Search Results (10,340)

Severe anaemia remains a major public health challenge, disproportionately affecting children and women of reproductive age in sub-Saharan Africa. In high-burden settings, the aetiology of severe anaemia is multifactorial, encompassing nutritional deficiencies, infections, and host genetic factors. Beyond its direct clinical consequences, severe anaemia is also associated with increased susceptibility to invasive bacterial infections, particularly those caused by enteric pathogens such as non-typhoidal Salmonella and Escherichia coli. In this review, we present an integrated framework linking severe anaemia and invasive bacterial infection through three interconnected biological pathways, collectively termed the gut–iron–immune axis: gut microbial dysbiosis and impaired intestinal barrier integrity; disrupted iron homeostasis; and impaired immune function. We examine context-specific modifiers in endemic settings, including iron deficiency, malnutrition, malaria, sickle cell disease, and environmental enteric dysfunction. We also discuss how management of severe anaemia, including blood transfusion and iron supplementation, reshapes the gut microbiome, with direct implications for microbial translocation, invasive bacterial infection, and clinical outcomes. Finally, we identify key knowledge gaps and research priorities to guide safer and more effective prevention and management of severe anaemia in high-burden settings. Full article

Pasteurella multocida is highly prevalent in animal populations. It is usually a component of the normal microbiome of the oral, nasopharyngeal and upper respiratory tracts of animals and can cause varying degrees of infection and even death in animals. P. multocida poses a threat to public health safety because humans can be infected by being bitten by infected animals or coming into contact with their nasal secretions. This article summarises the morphological and culture characteristics of P. multocida, in addition to serotyping, virulence factors and pathogenesis, aiming to explore the mechanism by which the pathogen establishes acute and chronic infections. The article also summarises the mechanism underlying the activation of inflammasomes after P. multocida infection, providing a reference for exploring the epidemiological laws and pathogenesis of the bacterium and for formulating prevention and control strategies. Full article

Numerous types of environmental toxicants alter human metabolomics, directly or indirectly, through gut microbial dysbiosis, upsetting immune homeostasis. Environmental toxicants capable of these direct and indirect effects have included heavy metals, pesticides, herbicides, polychlorinated biphenyl (PCB) congeners, and endocrine-disrupting chemicals. The cell and molecular events induced by some diverse toxicants are reviewed, along with their potential additive, synergistic, and antagonistic effects on immune homeostasis (increasing proinflammatory immune cell activation and suppressing immunoregulation), which leads to systemic oxidative stress (OS). As people are exposed in varying degrees to countless chemicals and environmental factors over a lifetime, it is challenging to correlate specific diagnoses to any single toxicant or exposure, which is often a key challenge in linking environmental exposure to health outcomes. However, many toxicants have the common mechanistic effect of OS. The effects of toxicants are more pronounced with aging due to cumulative exposures and immunoaging (immunosenescence), with chronic low-grade inflammation referred to as “inflammaging”. The cell and molecular mechanisms of toxicants include altered calcium flux, mitochondrial dysfunction, and increased levels of damage-associated molecular patterns (alarmins) that trigger an inflammatory response and possibly promote autoimmune and neurological disorders. OS skews type-1 immunity for defenses against pathogens and cancers more toward type-2 immune responses to self-antigens (autoimmunity). The toxicants may directly affect the innate and adaptive immune cells inducing this skewing, or they may modify portions of gut microbial species and strains and their production of metabolites that indirectly affect systemic immunity. These latter toxicant influences require metabolomic analysis of the differential structures and activities of the microbial metabolites. The damaging effects of OS and inflammation disrupting immune homeostasis and leading to disorders are reviewed and discussed. The need for well-designed studies that allow for standardized comparison of exposures and related effects are emphasized, and their real-world limitations noted. Full article

Protein intrinsically disordered regions (IDRs) play important biological roles despite lacking stable structures. IDRs drive the formation of both biomolecular condensates via liquid–liquid phase separation (LLPS) and solid fibrous amyloid aggregates. Amyloids can be pathogenic and may exhibit self-perpetuating (prion) properties. Relationships between LLPS and the amyloid-forming and prion-propagating abilities of IDRs remain poorly understood. The N-proximal IDR of the yeast translation termination factor eRF3 (Sup35) can form both liquid condensates and heritable amyloid-based prions and serves as a powerful model for investigating these phenomena due to the availability of simple phenotypic, cytological and biochemical assays. Deletion analysis demonstrates that the N-proximal prion domain (Sup35N) of Sup35 is sufficient for chaperone-dependent prion propagation and that various regions of this domain show differential impacts on LLPS, amyloid aggregation, and prion inheritance. Specifically, the N-terminal NQ-rich stretch and the region of oligopeptide repeats are the most important contributors to the LLPS and formation of amyloid fibrils, while oligopeptide repeats and the C-terminal region of Sup35N are crucial for prion inheritance. Contrary to previous reports, the NQ-rich stretch is not required for prion formation and inheritance in yeast. Our data indicate that, in addition to amino acid composition, specific sequence motifs control reversible and heritable assemblies of Sup35. Full article

Winter survival of crops is influenced by multiple environmental stress factors, including low temperature, excessive soil moisture, and pathogen pressure. With climate change, the role of flooding during cold acclimation has become increasingly important. This study examined the effect of cold flooding on frost tolerance of two winter rye (Secale cereale L.) lines differing in resistance to snow mould. Plants were subjected to cold acclimation for three weeks at 4 °C, followed by ten days of flooding at the same cold temperature. Cold flooding improved frost tolerance only in the snow mould-resistant line (343), which maintained the presence of a 50 kDa β-1,3-glucanase isoform and exhibited a flooding-induced decrease in cytosolic sucrose synthase (SuS) activity in leaves, while maintaining higher SuS activity in roots. In contrast, the less resistant line (620) lacked the 50 kDa isoform in roots and showed substantially lower SuS activity than line 343; however, leaf SuS activity increased during prolonged flooding to levels comparable with those of line 343. The 35 kDa isoform was no longer detectable in the leaves of either line after one or ten days of flooding, whereas in the roots of both lines, its accumulation was maintained after one day but was abolished after ten days of flooding. Additionally, line 620 exhibited prolonged flooding-induced upregulation of glu-8 and TLP3 genes, which, in the absence of protein accumulation, suggests post-transcriptional or translational constraints associated with prolonged stress. These findings demonstrate that higher frost tolerance under cold flooding involves the accumulation of specific pathogenesis-related (PR) proteins, maintaining a high reduced and oxidised glutathione ratio and metabolic adjustment of sucrose synthesis. Furthermore, cold acclimation alone did not differentiate frost tolerance between rye genotypes differing in snow mould resistance, whereas flooding under low-temperature conditions enhanced freezing tolerance only in the resistant line, indicating that flooding may function as a positive signal involved in frost tolerance induction. Full article

Chinese hickory (Carya cathayensis Sarg.) is an economically important tree species widely cultivated in southeastern China, where trunk canker disease caused by Botryosphaeria dothidea poses a serious threat to tree health and production. Pectin-degrading enzymes are important virulence-associated factors that facilitate fungal colonization and host tissue maceration, but their evolutionary diversification and functional roles in B. dothidea during woody host infection remain poorly understood. Comparative genomic analysis revealed lineage-specific variation in the GH28 glycoside hydrolase family among the examined Botryosphaeriaceae species, with B. dothidea exhibiting an expanded GH28 repertoire relative to the analyzed species. Expression analysis and functional assays revealed that BdGH28_3 showed the highest transcript abundance during infection stage and contributed to the full virulence of B. dothidea. A predicted protein–protein interaction (PPI) network suggested potential associations between BdGH28_3 and other pectinolytic enzymes, including polygalacturonases, pectin lyases, and pectinesterases. Collectively, these findings identify GH28 diversification as a distinctive feature of the B. dothidea genome and establish BdGH28_3 as a virulence-associated member, providing a foundation for investigating GH28-mediated pathogenicity in woody hosts. Full article

Background: Streptococcus suis serotype 2 is a major zoonotic pathogen responsible for severe systemic infections in pigs and humans, including septicemia, meningitis, and high mortality outcomes. Cefquinome, a fourth-generation β-lactam antibiotic widely used in veterinary medicine, is commonly applied for the treatment of S. suis infections. However, optimized dosing strategies remain insufficiently defined, particularly under conditions of varying bacterial burden, inoculum size, and reduced susceptibility or resistance phenotypes. These factors may significantly alter pharmacodynamic responses and compromise the predictive value of conventional MIC-based approaches. Objectives: This study aimed to characterize the pharmacokinetics (PK) and pharmacodynamics (PD) of cefquinome against S. suis serotype 2 using an integrated ex vivo serum time-kill experiments and semi-mechanistic PK/PD modeling. A secondary objective was to evaluate optimized dosing regimens across different inoculum levels and susceptibility phenotypes, including a cefquinome-resistant mutant. Methods: Cefquinome pharmacokinetics following intramuscular administration at 2 and 4 mg/kg in piglets were described using a two-compartment model. Dose proportionality, exposure linearity, and clearance parameters were assessed. Ex vivo serum time-kill experiments were conducted using a parental strain and a cefquinome-resistant mutant (M1) under normal-inoculum (NI), high-inoculum (HI), and mutant/resistant (MS) conditions. A semi-mechanistic PK/PD model incorporating logistic bacterial growth, sigmoidal Emax killing, nutrient limitation, and a time-delay function was developed to describe dynamic bacterial responses. Model parameters (k₀, k_max, EC₅₀) were estimated using nonlinear least-squares regression (Scientist v2.0), and simulations were performed by integrating time-varying PK input functions. Results: Cefquinome demonstrated linear pharmacokinetics with dose-proportional increases in Cmax and AUC between 2 and 4 mg/kg, with comparable clearance across doses. Ex vivo studies revealed time-dependent antibacterial activity with a pronounced inoculum effect. Higher bacterial burdens significantly reduced bactericidal efficiency and promoted regrowth during declining drug exposure. No tested concentrations achieved ≥3-log₁₀ killing in HI or MS conditions, whereas the NI group achieved a maximal reduction of 3.5-log₁₀ CFU/mL. MIC values in serum and medium were consistent (0.03, 0.06, and 0.24 µg/mL for NI, HI, and MS, respectively), indicating minimal protein binding influence. The semi-mechanistic model accurately described observed bacterial dynamics (R² > 0.99; MSC > 1.5), capturing delayed drug effects, inoculum-dependent growth suppression, and regrowth phenomena. Growth rates were reduced under serum conditions, reflecting nutrient limitation. Importantly, inoculum size exerted a stronger impact on pharmacodynamic outcomes than resistance phenotype, as reflected by reductions in kmax and increases in EC₅₀ under HI conditions. Although %T>MIC exceeded conventional β-lactam targets (>40%) in most regimens, MIC-based indices poorly correlated with observed dynamic killing responses. Conclusions: Cefquinome exhibited time-dependent antibacterial activity against S. suis serotype 2, strongly modulated by inoculum size and reduced susceptibility. The developed semi-mechanistic PK/PD model provided robust prediction of bacterial time-kill behavior and outperformed MIC-based metrics in guiding dose optimization. Simulation results support 2 mg/kg every 24 h for normal infections and 2 mg/kg every 12 h for high-inoculum or less susceptible infections, emphasizing the value of model-informed dosing strategies for optimizing β-lactam therapy. Full article

Androgenetic alopecia (AGA) is a prevalent clinical disorder, and the key pathogenic factor is dihydrotestosterone (DHT) present in the pilosebaceous unit. Current clinical therapeutic options are often associated with notable adverse effects, highlighting the urgent need for safer and more effective interventions. Herein, a novel amphiphilic covalent organic framework (amCOF) is designed and synthesized. By simultaneously incorporating hydrophilic functional groups and lipophilic alkyl chains into the covalent organic skeleton, the material exhibits excellent amphiphilicity, high specific surface area, and well-ordered porous structures. Owing to its amphiphilic nature, amCOF disperses uniformly in aqueous physiological media and adapts favorably to the lipophilic microenvironment within hair follicles. Furthermore, the ordered porous architecture endows amCOF with rapid DHT adsorption kinetics, high adsorption capacity, and high removal efficiency. Functional assays demonstrate that amCOF effectively reverses the inhibitory effects of DHT on the proliferation and migration of human dermal papilla cells. In animal models, topical application of amCOF significantly reduces local DHT concentrations, promotes hair regrowth, and shows favorable biosafety profiles. Collectively, this work provides a new strategy for treating androgenetic alopecia by scavenging pathogenic lipophilic molecules from sebum using amphiphilic porous materials and also establishes a solid foundation for expanding the biomedical applications of COFs. Full article

Background/Objectives: Achondroplasia is the most common genetic skeletal dysplasia associated with disproportionate short stature and is primarily caused by gain-of-function variants in the fibroblast growth factor receptor 3 (FGFR3) gene. Constitutive FGFR3 activation disrupts growth plate homeostasis and endochondral ossification through complex alterations in chondrocyte proliferation, differentiation, hypertrophy, extracellular matrix organization, and intracellular signaling. The increasing understanding of these mechanisms has enabled the transition from exclusively supportive management toward disease-modifying and precision-based therapeutic strategies. This narrative review aimed to critically synthesize current evidence on the genetic basis, molecular pathogenesis, growth plate abnormalities, and current and emerging targeted therapies in achondroplasia. Methods: A narrative literature review was conducted using PubMed/MEDLINE, Scopus, and Web of Science Core Collection, with Google Scholar used as a supplementary source, together with manual screening of the reference lists of relevant original studies, clinical trials, reviews, consensus documents, and clinical guidelines. The principal literature search covered publications from January 2010 to March 2026, while selected seminal primary studies published before 2010 were included when necessary to document the original identification of pathogenic FGFR3 variants and foundational mechanisms of FGFR3-mediated growth plate regulation. Particular emphasis was placed on FGFR3 variants, receptor activation mechanisms, growth plate dysfunction, intracellular signaling pathways, vosoritide, C-type natriuretic peptide-based therapies, FGFR3 inhibitors, ligand–receptor blockade, drug repurposing, Wnt/β-catenin modulation, and gene-based therapeutic approaches. Results: Achondroplasia is characterized by marked molecular homogeneity, with the recurrent p.Gly380Arg substitution accounting for most cases. Mutant FGFR3 displays sustained activity through partial ligand independence, enhanced receptor dimerization and kinase activation, increased receptor stability, and reduced degradation. Excessive signaling through MAPK/ERK, STAT, PI3K/AKT, IHH/PTHrP, and related pathways impairs chondrocyte proliferation and hypertrophic differentiation, alters extracellular matrix turnover, disrupts primary cilium function, and reduces longitudinal bone growth. Vosoritide provides clinical proof that pharmacological modulation of FGFR3-related signaling can improve growth velocity. Additional therapeutic strategies under clinical or preclinical investigation include long-acting CNP analogues, selective FGFR inhibitors, decoy receptors, RNA aptamers, repurposed drugs, Wnt/DKK1 pathway modulation, and gene- or enhancer-targeted interventions. Conclusions: Achondroplasia is increasingly understood as a disorder of dysregulated growth plate signaling rather than solely a condition of reduced stature. Although vosoritide has established the feasibility of disease-modifying treatment, substantial uncertainty remains regarding final adult height, skeletal proportionality, cranio-spinal development, orthopedic outcomes, and long-term safety. Future progress will depend on mechanistically informed therapeutic combinations, improved biomarkers, advanced cellular and animal models, and long-term clinical and real-world evidence. Full article

The incidence of fungal infections, particularly those caused by Candida species, has significantly risen among immunocompromised patients in recent years. Aim: This study evaluated the species distribution, antifungal susceptibility patterns, and virulence gene profiles of Candida species isolated from critically ill ICU patients while comparing the diagnostic performance of conventional phenotypic isolation media with molecular genotypic identification methods. Materials and Methods: A total of 211 clinical specimens were obtained from 200 hospitalized patients at Menoufia University Hospitals, Egypt. Candida species were phenotypically identified using cornmeal agar supplemented with Tween 80 (CTA) and CHROMagar^TM Candida (CMA) and were molecularly confirmed at the species level by sequencing PCR-amplified ITS regions. Antifungal susceptibility profiles to fluconazole, voriconazole, and amphotericin B were evaluated using the disk diffusion method. Furthermore, real-time PCR was deployed to detect genes encoding adherence factors and Secreted Aspartyl Proteinase. Results: Candida species were recovered from 45 out of 211 clinical specimens. The most frequently isolated species was Candida albicans (15/45, 33.3%), followed by C. parapsilosis (9/45, 20.0%), C. glabrata (7/45, 15.5%), C. tropicalis (7/45, 15.5%), C. krusei (4/45, 8.8%), and C. famata (3/45, 6.7%). Among the recovered Candida isolates, the percentage rates of the ALS1, ALS3, HWP1, and SAP4 genes were 40%, 42.22%, 44.4%, and 37.78%, respectively. HWP1 was the most frequently detected pathogenicity factor, whereas SAP4 was the least prevalent. Conclusions: In the studied immunocompromised cohort, non-albicans Candida species constituted a substantial proportion of clinical isolates. Notable antifungal resistance patterns were also observed, emphasizing the value of integrated phenotypic and genotypic identification for tailored management. Furthermore, virulence-associated genes (ALS1, ALS3, HWP1, and SAP4) were detected in isolates of several Candida species, highlighting their presence in clinical strains. Full article

Microphthalmia, anophthalmia and ocular coloboma (MAC) are rare developmental eye disorders. Although over 100 causative genes have been identified, the molecular spectrum and genotype–phenotype correlations remain incompletely understood, particularly in genetically diverse populations. We set out to molecularly characterize MAC in the Israeli population. Forty-seven MAC-affected individuals from 43 unrelated families were enrolled. DNA of all probands was subjected to whole exome sequencing. The most common phenotype was microphthalmia (64% of patients). Definite or possible molecular diagnoses were achieved in 13/43 probands (30%) and involved 10 different genes (MFRP, SMO, GJA8, SOX2, RARB, TSPAN12, SHH, PTPN11, BEST1, and TP63). An in vitro splicing assay was used to explore the pathogenicity of a variant in the SMO gene. Following stringent filtering of exome data, 226 rare possibly pathogenic variants were identified in 218 genes not previously associated with MAC. The rate of molecular diagnosis achieved in this Israeli MAC cohort is similar to the reported range in other studies. The results further demonstrate the genetic heterogeneity of MAC, while supporting the involvement of complex inheritance and/or environmental factors in many of the cases. Further studies are required to reveal these underlying etiological factors, and to support the novel genotype–phenotype associations suggested here. Full article

Background/Objectives: The apelin/APJ system has demonstrated neuroprotective effects in experimental studies by regulating key pathogenic mechanisms of ischemic stroke, including oxidative stress, apoptosis, cerebral edema, and inflammation. This study aimed to investigate the role of serum apelin levels measured within the first 24 h in predicting 28-day and long-term mortality in patients with ischemic cerebrovascular disease. Methods: This prospective cohort study included 44 patients hospitalized with a diagnosis of acute ischemic stroke due to large artery atherosclerosis. Serum apelin levels were measured using the ELISA method from blood samples obtained within the first 24 h after symptom onset. Patients were prospectively followed for 28-day and long-term mortality. Results: During the follow-up period, 32.6% of the patients died. The median serum apelin level was significantly higher in the deceased group compared to the survivors [105.0 pg/mL vs. 55.8 pg/mL]. In ROC analysis, the area under the curve (AUC) for apelin in predicting mortality was 0.727 (95% CI: 0.550–0.903). The optimal cut-off value was determined as ≥70.47 pg/mL (sensitivity: 85.71%, specificity: 62.07%). In Kaplan–Meier analysis, the 28-day mortality rate was 52.2% in the high-apelin group (≥70.47 pg/mL), whereas it was 10.0% in the low-apelin group (<70.47 pg/mL) (p = 0.004). In multivariate Cox regression analysis, an apelin level <70.47 pg/mL was identified as an independent prognostic factor (HR: 0.16; 95% CI: 0.03–0.94). The cumulative survival rates at days 28, 56, and 180 were 56.1%, 46.7%, and 11.7%, respectively, in the high-apelin group, while these rates were 100%, 100%, and 81.8%, respectively, in the low-apelin group. The mean NIHSS score was significantly higher in the high-apelin group, and a strong, positive, and highly significant correlation was found between serum apelin level and NIHSS score (r = 0.703, p < 0.001). Conclusions: High serum apelin levels measured within the first 24 h in acute ischemic stroke are associated with increased 28-day and long-term mortality. The association of high endogenous apelin levels with poor prognosis in the clinical setting suggests that apelin is mobilized as a stress response during ischemia, and that elevated circulating levels may actually reflect the severity of the ischemic insult. Full article

Background/Objectives: Mitochondrial Complex V (Complex V [CX-V], or ATP synthase) is the terminal enzyme of oxidative phosphorylation and is responsible for the majority of cellular ATP production. An increasing body of evidence suggests that CX-V dysfunction may contribute to mitochondrial impairment observed in neurodegenerative disease. This review evaluated current research on the structure, regulation, and function of CX-V, examined the consequences of CX-V dysfunction, and assessed its proposed role in neurodegenerative disorders. Methods: A comprehensive review of the published literature was carried out, with emphasis on primary research investigating CX-V structure and function, inherited CX-V disorders, and experimental evidence linking CX-V dysfunction to neurodegenerative disease. The reviewed studies used a range of experimental approaches, including structural biology, biochemical studies, patient-derived cellular models, animal models and post-mortem human tissue. Results: Current evidence demonstrates that disruption of CX-V impairs ATP production, alters mitochondrial membrane potential, and oxidative phosphorylation, and that pathogenic variants cause primary mitochondrial disease. Across Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis/frontotemporal dementia, glaucoma and inherited optic neuropathies, alterations in CX-V activity, regulation and structural integrity are consistently associated with mitochondrial dysfunction. Direct evidence supporting CX-V as a primary driver of neurodegeneration remains very limited, with many observations originating from broader studies of general mitochondrial dysfunction. Conclusions: CX-V dysfunction represents a recurring feature of mitochondrial impairment across a variety of neurodegenerative disorders and may exacerbate neuronal vulnerability by disrupting cellular bioenergetics. Current evidence indicates that CX-V may serve as a common downstream target of multiple pathological pathways rather than acting as a primary pathological factor. Future studies require direct assessment of CX-V activity in clinically relevant human models and patient tissues to determine its contribution to disease progression and examine its potential as a therapeutic target. Full article

(1) Background: methicillin‑resistant Staphylococcus aureus (MRSA) is a zoonotic pathogen, and its hemolysins serve as key virulence factors. Functional membrane microdomains (FMMs) are protein-enriching platforms and regulate diverse physiological functions by recruiting and assembling various proteins. However, whether and how FMMs regulate the hemolytic ability of MRSA remains unclear. This study aimed to investigate FMM-mediated regulation of MRSA hemolysins and the underlying mechanisms. (2) Methods: Homologous recombination was employed to generate FMM-disrupted (N315ΔfloA) and complemented (N315ΔfloA::floA) strains from the MRSA N315 wild-type strain (N315 WT). The three strains were compared with respect to hemolytic activity, transcript levels of key virulence and regulatory genes, and in vivo virulence. (3) Results: Disruption of FMMs significantly enhanced hemolytic activity compared with N315 WT and complemented strains. Meanwhile, FMM disruption repressed the two-component system genes (vraS and vraR), while activating the agr operon (agrB, agrD, agrC and agrA) and its effector molecule RNAIII, leading to upregulation of hemolysin genes (hla, hlb, hld). In vivo, N315ΔfloA infection markedly increased mortality in G. mellonella larvae and BALB/c mice, with significantly elevated pro-inflammatory factors (TNF-α, IL-6, and IL-1β) in mouse plasma. All these phenotypes were effectively reversed in N315ΔfloA::floA. (4) Conclusions: Disruption of FMMs potentiates both hemolytic activity and overall virulence in MRSA, with the potential underlying mechanism involving the VraS/R-Agr regulatory axis that drives transcriptional upregulation of hemolysin-encoding genes. Full article

Airborne bacterial diseases driven by pathogen aerosols in enclosed greenhouses spread rapidly, challenging traditional early-warning methods. This study developed a two-step monitoring system for cucumber angular leaf spot using low-cost particulate matter (PM) sensors, qPCR, and machine learning. Evaluated across spatially independent greenhouse trials using 732 plot-days of data, PM sensors were utilized as dynamic physical proxies alongside microclimate data. These proxies continuously estimated the fluctuations of pathogen aerosols suspended in the greenhouse air. When estimated aerosol risks exceeded a pathogenic threshold, targeted air sampling and qPCR quantification were triggered. For pathogen monitoring, the Extra Trees (ET) surveillance model accurately predicted the accumulation of airborne pathogen aerosols (R² = 0.884). For disease forecasting, by integrating the quantified aerosol loads with environmental factors, the XGBoost prediction model forecasted the daily disease index change rate with high precision (R² = 0.874). SHapley Additive exPlanations (SHAP) analysis confirmed that the concentration of airborne pathogen aerosols and vapor pressure deficit were primary drivers of disease expansion. By combining continuous physical sensing of greenhouse air with risk-triggered biological quantification, this framework provides a feasible strategy to partly compensate for the lack of biological specificity of PM sensors and supports early-warning management of airborne bacterial diseases in protected agriculture. Full article