Search Results (29,343)

Bone-resident macrophages are increasingly recognized as regulators of bone metabolism, yet their contribution to primary human osteoblast cultures remains poorly understood. We investigated the functional relevance of CD14-positive cells in primary human osteoblast cultures obtained using two isolation methods. CD14-positive cells were depleted by magnetic-activated cell sorting, and non-depleted and depleted cultures were compared regarding cell viability, matrix mineralization, osteogenic and macrophage-associated marker expression, and responses to IL-1β, IL-6, and TNF-α. CD14 depletion reduced cell viability under growth conditions and significantly impaired matrix mineralization in cultures obtained with both isolation protocols. Depletion markedly decreased CD14 and other monocyte/macrophage-associated markers, while the osteogenic cell population was largely preserved, although marker-specific changes suggested altered osteoblast maturation. Despite reduced basal mineralization, IL-1β and TNF-α significantly enhanced mineralization in both non-depleted and CD14-depleted cultures, whereas IL-6 had no significant effect. These findings indicate that CD14-positive cells support basal osteoblast viability, maturation, and mineralization but are not required for the mineralization-promoting effects of IL-1β and TNF-α. Primary human osteoblast cultures should therefore be considered multicellular systems in which macrophage-like cells contribute substantially to basal osteogenic function. Full article

Background: Post-cardiac arrest syndrome (PCAS) involves a complex interplay between systemic inflammatory and compensatory anti-inflammatory responses. The hyperacute kinetics of these cytokines and their incremental prognostic value beyond established brain injury biomarkers remain inadequately characterized. We aimed to evaluate whether the 6 h post–return-of-spontaneous-circulation (ROSC) cytokine profile predicts neurological outcome, with the Th1/Th2 ratio largely reflecting the IL-10 signal. Methods: This retrospective analysis of prospectively collected data from a single-center cardiac arrest registry included 56 cardiac arrest survivors (40 out-of-hospital, 16 in-hospital) treated with targeted temperature management (TTM) at 33 °C or 36 °C between January 2024 and December 2025. Serum IL-6, IL-10, IFN-γ (interferon-γ), and TNF-α (tumor necrosis factor-α) were measured at five time points (initial presentation (INIT), and 6, 24, 48, and 72 h post-ROSC). Neurological outcome was assessed using the Cerebral Performance Category (CPC) scale at 6 months after cardiac arrest, with poor outcome defined as CPC 3–5. Results: Eighteen patients (32.1%) had a good outcome (CPC 1–2) and 38 (67.9%) had a poor outcome at 6 months after cardiac arrest. Among the 38 poor-outcome patients, 2 were classified as CPC 3, 8 as CPC 4, and 28 as CPC 5 (death) at 6 months; the 6-month outcome was available for all 56 patients, with no loss to follow-up. Patients with poor outcomes exhibited a synchronized surge of IL-6 and IL-10 peaking at 6 h post-ROSC. IL-10 at 6 h showed the highest discriminative power among cytokines (area under the curve (AUC) 0.844) compared with IL-6 (AUC 0.761). Multivariable analysis using Youden-derived cut-offs revealed that IL-10 ≥ 154.32 pg/mL (adjusted odds ratio (aOR) 15.28, 95% CI 2.02–115.38, p = 0.008) and a Th1/Th2 ratio ≥ 0.0314 (aOR 0.09, 95% CI 0.01–0.61, p = 0.013) were independently associated with neurological outcome after adjustment for age and initial shockable rhythm. Conclusions: The 6 h post-ROSC window is a critical inflection point for immune dysregulation in PCAS. Early IL-10 elevation and collapse of the Th1/Th2 balance are independently associated with poor neurological recovery and add incremental prognostic information to established brain injury biomarkers. External validation in larger prospective cohorts is required. Full article

Probiotic interventions for inflammatory bowel disease (IBD) have become a hot research topic in this field. However, no previous studies have investigated whether fox-derived probiotics exert therapeutic effects against colitis. The present investigation evaluated the effects of Lactiplantibacillus plantarum (syn. Lactobacillus plantarum) J3, sourced from the intestines of healthy Arctic foxes, on colitis. In an in vitro LPS-stimulated Caco-2 cell model, strain J3 exhibited prominent anti-inflammatory and antioxidant capacities, indicating potential to preserve intestinal barrier integrity. Furthermore, in an in vivo DSS-induced colitis mouse model, oral J3 supplementation markedly alleviated body weight loss, lowered disease activity index (DAI), and ameliorated histopathological lesions in colon tissues. Mechanistic analyses revealed that the J3 group displayed significantly decreased colonic levels of TNF-α, IL-1β, IL-6, MPO, PGE₂, along with downregulated COX-2 mRNA expression (p < 0.05). By contrast, the levels of IL-10, TJ protein mRNA, and MUC2 mRNA were markedly upregulated, whereas serum LPS and D-Lac concentrations were significantly reduced (p < 0.05). In an exploratory analysis of 16S rDNA and short-chain fatty acids (SCFAs) in a subset of mice, J3 treatment showed a trend toward colonic microbial remodeling, accompanied by a significant increase in short-chain fatty acid production (p < 0.05). Overall, these findings indicate that Lactiplantibacillus plantarum J3 derived from foxes may alleviate DSS-induced colitis in mice, providing a basis for future translational research. Full article

The bystander effect describes the induction of responses in non-targeted cells through cell signaling by directly stimulated cells. While this phenomenon has been extensively studied in the context of ionizing radiation, its occurrence following electrical stimulation (ES) remains poorly understood. Conditioned medium from N2a neuroblastoma cells exposed to voltage-controlled biphasic pulses at 500 mV/mm and 100 Hz induced neuronal differentiation in non-stimulated cells through an ES bystander effect. Bystander medium promoted morphological changes associated with neuronal differentiation, including increased neurite outgrowth and a reduction in the proliferation marker KI-67, indicating that the effects of ES extend to neighboring non-targeted cells. Molecular analysis revealed increased expression and secretion of interleukin-6 (IL-6) following ES, while neutralization of the IL-6 receptor inhibited the effects of ES, highlighting the role of IL-6 as a key mediator of this effect. We provide the first evidence that ES promotes a differentiation-associated bystander effect mediated by IL-6. Full article

Senescence-associated secretory phenotype (SASP) signaling, along with key markers such as P16^INK4a/CDKN2A and LMNB1, has not been systematically studied in circulating lymphocyte subsets in head and neck squamous cell carcinoma (HNSCC). This study aimed to evaluate SASP-related genes and senescence markers in peripheral CD4⁺, CD8⁺, and CD19⁺ cells and assess their clinical relevance. Expression of IL-6, IL-1β, TNFα, CXCL1, P16^INK4a/CDKN2A, and LMNB1 was measured by RT-qPCR in sorted lymphocytes from 58 HNSCC patients at baseline, 31 post-treatment, and 13 controls. Statistical analyses included nonparametric tests, correlation analyses, and survival models (Kaplan–Meier, Cox regression). In the results, LMNB1 was significantly upregulated in all lymphocyte subsets of HNSCC patients. IL-6, CXCL1, and IL-1β were elevated in CD4⁺ T cells. A coordinated co-expression network involving IL-6, CXCL1, IL-1β, P16^INK4a/CDKN2A, and LMNB1 was observed. Clinically, IL-6 in CD8⁺ T cells was associated with higher nodal stage and worse survival, while CXCL1 in CD19⁺ B cells independently predicted survival. No differences were found between pre- and post-treatment samples. Circulating lymphocytes in HNSCC display coordinated expression of selected senescence-associated genes, with IL-6 and CXCL1 as candidate prognostic biomarkers linked to tumor progression that warrant further validation. Full article

This study investigates polymer/ionic liquid/polymer trilayer membranes for recovering aroma and fragrance compounds from a simplified synthetic model aqueous solution via pervaporation. The membranes featured organophilic polymer layers (PEBA and POMS) sandwiching an intermediate ionic liquid (IL) layer ([P₁₄₄₄][Tf₂N] and [Bmim][Tf₂N]), which were gelled with 12-hydroxystearic acid to ensure structural integrity. The trilayer architecture significantly enhanced separation performance compared with monophase membranes. The PEBA/[P₁₄₄₄][Tf₂N]/PEBA configuration achieved the highest enrichment factors, reaching 1626 for hexanal and 963 for linalool. Meanwhile, the POMS/[P₁₄₄₄][Tf₂N]/POMS system exhibited the highest selectivity relative to water. The introduction of the IL gel layer reduced overall mass transfer resistance while simultaneously suppressing water flux from 0.312 kg h⁻¹ m⁻² (in pure PEBA) to between 0.013 and 0.023 kg h⁻¹ m⁻². Overall, the results demonstrate that combining polymer matrices with gelled ILs in a trilayer design effectively optimizes mass transfer and selectivity, offering a promising strategy for the future valorization of aroma compounds from agro-industrial aqueous streams. Full article

Background/Objectives: Carbon tetrachloride (CCl₄) is a potent toxic agent that induces oxidative stress, inflammation, fibrosis, and apoptosis in various tissues, including the lungs. This study aimed to investigate the potential protective effects of curcumin against CCl₄-induced lung injury in rats using histopathological, biochemical, and immunohistochemical analyses. Methods: A total of 40 male Wistar albino rats were allocated to four experimental groups: control, curcumin, CCl₄, and CCl₄ + Cur. Curcumin was administered orally at 200 mg/kg/day for three weeks, whereas CCl₄ was administered intraperitoneally at 0.5 mL/kg as a 1:1 mixture with olive oil every other day for three weeks. Results: Histopathological examination revealed marked alveolar septal thickening, hemorrhage, vasocongestion, inflammatory cell infiltration, vacuolization, and epithelial desquamation in the CCl₄ group, whereas lung tissue architecture was largely preserved in the CCl₄ + Cur group. Biochemically, CCl₄ exposure significantly increased the MDA levels and decreased SOD activity, while curcumin administration significantly reduced the MDA levels and increased SOD activity. Immunohistochemical H-score analysis showed significantly higher TNF-α, IL-1β, TGF-β, and caspase-3 immunoreactivity in the CCl₄ group, whereas these alterations were significantly reduced following curcumin administration. Conclusions: These findings indicate that curcumin attenuated pulmonary histopathological, biochemical, and immunohistochemical alterations associated with CCl₄ exposure, accompanied by improved oxidant–antioxidant balance and reduced inflammatory, profibrotic, and apoptotic immunoreactivity. However, because hepatic injury was not evaluated, the relative contributions of direct pulmonary effects and indirect liver-mediated systemic effects could not be determined. Full article

Plant-mediated green synthesis of silver nanoparticles (AgNPs) predominantly relies on single botanical sources, constraining reduction efficiency and forfeiting the therapeutic potential of residual biomass. This study employed aloe vera and birch bark extracts as reducing agents. A combination of single-factor analysis and response surface methodology was employed to prepare monodisperse 30 nm AgNPs (with a Zeta potential of −35.3 mV and confirmed by XPS as metallic Ag⁰). It was loaded into carboxymethyl chitosan-vanillin-polyvinyl alcohol (CVP) gel microneedles using the vacuum casting method. The mechanical strength of these microneedles reaches 0.302 N/needle, exceeding the skin penetration threshold. Throughout the entire preparation process, both its Ag⁰ chemical state and crystal structure were maintained (by FT-IR and XRD). The MIC values of AgNPs@CVP against four pathogens ranged from 0.977 to 7.813 μg/mL, with a biofilm disruption rate exceeding 70%, and demonstrated excellent biocompatibility (hemolytic rate < 1.6%, cell survival rate > 80%). In a rat wound infection model, high-dose microneedle therapy reduced the residual wound area to 10.9% by day 9. This strategy inhibited the secretion of TNF-α and IL-6 while promoting epithelial regeneration, angiogenesis, and collagen deposition. This bifunctional Aloe-Birch strategy converges green nanomaterial synthesis with therapeutic delivery within a single bio-based platform, advancing sustainable nanomedicine paradigms and providing a resource-efficient blueprint for clinical infectious wound management. Full article

Bacterial infection triggered excessive inflammatory responses, yet the mechanisms linking inflammatory activation to immunometabolic adaptation remained incompletely understood. The mitochondrial translocator protein (TSPO) has been implicated in inflammatory activation and cellular metabolism. This study aimed to investigate the role of TSPO in inflammation mediated by Toll-like receptor 4 (TLR4). Herein, we integrated transcriptomic data from the human peripheral blood dataset GSE72829, and single-cell transcriptomic profiles from the CELLxGENE platform with cellular mechanistic experiments in BV2 microglia and RAW264.7 macrophages. Transcriptomic analyses revealed that TSPO expression was markedly upregulated in patients with bacterial infection (n = 52) and exhibited diagnostic potential to distinguish bacterial infection from healthy controls (HCs, n = 16) and viral infection (n = 92). TSPO-correlated genes were enriched in Toll-like receptor (TLR) signaling, inflammatory response, and immunometabolic pathways. Mechanistically, TSPO interacted with TLR4 and selectively modulated TLR4-driven inflammatory activation. TSPO deficiency augmented lipopolysaccharide (LPS) induced tumor necrosis factor‑α (TNF-α) and interleukin‑6 (IL-6) secretion, accompanied by disrupted Ca²⁺ homeostasis, impaired cholesterol balance, and compensatory metabolic remodeling characterized by elevated L-lactate and sustained Adenosine triphosphate (ATP) levels. Collectively, these findings identify TSPO as an immunometabolic regulator bridging TLR4 signaling and metabolic adaptation during inflammatory activation. TSPO represented a promising biomarker and therapeutic target to limit exaggerated inflammatory responses. Full article

Background: Psoriatic arthritis (PsA) is a chronic inflammatory disease frequently associated with obesity and metabolic comorbidities. Increasing evidence suggests that obesity is associated with systemic inflammation, insulin resistance, and adverse clinical outcomes; however, the immunometabolic profile associated with obesity in PsA has not been fully characterized. Objective: To investigate the relationship between obesity, inflammatory biomarkers, cytokine profiles, metabolic parameters, insulin resistance, and disease-related characteristics in patients with PsA. Methods: In this monocentric cross-sectional study, 224 consecutive patients fulfilling the Classification Criteria for Psoriatic Arthritis (CASPAR) for PsA were evaluated. Clinical, inflammatory, metabolic, and cytokine-related variables were analyzed within an integrated immunometabolic framework. Patients were stratified according to obesity status based on body mass index (BMI ≥ 30 kg/m²). Correlation analyses, multivariable regression analyses, and exploratory machine-learning approaches were applied to identify multidimensional patterns associated with obesity. Adjusted multivariable regression analyses were performed to account for available demographic, clinical, comorbidity-related, and therapeutic covariates. Results: Ninety-four patients (42.0%) were classified as obese and 130 (58.0%) as non-obese. Compared with non-obese patients, obese individuals exhibited significantly higher levels of C-reactive protein (CRP; 0.31 vs. 0.13 mg/dL, p < 0.001), erythrocyte sedimentation rate (ESR; 15.0 vs. 10.0 mm/h, p = 0.006), serum amyloid A (SAA; 7.7 vs. 6.4 mg/L, p = 0.008), insulin (8.0 vs. 6.1 μU/mL, p < 0.001), glycated hemoglobin (HbA1c; 38.0 vs. 37.0 mmol/mol, p = 0.003), Homeostasis Model Assessment of Insulin Resistance (HOMA-IR; 1.29 vs. 1.21, p = 0.007), triglycerides (106.0 vs. 85.0 mg/dL, p = 0.019), and Health Assessment Questionnaire (HAQ) scores (p < 0.001). Obese patients also showed a higher prevalence of hypertension (18.1% vs. 6.9%, p = 0.018). BMI was positively correlated with several inflammatory, metabolic, and disease-related variables, including CRP (ρ = 0.383), interleukin-6 (IL-6; ρ = 0.295), insulin (ρ = 0.289), ESR (ρ = 0.245), SAA (ρ = 0.228), HbA1c (ρ = 0.199), HAQ score (ρ = 0.351), and Disease Activity Index for Psoriatic Arthritis (DAPSA) score (ρ = 0.183), while showing an inverse correlation with high-density lipoprotein cholesterol (HDL-C) (ρ = −0.189). After adjustment for age, sex, disease duration, DAPSA, hypertension, type 2 diabetes mellitus, and current therapy class, obesity remained associated with higher CRP and fasting insulin levels and with greater odds of belonging to a higher HAQ category. Machine-learning analyses identified inflammatory biomarkers, insulin resistance indices, and lipid-related parameters as the most informative features associated with obesity-related phenotypes. Conclusions: Obesity in PsA was associated with a broader immunometabolic phenotype characterized by increased inflammatory burden, metabolic dysfunction, and worse functional outcomes. These findings support the integration of metabolic and cardiovascular assessment into routine rheumatology practice and highlight obesity as an important marker of increased immunometabolic and clinical burden in PsA. Although the cross-sectional design precludes causal inference, the observed associations may help identify patients requiring closer metabolic and cardiovascular assessment. Full article

Background/Objectives: Psoriasis is a systemic immune-mediated inflammatory disease associated with endothelial dysfunction and cardiovascular risk. This study evaluated relationships among clinical severity, cytokine activity, systemic vascular resistance, and skin microvascular reactivity in chronic plaque psoriasis before and after therapy. Methods: In this prospective longitudinal study, 34 patients with chronic plaque psoriasis and 19 matched controls were assessed. Patients were examined at baseline and after 12 months of clinically indicated systemic therapy. Psoriasis Area and Severity Index (PASI), serum IL-17A, IL-22, TNF-α, IL-12(p40), IL-10, VEGF-A, total peripheral resistance, and laser Doppler flowmetry post-occlusive reactive hyperemia indices were analysed. Results: PASI decreased markedly after therapy, from 20.6 ± 7.7 to 4.1 ± 5.3, with excellent discrimination between pre- and post-treatment states. IL-17A, IL-22, and IL-12(p40) decreased significantly, while TNF-α remained associated with disease severity. Total peripheral resistance and delayed psoriatic-skin hyperemia persisted and correlated with inflammatory/angiogenic markers, particularly IL-12(p40) and VEGF-A. Conclusions: Long-term therapy improves clinical and cytokine profiles in psoriasis, but vascular dysfunction may persist despite cutaneous improvement. Integrated cytokine–vascular assessment may complement PASI for evaluating systemic inflammatory burden and cardiovascular risk. Full article

Background/Objectives: Obesity is paradoxically associated with iron deficiency despite adequate dietary intake, driven by chronic inflammation and elevated hepcidin. Different dietary patterns may differentially affect iron metabolism in obese individuals, yet comparative evidence remains limited. Methods: We conducted a systematic literature review following PRISMA 2020 guidelines. Four databases (SciSpace, Google Scholar, PubMed) were searched through 2025 using terms related to obesity, iron deficiency, and three dietary patterns: Mediterranean diet, ketogenic diet, and intermittent fasting. Studies were screened using seven predefined criteria (three inclusion, four exclusion) with thresholds of ≥4.0/5.0 for abstract screening and ≥4.5/5.0 for full-text screening. Results: From 396 identified records (SciSpace n = 325, Google Scholar n = 57, PubMed n = 14), 38 studies were included after removing 62 duplicates and screening 334 unique records. Studies without accessible full text were excluded.The Mediterranean diet appears most protective for iron status due to its anti-inflammatory profile (omega-3 fatty acids, polyphenols, vitamin C) and bioavailable iron sources. Ketogenic diets may impair duodenal iron absorption through hepcidin-independent mechanisms and restrict dietary iron diversity. Intermittent fasting shows complex effects, remodeling iron metabolism with increased transferrin and decreased ferritin within physiological ranges. Weight loss per se consistently improves iron status by reducing adipose-driven inflammation and lowering hepcidin. Conclusions: Among the three dietary patterns examined, the Mediterranean diet appears most protective for iron status in obese individuals. The ketogenic diet may pose the highest risk due to restricted dietary iron diversity and potential hepcidin-independent absorption impairment. Direct comparative randomized controlled trials are urgently needed. Clinicians should routinely monitor iron biomarkers, including hepcidin, in obese patients undertaking any dietary intervention. Quantitative biomarker data from the 38 included studies showed serum ferritin reductions of 8–28%, hemoglobin levels remaining within clinically stable ranges, and IL-6 decreases of 15–42% across dietary patterns. Full article

Background/Objectives: Ferritin and soluble interleukin-2 receptor α (sIL-2Rα) are HLH-related biomarkers, but their comparative discrimination in pediatric critical illness is uncertain. We primarily compared their discrimination for adjudicated HLH in hyperferritinemic PICU children and secondarily assessed PICU mortality. Methods: This prospective single-center study enrolled 75 children aged 1 month–18 years with ferritin ≥500 ng/mL: 25 each with HLH, sepsis/septic shock, or other diseases. Both biomarkers were measured from the same admission sample. Research-use sIL-2Rα was reported in ng/mL without cross-calibration to the HLH-2004 U/mL scale; adjudicators were blinded to sIL-2Rα, whereas ferritin informed the reference process. Analyses used ROC, Firth regression, targeted post hoc paired AUC tests with Holm adjustment, bootstrap optimism correction, and cross-validation. Results: For adjudicated HLH, ferritin showed greater discrimination than sIL-2Rα (AUC, 0.898 vs. 0.690; ΔAUC, 0.208; Holm-adjusted p = 0.019). The exploratory 1614-ng/mL ferritin cutoff had 92% sensitivity and 76% specificity. Although sIL-2Rα remained associated with HLH after ferritin adjustment (OR, 1.089 per ng/mL; p = 0.002), adding it did not significantly improve discrimination beyond ferritin (p = 0.663). For secondary mortality, ferritin showed greater discrimination than sIL-2Rα (AUC, 0.754 vs. 0.495; Holm-adjusted p = 0.019). Adding ferritin to PRISM III increased the apparent AUC from 0.725 to 0.811, but the comparison was not statistically significant (p = 0.105); the bootstrap optimism-corrected AUC was 0.800. Conclusions: In this hyperferritinemic PICU cohort, ferritin showed greater discrimination for adjudicated HLH than the studied sIL-2Rα assay, and adding sIL-2Rα did not significantly improve discrimination. Findings should be interpreted in the context of the studied assay and reference process. The exploratory mortality model requires external validation. Full article

Butyl benzyl phthalate (BBP), a widely used endocrine-disrupting chemical, has been associated with reproductive toxicity; however, its long-term effects during aging remain poorly understood. In the present study, we examined the effects of prolonged BBP exposure on the male reproductive system using naturally aged C57BL/6J mice. Mice received BBP at 169 μg/kg/day in drinking water for 10 or 22 months and were analyzed at 24 months of age. No significant differences in body weight, food intake, or water consumption were observed among the experimental groups. Representative gross images showed apparent distension and dark-red discoloration of the seminal vesicles in BBP-exposed aged mice. Compared with Young mice, the BBP-exposed aged groups showed higher expression of IL-1β, IL-6, TNFα, SOD1, and SOD2 and lower CAT expression in the seminal vesicle. H₂DCFDA fluorescence showed a non-significant increasing trend. Because an untreated age-matched Old group was not included in the seminal vesicle analyses, the effects of aging and BBP could not be distinguished. In contrast, the testis showed limited changes in inflammatory cytokine-, antioxidant enzyme-, and steroidogenesis-related gene expression and in H₂DCFDA fluorescence relative to the untreated Old group. Exploratory miRNA sequencing of pooled testicular RNA and comparison with a TM3 Leydig cell dataset identified miR-664-5p as a candidate showing higher relative abundance in both datasets. TargetScan analysis predicted binding sites for miR-664-5p in FOXO1 and FOXO3. In BBP-treated TM3 cells, FOXO3 protein expression was decreased, and FOXO6 expression was increased, whereas FOXO1 showed no consistent dose-dependent change. These molecular findings do not establish direct regulation of FOXO proteins by miR-664-5p or explain the seminal vesicle findings. Full article

Acinetobacter baumannii, particularly colistin-resistant strains, represents a major therapeutic challenge because of multidrug resistance, biofilm formation, and limited treatment options. This study investigated the antibacterial, antibiofilm, immunomodulatory, and therapeutic potential of Withania somnifera ethanolic root extracts (WSEEs) against drug-sensitive (DS) and colistin-resistant (CR) A. baumannii. WSEE exhibited concentration-dependent antibacterial activity, with MIC/MBC values of 125/250 μg/mL against the DS isolate and 250/500 μg/mL against the CR isolate. Time–kill analysis demonstrated bactericidal activity at 250 μg/mL, and WSEE significantly reduced the biomass of preformed biofilms. In cyclophosphamide-induced leukopenic mice, oral administration of WSEE (100 and 200 mg/kg) restored leukocyte counts and significantly reduced pulmonary bacterial burden following infection with both isolates. The higher dose (200 mg/kg) achieved survival rates of 90% and 70% in mice infected with the DS and CR isolates, respectively, compared with 50% and 30% in the corresponding colistin-treated groups. WSEE also significantly decreased serum levels of the pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), indicating attenuation of infection-associated inflammation. Biochemical analyses further showed that WSEE did not produce detectable hepatotoxicity or nephrotoxicity under the experimental conditions. Collectively, these findings demonstrate that WSEE possesses antibacterial, antibiofilm, anti-inflammatory, and immunomodulatory activities and provides therapeutic benefit in experimental A. baumannii infection. These results support the potential of WSEE as a complementary therapeutic strategy against multidrug-resistant A. baumannii, while further mechanistic, pharmacokinetic, and translational studies are needed to validate its clinical potential. Full article