Search Results (492)

Toxocara spp. infection is a neglected zoonotic disease associated with exposure to companion animals and contaminated environments. However, information regarding its seroprevalence and associated risk factors among cat owners in Thailand, particularly in remote island communities, remains limited. This cross-sectional study aimed to determine anti-Toxocara spp. IgG seropositivity and identify associated risk factors among cat owners in Koh Yao District, Phang Nga Province, Thailand. A total of 291 cat owners participated in the study. Sociodemographic characteristics, health-related behaviors, serum anti-Toxocara spp. IgG antibodies, and hematological parameters were collected. Univariate and multivariable logistic regression analyses were performed to identify factors associated with seropositivity. The overall prevalence of anti-Toxocara spp. IgG seropositivity was 34.36%. In the univariate analysis, failure to wash hands after cat contact was significantly associated with higher odds of seropositivity (odds ratio [OR] = 1.96, 95% confidence interval [CI]: 1.16–3.33; p = 0.011). This association remained significant in the multivariable logistic regression model. These findings indicate substantial exposure to Toxocara spp. among cat owners in this island community and highlight the importance of personal hygiene, particularly handwashing after cat contact, in reducing exposure to infective Toxocara eggs. Targeted health education programs and preventive interventions should be strengthened to reduce the risk of Toxocara spp. exposure in endemic communities. Full article

Rett syndrome (RTT, OMIM 312750) is a complex multisystem neurodevelopmental disorder. Evidence suggests that RTT may have an autoimmune component and inflammatory activation. However, the autoimmune manifestations remain poorly described. Pemphigus foliaceus is a debilitating autoimmune blistering condition caused by IgG autoantibodies that target desmoglein-1 (Dsg1), resulting in widespread skin blistering and lesions. We report a case of pemphigus foliaceus in a 20-year-old female with RTT and discuss its clinical implications. Clinical data obtained from electronic health records were extracted and reviewed. Genetic testing was performed to identify the specific methyl-CpG-binding protein 2 (MECP2) mutation and on an expanded panel of 55 genes associated with pemphigus foliaceus and related blistering disorders. The individual had pemphigus foliaceus, which required immunosuppression, intravenous immunoglobulin (IVIg) therapy, and Rituximab. The disease trajectory was complicated by infections, aspiration pneumonia, and hypoxic cardiac arrest. There was progressive functional decline, and disease control was difficult to achieve, with frequent flares. Genetic testing confirmed a heterozygous pathogenic MECP2 variant (NM_001110792.1:c.952C>T; p.(Arg318Cys)). HLA genotyping identified alleles consistent with the HLA-DRB1*04:02–HLA-DQA1*03:01–HLA-DQB1*03:02 (DR4/DQ8) haplotype. Furthermore, genetic analysis identified a heterozygous DSG1 variant rs12967407. This study reports the first case of pemphigus foliaceus in RTT, expanding the clinical spectrum of RTT beyond its neurodevelopmental phenotype. The DR4/DQ8 haplotype, previously associated with pemphigus susceptibility, supports a background of genetic susceptibility in this individual. No causal association between RTT and pemphigus foliaceus can be inferred from this single case. Rather, this case demonstrates that a rare autoimmune disorder such as pemphigus foliaceus can co-occur with a pathogenic MECP2 mutation. The coexistence of a genetic and autoimmune disease can result in a more complex clinical presentation and treatment course. The case further emphasises the need for increased vigilance in identifying new and emerging systemic pathology alongside RTT. Full article

Background: Pediatric idiopathic nephrotic syndrome (INS) is classified primarily by corticosteroid response, delaying identification of steroid-resistant disease and exposing children to unnecessary treatment toxicity. Novel biomarkers could enable earlier biological stratification and treatment guidance. Objectives: The study aimed to map available evidence on candidate biomarkers in pediatric INS published since 2020, with emphasis on anti-nephrin autoantibodies and their potential for clinical translation. Data Sources: PubMed/MEDLINE and Web of Science Core Collection (January 2020–October 2025), with a supplementary verification search in Scopus and Embase and manual reference screening. Eligibility Criteria: Original studies reporting circulating, urinary, or tissue-based biomarkers in children aged 0–18 years with idiopathic NS, with outcomes related to diagnosis, treatment response, relapse prediction, or monitoring. Studies in adults only, secondary NS, or animal models were excluded. Results: After screening, 34 studies met the eligibility criteria and were included, grouped into five categories: autoantibodies, urinary markers, immune cell signatures, cytokines/chemokines, and exploratory markers (metabolomics, extracellular vesicles, lipid profiles, microRNAs). Anti-nephrin IgG emerged as the most mechanistically informative marker, with seroprevalence declining across phenotypes (SSNS 68%, SDNS 28%, non-genetic SRNS 14%, genetic SRNS 2%) and positivity predicting response to intensified immunosuppression. Of the candidates reviewed, urinary NGAL and peripheral B-cell subset monitoring are the most readily implementable with existing laboratory infrastructure. Conclusions: Pediatric INS encompasses a spectrum of immune-mediated podocytopathies that may soon be distinguishable by emerging biomarker profiles. Anti-nephrin autoantibodies provide the strongest mechanistic evidence for an autoimmune podocytopathy. Full article

Background/Objectives: Waning immunity after primary COVID-19 vaccination supports evaluation of additional doses. HXP-GPOVac is an egg-based, inactivated Newcastle disease virus (NDV)-vectored vaccine expressing a prefusion-stabilized SARS-CoV-2 HexaPro spike antigen. We evaluated the safety, tolerability, and immunogenicity of a single additional 10 µg dose of HXP-GPOVac administered to adults previously primed with two doses of either HXP-GPOVac or BNT162b2. Methods: Study GPO NDV-HXP-S 203 was an open-label phase II extension enrolling adults (18–75 years) who previously completed a two-dose primary series in Study 202 with either HXP-GPOVac or BNT162b2 (Pfizer–BioNTech; Comirnaty). All participants received a single additional 10 µg intramuscular dose of HXP-GPOVac ≥ 6 months after their second primary dose. Solicited local/systemic adverse events (AEs) were recorded for 7 days, unsolicited AEs through Day 28, and serious AEs (SAEs) and adverse events of special interest (AESIs) throughout follow-up. Neutralizing antibody titers (pseudovirus 50% neutralization titer, NT₅₀) and anti-spike IgG (BAU/mL) were assessed pre-dose (Day 1) and post-vaccination through 12 months; a predefined subset underwent IFN-γ and IL-5 ELISpot. SARS-CoV-2 infection during follow-up was assessed using anti-nucleocapsid (anti-N) IgG. Symptomatic COVID-19 was identified through symptom-reported, symptom-triggered RT-PCR testing; sequencing was performed when feasible. Results: All 219 participants received HXP-GPOVac (167 primed with HXP-GPOVac and 52 with BNT162b2). Any solicited local reaction occurred in 22.2% (37/167) of HXP-GPOVac-primed and 26.9% (14/52) of BNT162b2-primed participants; any solicited systemic reaction occurred in 10.8% (18/167) and 13.5% (7/52), respectively. No vaccine-related unsolicited AEs or AESIs were reported. Three deaths occurred during the 12-month follow-up; one (a sudden cardiac death in an HXP-GPOVac-primed participant) was assessed by the safety medical team as possibly related to vaccination, and two were assessed as not related. Neutralizing antibody GMTs increased from 46.33 at baseline to 1569.04 at Day 15 in HXP-GPOVac-primed participants and from 77.25 to 841.34 in BNT162b2-primed participants; corresponding SCRs were 78.8% and 76.9%. Anti-spike IgG GMCs increased from 48.79 to 1480.14 BAU/mL and from 194.48 to 1547.88 BAU/mL, respectively. Responses declined over time but remained above baseline through 12 months. In the cellular immunity subset, post-vaccination IFN-γ responses increased, with comparatively modest IL-5 responses and no pattern suggestive of Th2 predominance. Conclusions: A single additional dose of HXP-GPOVac administered ≥6 months after primary vaccination with HXP-GPOVac or BNT162b2 was generally well tolerated and elicited robust recall humoral responses, with supportive findings of cellular immunity. Trial registration: Thai Clinical Trials Registry, TCTR20230213001. Full article

Periodontitis and cardiovascular disease share inflammatory, immune, endothelial, oxidative, and lipid-related pathways. Although sex-related differences are well established for many cardiovascular biomarkers, it remains unclear whether sex modifies biomarker patterns at the intersection of periodontal and cardiovascular disease. PubMed, Scopus, and Web of Science were searched in accordance with PRISMA 2020. Eligible adult human studies evaluated periodontitis or periodontal inflammation together with atherosclerotic or related cardiovascular phenotypes and reported candidate biomarkers in blood or, as supportive evidence, oral fluids. High-throughput omics studies were eligible when available. Data on study design, periodontal and cardiovascular assessment, biological matrix, biomarker findings, sex-stratified analyses, and menopausal status were extracted. Twelve studies were included. Most assessed single biomarkers or small predefined panels rather than discovery-scale omics. Reported markers involved inflammation and immunity (CRP, hs-CRP, IL-6, LPS, and periodontal antibodies), endothelial or vascular injury, lipid and autoimmune pathways (PCSK9 and anti-ApoA-1 IgG), innate-immune and metabolic regulation (MBL and SIRT1), cardiac stress, and oxidative stress. Findings were heterogeneous across cardiovascular phenotypes, and several key associations were null or imprecise. Only two studies performed direct male–female comparisons: one enrolled women only, and none stratified women by menopausal status. No study derived and validated a sex-specific omics signature. The literature identifies overlapping candidate-biomarker pathways but does not establish a causal, clinically validated, sex-specific, or menopause-specific signature of periodontitis-associated cardiovascular disease. The current evidence should be considered hypothesis-generating. Full article

Background: Lymphoepithelial sialadenitis (LESA) is a chronic lymphoid-rich inflammatory disorder of the salivary glands that is strongly associated with Sjögren’s disease and may overlap clinically, radiologically, and histopathologically with IgG4-related sialadenitis, HIV-associated lymphoepithelial lesions, chronic sialadenitis, salivary gland tumors, and extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma). Objective: This scoping review mapped current evidence on diagnostic challenges, differential diagnostic criteria, management strategies, and surveillance considerations for LESA. Eligibility criteria: Sources were selected using the Population–Concept–Context framework and included the literature addressing salivary gland lymphoepithelial lesions, LESA, Sjögren’s disease-associated salivary gland involvement, or related lymphoid-rich salivary gland disorders published from 2010 onward. Sources of evidence and charting methods: Google Scholar was searched, records were screened in sequential stages, and relevant data were charted narratively across clinical, serological, imaging, histopathological, immunophenotypic, molecular, therapeutic, and follow-up domains. Results: Thirty-seven sources were included. The evidence indicates that LESA is usually characterized by chronic lymphoplasmacytic inflammation, acinar atrophy, lymphoepithelial lesions, and preserved lobular architecture; however, these findings may overlap with early or established MALT lymphoma. Immunohistochemistry, assessment of light-chain restriction, clonality testing, serological markers, and imaging are useful adjuncts, but no single test is independently definitive. Conservative management and symptomatic care are appropriate for stable disease, whereas corticosteroids, immunomodulatory therapy, sialendoscopy, surgery, radiotherapy, or systemic lymphoma therapy may be considered according to clinical context. Conclusions: LESA requires integrated clinicopathological interpretation and multidisciplinary follow-up. Key evidence gaps include the absence of standardized LESA-specific diagnostic criteria, limited validation of molecular and flow cytometric approaches in salivary gland specimens, and lack of consensus surveillance protocols. Full article

Porcine circovirus type 2 (PCV2) and Mycoplasma hyopneumoniae (Mhp) are major contributors to the porcine respiratory disease complex. Although PCV2-Mhp bivalent inactivated vaccines are useful for simultaneous disease control, their immunogenicity may be improved by adjuvant optimization. This study evaluated a composite adjuvant consisting of porcine interleukin-2 (IL-2), IL-4, IL-6 and MnJ(beta), a colloidal manganese adjuvant, in an initial murine immunogenicity model. Thirty female Kunming mice were assigned to three groups (n = 10/group): bivalent antigen plus IL-2/IL-4/IL-6/MnJ(beta), bivalent antigen plus MnJ(beta), or phosphate-buffered saline. Body weight, complete blood count, peripheral blood T- and B-cell subsets, PCV2-specific IgG and Mhp-specific indirect hemagglutination titers were monitored after primary and booster immunization. The composite formulation did not suppress body-weight gain or induce sustained abnormalities in erythrocyte- or platelet-related indices. WBC, neutrophil, lymphocyte and monocyte counts were elevated in group A at days 7 and 28 post-primary immunization, indicating transient immune activation. Day-56 flow cytometry indicated increased CD19+IgM-IgD- B-cell and effector/memory T-cell-associated responses. PCV2-specific IgG increased from day 14 onward. At day 56, the OD450 value in group A reached 1.532 ± 0.006, compared with 1.095 ± 0.004 in group C1 and 0.102 ± 0.002 in group C2, corresponding to approximately 1.40-fold and 15.09-fold higher levels than the MnJ(beta)-adjuvanted and PBS control groups, respectively. Mhp-specific IHA titers were also maintained at high levels after booster immunization; at day 56, group A showed a log2 endpoint titer of 13.00 ± 0.00, corresponding to a GMT of 1:8192, whereas group C1 showed a log2 endpoint titer of 12.00 ± 0.00, corresponding to a GMT of 1:4096, and group C2 remained negative. These results indicate that the IL-2/IL-4/IL-6/MnJ(beta) composite adjuvant demonstrates potential for improving antibody and peripheral lymphocyte responses to PCV2-Mhp bivalent antigen, but protective efficacy must be confirmed in target-species challenge studies. Full article

Background/Objectives: Dengue is an emerging arboviral disease in temperate South America, where urban expansion, climate variability, and social vulnerability favor transmission. In Argentina, the endemic circulation of dengue was established in the late 1990s and outbreaks are reported every three or four years. Methods: This cross-sectional study assessed dengue virus (DENV) seropositivity and associated sociodemographic, environmental, and knowledge-attitudes-practices (KAPs) factors in three socioeconomically vulnerable peripheral neighborhoods of Santa Fe, Argentina, between December 2019 and March 2020. Results: A total of 188 adults were surveyed and tested for anti-DENV IgG using ELISA. KAPs questionnaires and direct peridomiciliary observations were used to characterize exposure contexts. Apparent seropositivity was 16.5%, with an adjusted estimate of 10.7% after accounting for test performance, indicating substantial unrecognized DENV circulation. Most seropositive individuals had no previous dengue diagnosis, highlighting underdetection likely related to asymptomatic infections, limited healthcare access, or surveillance gaps. Although dengue awareness was high (98.4%), knowledge was often incomplete and was weakly correlated with preventive practices, suggesting that awareness alone does not translate into effective risk reduction under structural constraints. In multivariate analysis, living farther from vacant lots was associated with higher odds of seropositivity, consistent with transmission concentrated in denser urban settings. Conclusions: Integrating serology with KAPs surveys provides critical insights into hidden transmission and supports targeted surveillance and public health interventions in vulnerable urban settings. Full article

Alcohol-related liver disease (ALD) poses a significant global health burden, driven by complex mechanisms including oxidative stress, inflammation, and gut–liver axis disruption. While the individual roles of gut microbiota dysbiosis and ageing in ALD pathogenesis are increasingly recognized, their synergistic interaction remains poorly understood. This review synthesizes current evidence to argue that there is an interaction between ageing and the gut microbiota that collectively amplifies progression of ALD. Specifically, ageing promotes gut dysbiosis through immunosenescence (e.g., reduced IgA diversification and antimicrobial peptide decline), intestinal barrier failure, and altered microbial metabolite profiles (e.g., decreased short-chain fatty acids and dysregulated bile acid metabolism). Conversely, dysbiosis-derived metabolites and endotoxins modulate ageing-related signaling pathways, including SIRT1, FOXO, and Nrf2, thereby accelerating hepatic cellular senescence, inflammation, and fibrogenesis. Furthermore, we also discussed the typical microbial changes in ALD. These include an increase in the Proteobacteria, a decrease in the Bacteroidetes, as well as imbalances in fungi and viruses. In ageing, similar but distinct shifts occur, such as reduced microbial diversity, decreased short-chain fatty acid producers, and increased intestinal permeability. Therapeutic strategies targeting the gut microbiota (probiotics, fecal microbiota transplantation) or ageing-related pathways (SIRT1 activators) hold promise. Future research priorities include validating ageing-associated microbial signatures as predictors of ALD progression and testing microbiota-targeted interventions in aged preclinical models. Collectively, this review identifies the microbiota–ageing axis as a tractable therapeutic target for ALD and provides a framework for future mechanistic and translational studies. Full article

Wilson’s disease (WD) is traditionally known as a monogenic disorder of copper transport, but immune activation is now being increasingly recognized in a subset of patients. In a single-center retrospective cohort study of 86 treatment-naïve WD patients who were rigorously diagnosed using the Leipzig score, Jiang et al. systematically evaluated the prevalence, clinical impact, and prognostic significance of autoimmune phenomena (AP), defined by autoantibody positivity and/or elevated immunoglobulin G (IgG). They found that 55.8% of patients met the criteria for AP, with about half showing at least one autoantibody, primarily low-titer antinuclear antibodies (ANAs), indicating that immune activation is common in newly diagnosed WD. Notably, patients with WD and AP (AP-WD) had more advanced hepatic dysfunction at baseline, including higher bilirubin levels, worse synthetic function, greater cirrhosis and ascites burden, and higher composite liver scores, as well as increased urinary copper excretion. Histological analysis in a subset of patients who underwent biopsy showed more intense portal inflammation and plasma cell infiltration in AP-WD, suggesting a distinct immunopathological phenotype. Over a 60-month period, AP-WD patients had a higher incidence of liver-related adverse events (death or liver transplantation), with a nearly fourfold increased hazard compared to patients without AP. Collectively, these findings support AP as a clinically significant modifier of disease expression and outcome in WD, emphasizing the importance of routine assessment of autoantibodies and IgG at diagnosis to improve risk stratification and guide follow-up care. Full article

Background: Systemic sclerosis (SSc) is a heterogeneous autoimmune disease characterized by inflammation, vasculopathy, and fibrosis. It is associated with the highest mortality among rheumatic diseases. Very early SSc may represent a critical phase with risk of developing progressive disease. Although timely treatment may be effective in patients with progressive disease, it carries risks of adverse events, underscoring the need for early identification of individuals at risk. Biomarkers for progression in the early stage offer opportunities for timely intervention and improved long-term outcomes. Therefore, validating biomarkers that predict progression is an important research priority. In this narrative literature review, we summarize and evaluate blood circulating biomarkers associated with different progression endpoints in (very) early SSc. Methods: The literature search was conducted using PubMed. Eligible studies assessed biomarkers in very early SSc or early SSc cohorts with longitudinal follow-up and progression-related outcomes. Results: The identified studies investigated biomarkers associated with interstitial lung disease (ILD), skin progression, overall disease progression, and mortality. Anti-topoisomerase I was associated with ILD development. A high interferon score was linked to reduced lung function and mortality. KL-6 was associated with progression in early SSc-ILD. PRO-C3 and PRO-C6 showed the strongest associations with skin involvement. Finally, IgG anti-centromere antibody was associated with organ involvement and progression to definite SSc. CXCL10 and TNFRII were linked to progression and significant survival differences in the discovery and replication cohorts. However, effect sizes were often modest, and findings were inconsistent across cohorts. Substantial heterogeneity in study design, populations, endpoints, and biomarker assessment methods limited comparability. Moreover, most biomarkers demonstrated associations at the group level but lacked sufficient discriminatory power for individual risk prediction. Only a minority of studies included validation cohorts, and replication of findings was limited. Conclusions: Multiple biomarkers show promising associations with progression in very early and early SSc, but a single biomarker is unlikely to reliably predict disease progression. Full article

Toxoplasmosis remains one of the most common parasitic infections affecting humans, with significant implications for pregnancy and fetal health. Maternal primary infection during gestation can result in transplacental transmission of Toxoplasma gondii, leading to a wide spectrum of congenital disease. The risk of vertical transmission increases with gestational age, whereas disease severity is inversely related—early infections causing severe neurological and ocular damage, and late infections often resulting in subclinical forms. Advances in serological testing, including IgG avidity assays and molecular diagnostics such as PCR on amniotic fluid, have improved early detection and management. Prenatal treatment with spiramycin or pyrimethamine–sulfadiazine–folinic acid combinations has been associated with reduced transmission and less severe fetal disease in several studies, although the magnitude of benefit remains debated. Long-term follow-up is essential, as late-onset manifestations, particularly chorioretinitis and neurodevelopmental impairment, are common. This narrative review was based on a comprehensive literature search of major medical databases and summarizes current knowledge on the epidemiology, pathophysiology, diagnosis, treatment, and outcomes of toxoplasmosis in pregnancy. Particular emphasis is placed on high-prevalence countries, where greater parasite genetic diversity, distinct epidemiological patterns, and a higher burden of congenital disease pose unique clinical and public health challenges. Despite progress in understanding parasite biology, pathogenesis, and treatment efficacy, congenital toxoplasmosis continues to be underdiagnosed and underreported, especially in low-resource settings. Ongoing challenges include optimizing screening strategies, ensuring access to standardized therapies, and strengthening surveillance systems. Full article

Background: Toxoplasmosis is a prevalent zoonotic disease worldwide, affecting approximately one-third of the global human population. Primary infection with Toxoplasma gondii during pregnancy can induce miscarriage or congenital infection, leading to irreversible damage to the foetus. Moreover, reactivation of T. gondii infection in immunosuppressed individuals can result in fatal outcomes. No vaccine exists to prevent human disease caused by this parasite. Thus, a vaccine that could induce complete and lasting protection against human toxoplasmosis is an unmet need. Method: In this work, BALB/cByJ mice were intranasally immunised with a subunit vaccine consisting of T. gondii membrane proteins (TGMP) from the T. gondii Me49 strain plus CpG-oligodeoxynucleotide adjuvant (CpG). Antibody responses were analysed by ELISA, while T-cell responses were evaluated by flow cytometry. The immunogenic proteins present in TGMP were identified by mass spectrometry, and parasite burden was quantified by qPCR. Result: The results showed raised TGMP-specific serum IgG and intestinal IgA antibody levels, and parasite-specific IFN-γ-producing CD4⁺ and CD8⁺ memory T cells. Dense granule proteins (GRA) 2 and 7, surface antigen (SAG)-related sequences 25, 29B, and 34A, microneme protein (MIC) 10, toxofilin, nascent polypeptide-associated complex (NAC) domain-containing protein, and NAC subunit beta were identified as immunogenic proteins. Mice immunised with TGMP+CpG were challenged with T. gondii tachyzoites and showed a significant reduction in the parasitic burden in the peritoneal exudate, spleen, and lungs, compared to mice sham-immunised with CpG alone. Conclusions: Altogether, these results indicate that mucosal immunisation with TGMP plus CpG adjuvant is worth exploring as a vaccination approach to prevent toxoplasmosis. Full article

IgG4-related disease (IgG4-RD) is a systemic fibroinflammatory disorder characterised by elevated serum levels of IgG4 and multiorgan damage. Its diagnosis is challenging and requires a careful integration of clinical, radiological, serological and histological data. Pancreatic and biliary involvement is one of the most common manifestations of IgG4-RD, presenting as type 1 autoimmune pancreatitis (AIP) and IgG4-related sclerosing cholangitis (IgG4-SC), two entities that often occur synchronously and may mimic malignancy in the form of pancreatic ductal adenocarcinoma (PDAC) and cholangiocarcinoma, respectively. The main objective of this article is to illustrate the key imaging features of AIP and IgG4-SC on computed tomography (CT) and magnetic resonance imaging (MRI), providing a comprehensive review of their current diagnostic criteria and discussing their differential diagnosis with other benign and malignant conditions. Full article

Non-cystic fibrosis bronchiectasis (NCFB) is a heterogeneous chronic airway disease characterized by irreversible bronchial dilatation, impaired mucociliary clearance, and recurrent infection. Historically, research and clinical practice have focused mainly on bacteria, particularly Pseudomonas aeruginosa, as major drivers of exacerbations and disease progression, whereas the contribution of fungi has received far less attention. Over the last decade, evidence from mycobiome studies, large registries, and prospective cohorts has increasingly identified Aspergillus spp. as clinically relevant contributors in a substantial subset of patients with bronchiectasis. Data from the European Bronchiectasis Registry (EMBARC) indicate that approximately one quarter of patients exhibit Aspergillus-related immunological signals, including allergic bronchopulmonary aspergillosis (ABPA), Aspergillus sensitization, and elevated Aspergillus-specific IgG, and that these phenotypes are associated with more severe disease and worse clinical outcomes. Mechanistic studies further suggest that Aspergillus-related disease in bronchiectasis is underpinned by distinct molecular and immunological programs involving epithelial dysfunction, impaired mucociliary clearance, innate fungal sensing, inflammasome-related signaling, and divergent type-2 versus non-type-2 inflammatory responses. In parallel, mycobiome and multi-biome studies indicate that Aspergillus should be interpreted within a broader airway interactome shaped by cross-kingdom relationships with bacterial pathogens and by host immune tone. In this review, we synthesize current evidence on the epidemiology, molecular pathobiology, inflammatory endotypes, biomarker profiles, clinical–radiologic spectrum, and therapeutic implications of Aspergillus in bronchiectasis. Current evidence suggests that Aspergillus-related findings in bronchiectasis should be interpreted within a structured clinical, radiological, microbiological, and immunological framework rather than considered solely as isolated culture results. However, most data remain observational or extrapolated from related airway diseases, and bronchiectasis-specific interventional evidence is limited. A cautious biomarker-informed approach may help standardize phenotyping, identify patients requiring closer follow-up, and define priorities for future prospective trials. Full article