explore the progression profiles of valvular and vascular disorders associated with BAV in children and to achieve an optimal approach to pediatric bicuspid aortopathy. Full article

Cercospora beticola, the causal agent of Cercospora leaf spot (CLS), is a major pathogen affecting beet (Beta vulgaris) worldwide. Rapid and accurate detection is critical for effective disease control. This study validated a diagnostic framework combining portable quantitative PCR (qPCR) and laboratory-based digital droplet PCR (ddPCR) assays to detect and quantify C. beticola in leaves, seeds, and soil-associated crop residues. We used two portable qPCR systems (Biomeme Franklin^® Three9 and Hyris bCUBE^™) for in-field diagnostics, and ddPCR (Bio-Rad Laboratories) for laboratory analysis. Two rapid DNA extraction protocols, the Sigma-Aldrich REDExtract-N-Amp Plant PCR Kit (brief incubation at 95 °C) and the BN QuickPick Plant DNA Kit (magnetic-bead-based), were evaluated. The optimized portable qPCR assays achieved detection limits of 1 pg μL⁻¹, PCR efficiencies of 96–102%, and R² > 0.98. The ddPCR assay enabled accurate and absolute quantification even at low target concentrations and was resilient to common PCR inhibitors. Both methods proved robust in complex environmental matrices, with a detection threshold of 1% in infected residue soil. The framework’s sensitivity, specificity, and portability support timely on-site CLS diagnosis and informed management. This integrated approach advances portable molecular diagnostics and provides a platform for future field-ready disease surveillance and sustainable crop protection. Full article

Coxiella burnetii, the etiological agent of Q fever, is a globally distributed zoonotic pathogen and a One Health priority. Despite increasing recognition of wildlife as potential reservoirs, data on C. burnetii circulation in European wild ungulates remain scarce. This study estimated exposure to C. burnetii in free-ranging wild boar (Sus scrofa) and red deer (Cervus elaphus) from two major hunting regions in east-central and northeastern Portugal and evaluated the performance of a commercial multi-species ELISA in these hosts. Between 2011 and 2021, 279 serum samples (162 wild boar; 117 red deer) from legally hunted animals in Portugal were tested using an indirect multi-species ELISA using an empirical species-specific threshold derived from a Gaussian mixture model. Overall seroprevalence was 6.8% (CI 95%; 3.4–11.8) in wild boar and 13.7% (CI 95%; 8.0–21.3) in red deer, with higher exposure in wild boar from Beira Baixa (east-central Portugal) than from Trás-os-Montes (northeastern Portugal). The manufacturer’s ruminant cut-off classified almost no animals as seropositive (0.6% and 2.6%, respectively) and showed slight to fair agreement with the species-specific thresholds, underscoring the need for validated, wildlife-appropriate diagnostic criteria. These findings confirm exposure to C. burnetii in both species, suggesting their possible involvement in local maintenance of the pathogen at the wildlife–livestock–human interface. The results reinforce the value of integrating wildlife surveillance into national Q fever surveillance and control strategies to safeguard both public health and livestock production within a One Health context. Full article

Antimicrobial resistance is a growing global crisis that threatens to return humanity to a pre-antibiotic era where common infections become deadly. This narrative review synthesizes evidence from 2000 to early 2026, including Global Research on Antimicrobial Resistance data and World Health Organization surveillance, to outline the problem’s scale, drivers, and solutions. In 2019, bacterial resistance directly caused 1.27 million deaths and was linked to 4.95 million more. Low- and middle-income countries bear the heaviest burden. ESKAPE pathogens, especially carbapenem-resistant Acinetobacter baumannii and NDM-producing Klebsiella pneumoniae, drive intensive care unit mortality near 50% and cause untreatable neonatal sepsis. One Health drivers include antibiotic overuse in humans, with 30% of prescriptions unnecessary in high-income settings; agriculture, consuming 70% of global antibiotics; and environmental pollution, with resistance genes found in 72% of rivers. Bacteria spread resistance through horizontal gene transfer and mutations such as gyrA S83L, creating pan-drug-resistant strains that make surgeries, transplants, and cancer treatment risky. Economic modeling studies suggest that unchecked antimicrobial resistance could reduce annual global GDP by 1.1–3.8%, with some scenarios projecting losses of up to approximately 5% by 2050, depending on assumptions about healthcare costs, labor productivity, and livestock production. Solutions require subscription-based payment models, enforceable agricultural regulations, integrated genomic surveillance, and equity-focused diagnostics for low- and middle-income countries. Without binding 2030 targets, the post-antibiotic era would become a clinical reality within a decade. Full article

Background: Infantile dilated cardiomyopathy (DCM) is uncommon but carries substantial mortality, particularly when accompanied by neurological, ocular, or metabolic abnormalities. Long–Olsen–Distelmaier syndrome is a rare mTORopathy caused by heterozygous gain-of-function variants in RRAGC and may include cortical malformations, congenital cataracts, mineral disturbances, and early-onset DCM. Case Summary: We describe a term male infant born to consanguineous parents with hypocalcemia and hyperphosphatemia, bilateral frontoparietal polymicrogyria, bilateral congenital lamellar cataracts, small patent ductus arteriosus and ventricular septal defect, and initially preserved biventricular function. At 53 days of age, he developed cardiogenic shock, severe lactic acidosis, and hyperkalemia during a rhinovirus/enterovirus-positive respiratory illness. Echocardiography showed severe DCM with marked left ventricular dilatation and an ejection fraction of 27%. Despite multi-agent inotropic support, ventricular function did not recover, and he died at approximately two months. Accordingly, the contemporaneous clinical WES record documented a heterozygous RRAGC c.343T>C, p.(Trp115Arg) variant, reported by the diagnostic laboratory as likely pathogenic. The variant was subsequently standardized in this manuscript as NM_022157.4:c.343T>C, and an independent manuscript-level ACMG/AMP reassessment was concordant. Conclusions: Because p.(Trp115Arg) was previously reported, the principal contribution is detailed documentation of rapid progression from preserved neonatal ventricular function to fatal infantile DCM, while extending the clinical and geographic spectrum of RRAGC-related Long–Olsen–Distelmaier syndrome. Respiratory viral detection should be interpreted cautiously because myocarditis was not established; early exome-based testing should be considered in infants with cardiomyopathy and multisystem abnormalities. Full article

Soilborne diseases caused by Rhizoctonia solani, Fusarium oxysporum f. sp. betae, Aphanomyces cochlioides, and Pythium spp. constrain sugar-beet production worldwide, with yield losses exceeding 50% in severely affected fields. These pathogens frequently co-occur, yet most biological control and microbiome studies address them individually, and recommendations from model crops often fail to translate to sugar beet’s distinctive root biology and rotation systems. This critical review synthesises evidence on the rhizosphere microbiome as a plant protection resource, organising the literature by agronomic applicability: crop rotation, organic amendments, soil physicochemical management, microbial inoculants and synthetic communities, and microbiome-informed breeding and diagnostics. For each strategy, we state the evidence directness (direct sugar-beet field trials, greenhouse data, cross-crop extrapolation, or mechanistic inference) and evaluate the gap between experimental efficacy and field-ready recommendations. Direct field evidence remains limited: the best-characterised example is Rhizoctonia-suppressive soil linked to non-ribosomal peptide synthetase (NRPS)-producing Pseudomonadaceae and Burkholderiaceae, with 2,4-DAPG-producing Pseudomonas populations also being correlated with disease suppression in sugar-beet seedlings, plus one integrated fungicide-biocontrol field trial. We identify multi-pathogen challenge experiments, multi-site field validation of synthetic communities, and microbiome-informed breeding as priority research gaps. Rhizosphere microbiome management should be integrated into existing disease programmes rather than deployed as a stand-alone replacement. Full article

Macacine alphaherpesvirus 1 (McHV-1, commonly known as Monkey B Virus) is a fatal zoonotic pathogen naturally prevalent in macaques. In this study, we developed and conducted a proof-of-concept analytical validation of a HotStart Loop-Mediated Isothermal Amplification (LAMP) assay targeting a conserved, moderately GC-rich (61–62%) region of the UL1 gene in McHV-1. The reaction was optimized at 70 °C using engineered HotStart Bst 3.2/4.2 DNA Polymerase, tracked via real-time fluorescence and closed-tube visual colorimetric detection (pre-added L-HNB dye) without post-amplification tube opening to reduce the risk of post-amplification aerosol carry-over contamination. The assay achieved a preliminary practical analytical limit of detection (analytical LOD) of 100 copies/reaction (3/3 replicates) within a 15–30 min diagnostic cutoff window, matching the practical sensitivity of reference qPCR. Strict analytical specificity was demonstrated against a comprehensive panel of human herpesviruses (HHV-1 through HHV-5) and host macaque genomic DNA. As a single-target analytical prototype, this visual HotStart LAMP platform provides a rapid, equipment-free molecular tool with promising potential for McHV-1 surveillance in resource-limited settings and macaque breeding facilities upon further clinical validation. Full article

Facioscapulohumeral muscular dystrophy (FSHD) is a genetically and epigenetically complex autosomal dominant myopathy that presents formidable challenges to molecular diagnosis and reproductive intervention. The disease is caused by aberrant derepression of the DUX4 retrogene within the D4Z4 macrosatellite repeat array at chromosome 4q35, triggered either by pathological contraction of the array on a permissive 4qA haplotype (FSHD1, ~95% of cases) or by mutations in epigenetic modifier genes SMCHD1, DNMT3B, and LRIF1 that lead to global D4Z4 hypomethylation (FSHD2, ~5% of cases). Traditional approaches (Southern blotting, optical genome mapping, bisulfite sequencing) are discontinuous and labor-intensive. Nanopore ultra-long read sequencing spans the entire D4Z4 array in single reads, simultaneously resolving repeat number, haplotype, and allele-specific CpG methylation without bisulfite conversion. With the telomere-to-telomere (T2T-CHM13) reference genome, long-range haplotype phasing enables preimplantation genetic testing for monogenic conditions (PGT-M) for families with de novo pathogenic variants and somatic mosaicism, groups previously excluded from reproductive genetic intervention. This review systematically examines FSHD molecular mechanisms, the Nanopore diagnostic workflow integrated with T2T-CHM13, Nanopore-based PGT-M clinical data, and future perspectives including R11 pore chemistry, AI-driven bioinformatics, CRISPR-targeted enrichment, and multi-omics integration. Full article

Background/Objectives: Prompt identification of bloodborne pathogens and their antimicrobial resistance is critical for effective sepsis management. Direct molecular testing of blood offers faster results than blood culture; however, its clinical utility has been limited by suboptimal sensitivity and procedural complexity. This study evaluated an automated rapid multiplex PCR assay (BPID^® system) and compared its performance with gold-standard methods. Methods: This was a preliminary, single-centre diagnostic-agreement study. Forty-three whole-blood samples were collected from patients with suspected bloodstream infection at Tri-Service General Hospital, Taipei, Taiwan, between January 2025 and January 2026, and were analysed. Three molecular methods and two culture-based methods were compared: the BPID^® system, a Qiagen^®-based workflow, the BioFire^® FilmArray^® BCID2 panel, blood culture, and MALDI-TOF MS identification. Positive percent agreement (PPA) was calculated at the organism level against a composite reference standard. Analytical sensitivity (limit of detection, LoD) was assessed in whole blood spiked with serial dilutions of ten reference organisms. Results: The composite reference standard yielded 47 reference-positive organisms across 42 samples. The BPID^® system achieved a PPA of 95.74% (95% CI, 85.8–98.8), numerically similar to the post-culture BCID2 panel (93.62%; p = 1.00, exact McNemar test), and higher than the Qiagen^® workflow (72.34%; p = 0.001), blood culture (72.34%; p = 0.007), and MALDI-TOF MS (74.47%; p = 0.013). In a sensitivity analysis using a composite reference standard from which the index test was excluded, 46 organisms remained reference-positive and the PPA of the BPID^® system was 95.65% (44/46; 95% CI, 85.5–98.8), again numerically similar to the BCID2 panel (93.48%; p = 1.00). For antimicrobial resistance determinants covered by both panels, the BPID^® system reproduced the BCID2 determinant profile in all 16 specimens in which such a determinant was reported (100%), versus 10 of 16 specimens (62.5%) for the Qiagen^® method. Confirmed LoD values for the BPID^® system were 0.67–20.81 CFU/mL, an 8.8- to 24.3-fold improvement over the Qiagen^® method (6.51–224.61 CFU/mL). Conclusions: The automated BPID^® system substantially improves PCR-based diagnostic sensitivity for bacteremia and, by operating directly on whole blood, removes the culture-incubation step that post-culture molecular panels require. Because the study was not designed as an equivalence or non-inferiority trial and evaluated only 43 specimens, the similar agreement observed for the BPID^® system and the BCID2 panel should not be interpreted as demonstrated equivalence; these findings should be regarded as a preliminary clinical evaluation requiring confirmation in larger multicentre studies that also enrol culture-negative and uninfected controls. Full article

Urinary tract infections (UTIs) represent a major global health burden, traditionally defined as microbial invasion of a sterile urinary tract, but now increasingly understood as a state of microbial dysbiosis involving disruption of the urinary microbiome. This review aims to synthesize current knowledge on the molecular mechanisms, etiological agents, clinical classification, and emerging therapeutic strategies in UTIs. The analysis integrates recent advances in microbiome research, molecular pathogenesis, and clinical guidelines. Uropathogenic Escherichia coli (UPEC) remains the predominant pathogen, utilizing virulence factors such as adhesins and intracellular bacterial community formation to establish persistent infection, while other organisms including Klebsiella pneumoniae, Proteus mirabilis, and Enterococcus faecalis contribute to disease complexity. The emergence of multidrug-resistant organisms, particularly among ESKAPE pathogens (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species), poses significant therapeutic challenges through mechanisms such as β-lactamase production, efflux pumps, and biofilm formation. Clinically, evolving classification systems emphasize infection localization rather than host factors, improving diagnostic and therapeutic precision. Diagnostic strategies rely on clinical assessment, urinalysis, and urine culture, while treatment increasingly incorporates antimicrobial stewardship principles. Emerging approaches, including immunoprophylaxis, bacteriophage therapy, and microbiome-targeted interventions, demonstrate promising results. In conclusion, UTIs are complex, multifactorial diseases requiring integrated molecular, clinical, and therapeutic approaches, with future advancements likely driven by precision medicine and artificial intelligence. Full article

Background/Objectives: Chromosomal microarray analysis (CMA) is widely used in the genetic evaluation of autism spectrum disorder (ASD), yet its diagnostic contribution in clinically nonsyndromic ASD, particularly in Brazilian populations, remains insufficiently characterized. This study aimed to determine the diagnostic yield of CMA and characterize clinically relevant copy number variants (CNVs) in a cohort of individuals with clinically nonsyndromic ASD from southern Brazil. Methods: In this observational cohort study, 215 individuals with clinically diagnosed ASD underwent high-resolution CMA using the Agilent CGH + SNP Array 180K platform. Individuals with dysmorphic features, known or suspected genetic syndromes, major congenital malformations, epilepsy, or macrocephaly/microcephaly were excluded. CNVs were classified according to American College of Medical Genetics and Genomics guidelines, and the diagnostic yield was compared with that of national and international reference cohorts using Fisher’s exact test. Results: Pathogenic or likely pathogenic CNVs were identified in six individuals, corresponding to a diagnostic yield of 2.8% (95% CI, 1.3–6.1%). These included deletions at 2q11.1–q11.2, 2p16.3 (NRXN1), 15q11.2 (BP1–BP2), and 3q29, and duplications at 16p11.2 and 6p22.3–p22.2. Although the diagnostic yield was lower than that reported in phenotypically heterogeneous ASD cohorts, it did not differ significantly from yields observed in comparably selected nonsyndromic subgroups. Conclusions: CMA identified clinically relevant recurrent CNVs at neurodevelopmental loci even in a clinically nonsyndromic ASD cohort. The comparatively low diagnostic yield highlights the substantial influence of clinical and phenotypic selection on the diagnostic contribution of CMA. Full article

Germline Whole-Exome Sequencing (WES) has emerged as a powerful genomic approach for investigating Hereditary Cancer predisposition through the comprehensive analysis of coding regions across the genome. Although multigene panels currently represent the standard diagnostic approach for Hereditary Cancer assessment, a substantial proportion of high-risk individuals and families remain molecularly unexplained. In this setting, germline WES may serve as a valuable second-tier strategy by identifying pathogenic variants in genes not routinely included in conventional testing panels and by addressing part of the unresolved “missing heritability” observed across Hereditary Cancer syndromes. Increasing evidence supports its application in hereditary breast and ovarian cancer, Lynch-like syndrome, colorectal polyposis, hereditary diffuse gastric cancer, and ovarian cancer predisposition, where WES has contributed to the identification of additional susceptibility genes and improved molecular characterization. Beyond Hereditary Cancer diagnostics, exome-based approaches have also been explored for tumour profiling, homologous recombination deficiency (HRD) assessment, biomarker discovery, and therapeutic stratification. However, despite its significant potential, the clinical implementation of WES remains challenging because of the high burden of variants of uncertain significance (VUS), difficulties in variant interpretation, incidental findings, and the need for robust functional validation of candidate genes. This review critically examines the current evidence supporting the clinical utility of germline WES in Hereditary Cancer syndromes, focusing on the clinical scenarios in which WES may provide meaningful additional information beyond multigene panels, its diagnostic yield, limitations, and future perspectives in precision oncology. Full article

Background/Objectives: Streptococcus parasuis is an under-recognized member of the Streptococcus suis complex that can be misidentified by routine diagnostic methods. Human clinical isolates remain sparsely characterized. This study investigated the antimicrobial phenotype, genomic features, population position, and larval pathogenicity of a human pleural-fluid isolate. Methods: Strain HUGSPH was recovered during the care of a patient with pneumonia. Hybrid whole-genome sequencing (WGS), average nucleotide identity analysis, multilocus sequence typing (MLST), core-genome phylogenetics, comparative pan-genomics, and an exploratory host-origin association analysis were performed. Minimum inhibitory concentrations (MICs) were determined using the VITEK 2 Compact system with an AST-ST03 card, and virulence was evaluated in Galleria mellonella larvae. Results: Genome-based analysis confirmed HUGSPH as S. parasuis and assigned it to the novel sequence type (ST) 181. The isolate clustered within a predominantly human-origin phylogenetic clade. Because species-specific clinical breakpoints are unavailable, the MICs were interpreted provisionally using explicitly stated surrogate Clinical and Laboratory Standards Institute (CLSI) criteria; erythromycin, clindamycin, and levofloxacin were categorized as resistant under those criteria. Several predicted antimicrobial-resistance-associated genes were detected. In a restricted comparison of seven human-origin and nine swine-origin genomes, eight genes were present in all included human-origin isolates and absent from all included swine-origin isolates, whereas metQ, metP, and metN showed the reciprocal pattern. HUGSPH caused dose-dependent larval mortality, reaching 100% at 10⁷ colony-forming units (CFU) by 96 h. Conclusions: HUGSPH expands the genomic record of human clinical S. parasuis and highlights the diagnostic and surveillance relevance of antimicrobial resistance in this species. The susceptibility categories, source-associated genes, and larval phenotype require validation by reference susceptibility testing, broader phylogenetically balanced collections, comparative strains, and mammalian models. Full article

Background: Complicated and recurrent urinary tract infections (cUTI/rUTI) remain diagnostically challenging, particularly after antimicrobial exposure and in polymicrobial or fastidious infections. Multiplex PCR may address some limitations of culture, but panel composition requires periodic refinement as epidemiological, resistance, and clinical evidence evolves. This study describes the transition of the DocLab UTM™ multiplex PCR assay from the prospectively evaluated V2 configuration to the redesigned V5 configuration. Methods: V2 pathogen-level agreement with quantitative urine culture and molecular AMR target–phenotypic AST agreement were characterized using 773 baseline specimens from the prospective multicenter NCT06996301 study. V2-to-V5 panel reconfiguration incorporated US epidemiological and AMR evidence, clinical and antimicrobial-stewardship considerations, and species-level reporting value. V5 was assessed retrospectively using 743 evaluable archived specimens from the same NCT06996301 cohort. Pathogen and AMR agreement were evaluated against the original parent-study quantitative culture and phenotypic AST comparators, and directly shared V2–V5 targets were compared within the common paired cohort using McNemar testing with Holm adjustment for multiple target-specific comparisons. Six newly introduced pathogen targets and one internal process-control target underwent limited contrived-urine feasibility testing. Results: V2 showed high agreement for most established pathogen and AMR targets, although lower negative percent agreement was observed for selected composite pathogen groups. V5 separated several composite targets into species-level outputs and modified selected AMR reporting, principally the qnr architecture. Across evaluated V5 AMR targets, positive percent agreement ranged from 94.9% to 100.0% and negative percent agreement from 96.6% to 99.6%. After Holm adjustment, paired V2–V5 comparisons identified no statistically significant differences in molecular classifications among the directly shared pathogen or AMR targets (all adjusted p > 0.05). All tested spiked-positive and negative contrived specimens were classified as expected under the predefined feasibility conditions. Conclusions: V5 increased species-level reporting resolution while retaining generally high retrospective pathogen and AMR agreement with the original parent-study comparators. Paired analyses did not identify statistically significant directional changes in shared-target classifications. Newly introduced targets require comprehensive validation, and prospective evaluation of the final V5 configuration is needed before conclusions regarding clinical or stewardship benefit can be made. Full article

Exosomes are small extracellular vesicles (EVs) generated through the endosomal pathway that mediate intercellular communication by transferring proteins, lipids, and regulatory RNAs. In parallel, the NLRP3 inflammasome is a key signaling platform of the innate immune system that integrates cellular stress signals to drive inflammatory responses. Recent studies suggest that exosome biology and NLRP3 signaling intersect at fundamental levels of cell organization. On one hand, inflammasome activation can promote exosome biogenesis and secretion through caspase-1-dependent remodeling of intracellular trafficking, including cleavage of Rab-interacting lysosomal protein (RILP) and redistribution of multivesicular bodies (MVBs). These processes influence the selective loading of exosomal cargo, notably miRNAs, through sequence-dependent mechanisms involving RNA-binding proteins and the endosomal sorting machinery. Conversely, exosomes can modulate inflammasome activity in recipient cells by delivering regulatory molecules that affect NLRP3 priming and signaling. Although exosome release is increased in several inflammatory disorders, including ischemia/reperfusion injury, diabetes and neurodegenerative disease, the mechanistic relationship between exosome pathways and NLRP3 remains incompletely understood. In addition to their pathogenic and diagnostic relevance, exosomes are increasingly being explored as innovative acellular biologics and therapeutic delivery platforms due to their immunomodulatory and regenerative properties. In particular, mesenchymal stem cell (MSC)-derived exosomes have shown promising anti-inflammatory effects through modulation of NLRP3 pathways in preclinical models of kidney, cardiovascular, neurological and inflammatory diseases. Here, we review current evidence connecting NLRP3 inflammasome activation to EV trafficking, exosome formation, and cargo selection, and discuss how exosome-mediated communication shapes inflammasome signaling across cells and tissues in health and disease. Full article