Search Results (362)

Andes virus (ANDV) is the only hantavirus with well-documented evidence of person-to-person transmission. However, key parameters related to transmission timing, viral shedding, exposure contexts, and public health management remain incompletely defined. We conducted a systematic review in accordance with PRISMA 2020. MEDLINE/PubMed, Scopus, and Web of Science were searched from database inception up to 14 May 2026. Eligible studies reported epidemiological, virological, clinical, or public health data relevant to ANDV infection, person-to-person transmission, viral shedding, and/or outbreak control. Thirty-three studies, including 17,204 individuals, 2221 laboratory-confirmed ANDV cases, and 135 documented secondary cases, were included. Person-to-person transmission was identified as a primary or co-occurring route in 20 papers. The median incubation period among ANDV cases was 20.8 days, and the median serial interval was 21.8 days (upper bounds near 40 days). Secondary attack rates were higher among sexual and other close contacts. ANDV RNA was consistently detected in blood and occasionally in saliva, respiratory secretions, urine, breast milk, and semen, although RNA detection alone does not necessarily imply infectious virus. Rare reports of culture-confirmed isolation of replication-competent virus support the biological plausibility of transmission via close mucosal or respiratory exposure. Unlike other hantaviruses, Andes virus can spread person to person through close contact, supporting prolonged monitoring and risk-stratified follow-up of high-risk contacts based on ANDV-specific epidemiological evidence. Possible recommendations, including post-discharge counselling regarding possible sexual transmission, remain provisional and require further evidence. Preparedness activities against outbreaks should also be implemented in non-endemic regions, while future research should prioritize prospective contact studies, standardized virological sampling, and genomic confirmation. Full article

Mucosal immunity in the respiratory tract provides the first line of defense against airborne pathogens, yet most current vaccines fail to induce strong and durable immune responses at these sites. Respiratory viruses, including respiratory syncytial virus (RSV), influenza viruses, and coronaviruses, remain major global health threats, in part due to their ability to evade long-term mucosal protection. Although systemic vaccination generates robust circulating immunity, it induces limited local responses, particularly secretory immunoglobulin A (IgA), which is critical for preventing viral entry and transmission at the airway surface. The mechanisms regulating B cell responses within the airway mucosa are not fully understood. B cell–activating factor (BAFF), a member of the tumor necrosis factor (TNF) superfamily, has emerged as an important context-dependent regulator of mucosal B cell immunity. BAFF is produced by airway epithelial cells and multiple myeloid populations, including dendritic cells and neutrophils, and is rapidly induced during respiratory viral infection through type I interferon–dependent pathways. Functionally, BAFF supports B cell survival, differentiation, and class-switch recombination, promoting the generation of antibody-secreting plasma cells and enhancing IgA production. In the lung, these effects align with early, intermediate, and late stages of the response, supporting initial local antibody production, the formation of inducible bronchus-associated lymphoid tissue (iBALT), and the development of tissue-resident memory B cells that sustain long-term immunity. Although BAFF plays an essential role in mucosal immunity, its activity requires tight regulation to maintain immune balance. Current evidence supports BAFF as a promising immunomodulatory component and highlights its potential as an adjuvant platform for enhancing mucosal vaccine efficacy, warranting further investigation as a potential adjuvant in this context. Full article

This study aimed to determine whether intranasal hinokitiol modulates short-term salivary secretory IgA (SIgA) secretion dynamics and IgA antibody-forming cell (AFC) activity in the submandibular glands of aged mice, a model of age-associated mucosal immune decline. Aged BALB/c mice received intranasal hinokitiol (50 μg) once weekly for 4 weeks. Saliva was collected on days 0, 7, 14, and 21 at baseline, 0.5 h, 1.5 h, 3 h, and 6 h after each administration. SIgA levels were measured using an enzyme-linked immunosorbent assay. On day 21, IgA AFCs were enumerated using an enzyme-linked immunosorbent spot assay, and their viability and proliferative activity were assessed using the MTT assay. Salivary SIgA rose transiently after each dose, peaking at 1.5 h and returning to baseline by 6 h. By day 21, baseline SIgA secretion was significantly higher than at day 0, indicating a cumulative effect. IgA AFCs were unchanged in number, but viability and proliferation increased at 0.5 and 1.5 h, coinciding with SIgA peaks. Flow cytometry revealed significant expansion of B220⁺CD38⁺ memory B-cells; B220⁺CD138⁺ plasma cells were unaffected. Intranasal hinokitiol transiently enhances salivary SIgA secretion in aged mice, likely through short-term modulation of salivary gland immune activity. This non-invasive approach may aid mucosal defense in aging populations. These findings suggest that intranasal HNK may represent a novel non-invasive approach for enhancing mucosal immune function during aging and may provide a basis for future preventive strategies against oral and respiratory infections. Full article

Salivary aldehyde dehydrogenases (ALDHs), particularly ALDH3A1, are increasingly recognized as potential contributors to oral defense against aldehyde-associated stress at the oral–environment interface. Unlike freely secreted salivary enzymes, measurable salivary ALDH activity primarily reflects intracellular and vesicle-associated enzymes derived from salivary gland epithelial cells, oral mucosal cells, immune cells, and exfoliated cellular components. Within the oral exposome, ALDHs expressed in oral epithelial and salivary gland tissues participate in the detoxification of reactive aldehydes, while salivary ALDH activity may serve as an indicator of local aldehyde-detoxification capacity and tissue redox status. Beyond aldehyde metabolism, emerging evidence suggests that ALDH-associated pathways are linked to redox regulation, epithelial stress adaptation, inflammatory signaling, and tissue repair through NAD(P)⁺-dependent processes and stress-responsive networks such as Nrf2 and SIRT1. This review provides a saliva-focused synthesis of ALDH biology, emphasizing isoform-specific functions and the potential importance of ALDH3A1 in oral epithelial defense. Altered salivary ALDH activity has been reported in association with oral conditions including periodontitis, oral lichen planus, radiation-induced salivary dysfunction, and oral squamous cell carcinoma (OSCC). Genetic factors, particularly ALDH2 polymorphisms, together with environmental exposures and microbial dysbiosis, may further influence aldehyde burden and oral disease susceptibility. Although current evidence supports the biological relevance of salivary ALDHs, their utility as clinical biomarkers or therapeutic targets remains investigational and requires further mechanistic and clinical validation. Full article

Background: Existing therapies for xerostomia are primarily symptomatic, providing temporary mucosal hydration without addressing underlying pathological changes in the oral cavity. In this context, medicated chewing gums containing ascorbic acid and lysozyme hydrochloride offer a promising approach, combining antimicrobial, antioxidant, and trophic effects with physiological salivary stimulation and prolonged local delivery. Methods: For the development of compressed chewing gum formulation, the physicochemical (particle size distribution, moisture absorption capacity, and microscopic characteristics) and technological (flowability, angle of repose, bulk and tapped density, Carr’s index (CI), and Hausner ratio (HR)) properties of the active substances and their formulations with excipients were evaluated. Pharmacological activity was assessed in an atropine-induced xerostomia rat model. Results: The physical mixture of all components showed inferior flow properties compared with the formulation containing pre-granulated lysozyme hydrochloride, as evidenced by higher Carr’s index and Hausner ratio values (CI = 17, HR = 1.20 vs. CI = 13, HR = 1.14), indicating improved processability after pre-granulation. The effect of relative humidity during formulation was also assessed, with an optimal level of 40% required to ensure process stability due to the hygroscopic nature of the components. Based on these data, technological approaches ensuring processability were established, including wet pre-granulation of lysozyme hydrochloride and premixing of ascorbic acid to reduce oxidation risk. These approaches resulted in an optimized compression mass with excellent flowability (CI = 8, HR = 1.09), suitable for the preparation of medicated chewing gum. An optimal compression force (7 kN) ensured suitable rheological and textural properties, resulting in rapid and nearly complete release of the active ingredients from the medicated chewing gum, consistent with kinetic analysis. In vivo studies using an atropine-induced xerostomia rat model demonstrated that the combination of ascorbic acid and lysozyme hydrochloride significantly increased salivary secretion (2.17-fold vs. control pathology group) and reduced salivary gland mass coefficients (by 13–18% compared with the control pathology group and groups receiving individual active ingredients), alongside improvement of oxidative stress markers, including a reduction in TBA-reactants (by 51.6%) and an increase in catalase activity (by 51.0%). Conclusions: The developed medicated chewing gum showed favorable technological properties, efficient release of active ingredients, and anti-xerostomic activity in vivo, indicating its potential for xerostomia relief and oral health support. Full article

Background/Objectives: Dry eye disease (DED) is a multifactorial ocular surface disorder characterized by tear film instability and decreased tear secretion, largely driven by chronic ocular surface inflammation. Although current therapies primarily target inflammation and tear film stabilization, their clinical efficacy is often limited by insufficient ocular surface retention. In this study, we explored a drug repositioning strategy for DED by developing a nanocrystalline formulation of troxipide (TRO), a gastric mucosal protective agent with cytoprotective properties. Methods and Results: A TRO nanosuspension (TRO-NPs) was successfully prepared by wet bead milling, yielding particles with a mean diameter of approximately 100 nm. Physicochemical characterization revealed that the crystalline structure, solubility, viscosity, pH, and osmolarity of the nanosuspension were comparable with those of the conventional TRO microsuspension (TRO-MPs). In contrast, the TRO-NPs exhibited markedly improved dispersion stability, maintaining particle suspension for at least 1 month after preparation. Repeated topical instillation of the TRO-NPs did not induce corneal toxicity or inflammation in rabbits, and resulted in significantly higher drug retention in the tear fluid than that observed for the TRO-MPs. Furthermore, in an N-acetylcysteine-induced rabbit dry eye model, repetitive instillation of the TRO-NPs significantly increased tear volume and mucin levels, leading to improved tear film stability. Conclusions: These findings demonstrate that nanosuspension-based formulations can enhance ocular surface retention and therapeutic efficacy of TRO. TRO-NPs therefore represent a promising nanomedicine-based repositioned therapy for the treatment of DED. Full article

Background/Objectives: The induction of anti-SARS-CoV-2 antibodies by COVID-19 vaccination reduces morbidity and mortality, but immune responses may be compromised in people living with HIV (PLWH). The aims of the current study were to determine whether viral suppression (VS) or immune reconstitution (IR) in PLWH directly affected their ability to produce effective levels of anti-SARS-CoV-2 antibodies in mucosal secretions or blood induced by vaccination. Methods: Anti-SARS-CoV-2 spike IgG, IgA and secretory IgA (SIgA) antibodies and their avidities were measured by ELISA in HIV-negative healthy controls (HC; n = 49) and PLWH (n = 94) using stimulated oral fluid (SOF) and serum. Frequencies of CD4/CD8 T cells and their expression of exhaustion/senescence were determined by flow cytometry. Cytokine levels were measured by cytokine bead arrays. Results: We showed that higher HIV burden negatively impacted the levels of systemic and mucosal anti-SARS-CoV-2 spike IgG antibodies produced. This differential IgG antibody production was unaffected by IR status, antiretroviral therapy duration or T cell exhaustion/senescence. PLWH elicited higher anti-SARS-CoV-2 spike IgA antibodies both in peripheral blood and oral mucosa and highr secretory IgA (SIgA) antibodies in the oral mucosa. PLWH with higher HIV RNA copies elicited lower IgG avidity but the IgA avidity indices remained unaffected. PLWH expressed higher levels of innate immunity cytokines in the oral mucosa, irrespective of the HIV RNA copies. Conclusions: Significantly fewer breakthrough infections in PLWH compared with HC, along with high IgA/SIgA antibodies and increased innate immunity cytokines in the SOF, suggest a potential role for mucosal immunity in the immunopathogenesis of COVID-19. Full article

Background/Objectives: Sleep deprivation (SD) induces the accumulation of reactive oxygen species (ROS) in the intestine, causing inflammation in the intestine, thereby damaging the intestinal epithelial barrier function. As a traditional Chinese medicine, Dendrobium huoshanense (DHS) modulates intestinal flora, maintains the intestinal mucosal barrier, and promotes gastrointestinal motility and digestive secretion. However, the role and mechanism of DHS in improving SD-induced intestinal injury have not been fully studied. Methods: The SD model was established by subjecting rats to complete SD using a specialised SD instrument. Hematoxylin and eosin (HE) staining was performed to evaluate pathological injury in ileal tissues. Enzyme-linked immunosorbent assay (ELISA) and biochemical methods were used to quantify the main inflammatory cytokines, oxidative stress markers, and hypothalamic–pituitary–adrenal (HPA) axis activity. The expression levels of E-cadherin and Occludin proteins in the ileum tissue were analyzed by Western blotting. Additionally, the pH value of ileal mucus, unit secretion, water content, and dry matter weight were measured. Differential metabolites in rat ileum mucus were profiled using ultra-high-performance liquid chromatography–quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MS). Results: DHS alleviated the pathological injury of the ileum induced by SD. DHS reduced the levels of serotonin (5-HT), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), while increasing interleukin-10 (IL-10) levels, thereby attenuating systemic inflammatory responses. Furthermore, DHS decreased malondialdehyde (MDA) content and elevated glutathione (GSH) and superoxide dismutase (SOD) levels in ileal tissues. DHS also upregulated the protein expression of E-cadherin and Occludin in intestinal tissues. In addition, DHS decreased the pH of ileal mucus, promoted intestinal mucus secretion, and increased dry matter content, facilitating the restoration of the mucus barrier. DHS may alleviate SD-induced ileal injury by modulating steroid hormone biosynthesis. DHS decreased the levels of adrenocorticotropic hormone (ACTH), cortisol (CORT), and corticotropin-releasing hormone (CRH), indicating that DHS suppresses the abnormal activation of the hypothalamic–pituitary–adrenal (HPA) axis. Conclusions: In this study, a comprehensive multi-index evaluation showed that DHS could significantly improve the ileal injury caused by SD in rats. The mechanism involved regulating the balance of serum neurotransmitters and inflammatory factors, reducing oxidative stress in tissues, and improving the physicochemical properties of intestinal mucus. Metabolomic analysis further revealed that these protective effects may be mediated via the regulation of steroid hormone biosynthesis pathways and are associated with the inhibition of abnormal HPA axis activation. Full article

Fermentation is widely used to enhance the bioactivity of herbal phytochemicals through microbial bioconversion. Rehmannia glutinosa contains catalpol, an iridoid glycoside with metabolic and immunomodulatory potential; however, its efficacy in the unfermented form is limited. This study investigated whether fermentation enhances catalpol production and improves metabolic and immune-regulating functions via glucagon-like peptide-1 receptor (GLP-1R) signaling. Rehmannia glutinosa extract was fermented under optimized conditions, and catalpol and iridoid precursor levels were quantified to assess bioconversion efficiency. Biological effects were evaluated in intestinal epithelial cells, macrophages, and an Artemia model, focusing on glucose transport, GLP-1 secretion, dipeptidyl peptidase-4 (DPP-4) expression, mucosal defense, and GLP-1R/protein kinase A/cAMP response element-binding protein (PKA/CREB) signaling. Fermentation significantly increased catalpol content while reducing iridoid precursors. The fermented extract suppressed intestinal glucose absorption by downregulating sodium–glucose cotransporter 1 (SGLT1) and glucose transporter 2 (GLUT2). It also enhanced GLP-1 secretion and reduced DPP-4 expression, leading to activation of GLP-1R/PKA/CREB signaling. This activation increased mucin 2 (MUC2) expression and promoted anti-inflammatory. Full article

Lymphoplasmacytic gastritis (LPG) is one of the most prevalent chronic diseases affecting cheetahs (Acinonyx jubatus) under human care, yet its underlying cause remains unresolved. Gastric inflammation occurs in the majority of adult captive cheetahs but is uncommon in free-ranging populations, suggesting that management-related factors contribute to disease pathogenesis. This review proposes that LPG represents a bile acid-driven gastroenteropathy arising from disruption of the natural feeding ecology of the cheetah. In free-ranging systems, cheetahs consume large episodic meals separated by prolonged fasting intervals and ingest whole-prey containing substantial connective tissue and collagen. In captivity, feeding patterns are typically characterized by smaller, more frequent meals and diets dominated by lean skeletal muscle with reduced structural complexity. I hypothesize that this mismatch alters gastric emptying kinetics, disrupts coordinated pancreatic and biliary secretion, and destabilizes fat digestion. Inefficient lipolysis may impair micelle formation and promote bile acid mislocalization within the gastrointestinal tract, increasing mucosal exposure to hydrophobic bile acids capable of inducing chemical epithelial injury. Within this framework, lymphoplasmacytic gastritis is interpreted as a secondary inflammatory reaction to chronic bile acid-mediated mucosal stress rather than a primary immune-mediated disorder. The model also provides a mechanistic explanation for the frequent coexistence of gastritis with fat and protein maldigestion in captive cheetahs. Differential responses to antimicrobial therapy, glucocorticoids, sulfasalazine, pancreatic enzyme supplementation, and bile acid-modifying agents are broadly consistent with this proposed mechanism. Recognition of LPG as a physiologically driven gastroenteropathy has important implications for management, emphasizing restoration of feast–fast feeding patterns, inclusion of collagen-rich carcass components, and targeted modulation of bile acid composition and signaling. Full article

Fructose, a key component of modern diets, is closely linked to the growing prevalence of pediatric obesity and metabolic alterations. Although numerous studies highlight its systemic consequences, including altered carbohydrate and lipid metabolism and increased cardiovascular risk, the direct impact of fructose, particularly its role in modulating mucin composition, a key determinant of the mucosal barrier, remains poorly explored. This study investigated whether fructose supplementation modifies high-fat diet (HFD)-induced changes in duodenal mucin production and whether these effects vary depending on age in animals. To this end, young and adult mice were fed a normal diet (ND), HFD, or an HFD supplemented with 30% fructose (w/v) in drinking water (HFD+Fru) for 16 weeks. Brunner’s glands and villus goblet cells were then analyzed using conventional histochemistry and a panel of lectins to evaluate possible alterations in intestinal mucus glycosylation. Results showed that both HFD and HFD+Fru significantly increased body weight. In young mice, HFD+Fru induced a compensatory mucosal phenotype characterized by increased villus PAS (Periodic Acid–Schiff) reactivity (2% vs. ND), elevated sialylated mucin secretion rate (SSR) in Brunner’s glands (25% vs. ND) and villi (17% vs. ND), and higher SNA (up to 46% vs. ND) and PNA (up to 39% vs. ND) in villus goblet cells. In contrast, adult mice receiving HFD+Fru exhibited a maladaptive response, characterized by a reduction in villus PAS-positive mucins (6% vs. ND), decreased villus SSR (5% vs. ND), diminished sialylation (up to 43% SNA vs. ND) and GlcNAc (up to 50% reduction in WGA vs. ND) in villus goblet cells, and marked loss of fucosylation in Brunner’s glands (81% vs. ND) and villus goblet cells (66% vs. ND). These results reveal that fructose-enriched HFD remodels duodenal mucin O-glycosylation in an age-dependent manner, suggesting that while young mice exhibit transient adaptive responses, prolonged exposure can deplete these mechanisms, leading to a compromised adult epithelial barrier. This age-specific vulnerability may significantly contribute to the pathogenesis of diet-related intestinal disorders and obesity-related complications in later life, highlighting the need for early dietary interventions. Full article

Porcine β-defensin 2 (pBD2) possesses broad-spectrum antimicrobial properties and is crucial for gastrointestinal mucosal repair. Lactic acid bacteria (LAB) serve as optimal vectors for exogenous protein delivery due to their high biosafety, intestinal colonization capacity, and ability to modulate gut microecology. In this study, we engineered a recombinant Lactobacillus paracasei strain (pPG-N1-pBD2/27-2) that efficiently secretes pBD2. In vitro, this recombinant strain significantly enhanced the proliferation and migration of porcine intestinal epithelial cells (IPEC-J2). In vivo, oral administration of pPG-N1-pBD2/27-2 markedly alleviated dextran sulfate sodium (DSS)-induced colitis in mice. This protective effect was evidenced by reduced Disease Activity Index (DAI) scores, prevention of colon shortening, and decreased colonic activities of myeloperoxidase (MPO) and eosinophil peroxidase (EPO), alongside normalized N-acetyl-β-D-glucosaminidase (NAG) levels. Histopathological analysis revealed that the treatment preserved mucosal architecture, including goblet cells and crypts, and fortified the physical barrier by upregulating tight junction proteins. Mechanistically, the recombinant strain suppressed the colonic iNOS/COX-2 inflammatory axis, decreased serum pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α), and elevated the anti-inflammatory cytokine IL-10. Furthermore, it restored systemic immune homeostasis by normalizing the proportions of splenic macrophages, T/B lymphocytes, and natural killer (NK) cells. In conclusion, pPG-N1-pBD2/27-2 mitigates colitis through a dual mechanism: reinforcing the intestinal physical barrier and rebalancing the innate–adaptive immune axis. These findings highlight the potential of pBD2-engineered probiotics as novel biological therapeutics for intestinal inflammatory diseases. Full article

The gut microbiota serves as a critical interface for host immunity, making it a promising target for probiotic intervention. In this study, we investigated the immunomodulatory potential of the strain Bifidobacterium breve (B. breve) MN15965 and the underlying role of gut bacterial communities in this process. We first assessed its in vitro immunomodulatory activity by measuring nitric oxide and cytokine secretion in THP-1 macrophages. Subsequently, an immunosuppressed mouse model was established by treating BALB/c mice with cyclophosphamide (CTX), a chemotherapeutic agent known to cause immune dysfunction and mucosal damage. In this model, we performed a series of analyses, including H&E staining, measurement of hematological parameters and serum cytokines/immunoglobulins, quantification of fecal short-chain fatty acids (SCFAs) by gas chromatography, and profiling of gut microbiota composition via 16S rRNA gene amplicon sequencing. The results showed that MN15965 supernatant enhanced TNF-α, IL-1β, and GM-CSF secretion in THP-1 cells, promoting M1 macrophage activation in vitro. In the in vivo model, MN15965 administration restored spleen and thymus tissue integrity and improved physiological indices, hematological parameters, and immunoglobulin levels. Furthermore, MN15965 increased fecal SCFAs, particularly butyric and valeric acid, increased gut bacterial diversity, and enriched potentially beneficial SCFA-producing taxa, including Lachnospiraceae and Eubacterium. These findings demonstrate that B. breve MN15965 alleviated CTX-induced immunosuppression by activating immune responses, regulating gut bacterial communities, and boosting SCFA production. Full article

Streptococcus canis is an opportunistic pathogen that colonises the mucosal surfaces and skin of its host. Though predominantly a veterinary pathogen affecting cats and dogs, S. canis has also been identified as the causative agent in severe human disease. IdeC is a secreted cysteine protease of S. canis that has a high specificity for IgG, cleaving at the hinge region. We show here that the protein binds back to the surface of the bacteria. Additionally, the protein contains a conserved Arg-Gly-Asp (RGD) motif, the minimal peptide sequence required for integrin binding. Several bacterial proteins containing RGD motifs have been implicated in adhesion and invasion of host cells. This RGD motif along with the ability of IdeC to bind back to the bacterial surface after secretion is the basis for this study into a potential secondary function of IdeC in adhesion and/or invasion. We used protein-coated latex beads to investigate the interaction of IdeC with epithelial and endothelial cells and, further, the extent to which the RGD motif is involved in this interaction by utilising an RGD->RGE recombinant protein. We also report here that the deletion of IdeC in S. canis results in a significant reduction in invasion into epithelial cells. Full article

Oral mucosal ulcers sustain a persistent inflammatory and oxidative microenvironment that interferes with epithelial repair and delays healing. Although hyaluronic acid (HA) is used in oral wound management due to its biocompatibility and hydrating properties, its biological activity is highly context-dependent and can be compromised under inflammatory conditions. In contrast, N-acetyl-L-cysteine (NAC) is a well-established antioxidant with documented anti-inflammatory effects, yet its rapid clearance limits its effectiveness when applied locally. In this study, the effects of HA and NAC, individually and in combination, on metabolic activity and inflammatory responses of TNF-α–stimulated human gingival keratinocytes were evaluated. In parallel, the individual immobilization of HA or NAC onto plasma-activated decellularized extracellular matrix (dECM) films was investigated as a materials-oriented approach for potential localized intraoral applications. NAC significantly attenuated TNF-α-induced IL-6 and IL-8 secretion, reducing both cytokines by approximately 99%, while preserving keratinocyte metabolic activity. HA displayed limited immunomodulatory effects. The combined HA + NAC condition did not improve the response compared with NAC alone. Plasma treatment enabled stable individual grafting of HA and NAC onto dECM films, and both functionalized surfaces retained chemical stability under saliva-like conditions. Collectively, these findings identify NAC as the most effective anti-inflammatory candidate under the tested cellular conditions and support plasma-functionalized dECM films as a feasible platform for future biological evaluation in intraoral applications. Full article