Search Results (8,193)

In recent years, an increasing amount of research has investigated the impact of chronic inflammation on the development and progression of both neurological and psychiatric disorders, including epilepsy, depression, schizophrenia, and bipolar disorder. Moreover, growing attention is being paid to how inflammatory processes contribute to disease mechanisms, influence symptom severity, and interact with pharmacological treatments in these conditions. Changes in the levels of inflammatory biomarkers, such as cytokines and C-reactive protein, may signal the early stages of neurological disorder development. Furthermore, specific biomarker profiles have been identified for individual diseases, and chronic treatment may affect their blood levels. Over the last two decades, significant progress in the study of inflammatory biomarkers in psychiatric disorders and epilepsy has been achieved, demonstrating an association between biomarkers with symptoms, a potential prognostic role, and possible use in personalising therapy. Furthermore, widely used methods for biomarker evaluation, such as immunoenzymatic assays and flow cytometry, remain essential tools for current research. Despite numerous indications of the importance of inflammation in psychiatry and neurology, the available studies are characterised by considerable heterogeneity in terms of both population selection and methodology. Based on the available data, inflammatory biomarkers represent a promising diagnostic and therapeutic tool for epilepsy and psychiatric disorders. Although existing studies suggest a correlation between inflammation and the symptoms of various disorders, inconsistent results highlight the need for further research to enable wider implementation of these findings in psychiatric and epilepsy practice. Advancing knowledge of inflammatory biomarkers is essential for improving treatment outcomes and promoting the development of targeted interventions. Full article

Pediatric asthma and allergic rhinitis are prevalent chronic inflammatory diseases ruled by complex interactions among genetic, environmental, and nutritional factors. Zinc, an essential trace element, plays a crucial role in immune modulation, oxidative stress regulation, and epithelial barrier maintenance, all of which are significant in the context of allergic airway diseases. This review aimed to explore and synthesize current evidence on the biological mechanisms and clinical implications of zinc in pediatric asthma and allergic rhinitis. A comprehensive literature search was conducted through PubMed and the Cochrane Library for studies published between 2015 and 2025. Eligible studies included observational and interventional research focused on zinc status or supplementation in children with asthma or allergic rhinitis. Numerous observational studies and meta-analyses indicated reduced circulating zinc levels in children with asthma, often correlating with poor symptom control, increased oxidative stress, and lower pulmonary function. In allergic rhinitis, zinc depletion in nasal mucosa was associated with elevated local inflammation, although paradoxical increases in zinc concentrations have been observed in nasal secretions during active disease. Interventional trials in pediatric asthma populations showed that zinc supplementation may improve clinical symptoms, reduce inflammation, and enhance lung function, although the results were inconsistent and limited by methodological variability. In conclusion, zinc plays a multifactorial role in modulating immune responses and maintaining mucosal health in pediatric allergic airway diseases. While zinc supplementation holds promise as a safe and accessible adjunctive therapy, further high-quality randomized controlled trials are needed to define its clinical utility and establish evidence-based guidelines. Full article

Oxidative stress is one of the key elements in lung-related complications such as cystic fibrosis, acute lung injury, pulmonary hypertension, bronchopulmonary dysplasia, chronic airway diseases, lung cancer, COVID-19, and many others. Antioxidant and anti-inflammatory therapy can be considered as supportive alternatives in their management. However, most naturally derived antioxidants face issues with poor aqueous solubility and stability, which hinder their clinical utility. Remarkably, local pulmonary delivery circumvents the severe limitations of oral delivery, including hepatic first-pass metabolism and organ toxicity, and enables a higher drug payload in the lungs. Here, in this review, we present cyclodextrin as a potential drug carrier for pulmonary administration, exploring the possibilities of its surface modification, complexation with other drug transporters, and loading of cannabidiols, siRNA, and antibodies as future trends. However, the lack of a robust physiological model for assessing the efficacy of lung-oriented drug targeting is a significant concern in its path to clinical and commercial success. Full article

Current therapies for inflammatory bowel disease (IBD), such as olsalazine and cyclosporine, often exhibit limited long-term efficacy and are associated with adverse effects. Cannabidiol (CBD), a non-psychoactive phytocannabinoid, shows promise for its anti-inflammatory properties, though its effectiveness as a monotherapy remains inconclusive. This study investigates the therapeutic potential of combining low-dose CBD (10 mg/kg) with olsalazine (50 mg/kg) or cyclosporine (2.5, 5 mg/kg) in dextran sulphate sodium (DSS)-induced acute and chronic colitis models in mice. Disease severity was assessed via disease activity index (DAI), colon morphology, cytokine and chemokine expression, myeloperoxidase (MPO) activity, systemic inflammatory markers, and glucagon-like peptide-1 (GLP-1) regulation. Safety evaluations included haematology and plasma biochemistry. DSS-treated mice showed elevated DAI scores, colon shortening, heightened inflammation, and organ enlargement. Combination therapies significantly ameliorated colitis, reducing DAI, MPO activity, and inflammatory cytokines, while restoring colon length and GLP-1 levels—without inducing liver or kidney toxicity. These findings demonstrate that combining a low dose of CBD with standard IBD drugs enhances therapeutic efficacy while minimizing side effects, supporting its integration into future combination strategies for more effective and safer IBD management. Full article

Chronic obstructive pulmonary disease (COPD) is a heterogeneous syndrome with multiple clinical and inflammatory phenotypes. The coexistence of bronchiectasis, known as bronchiectasis–COPD overlap (BCO), identifies a subgroup with increased morbidity and mortality. Non-invasive breath analysis using electronic noses (e-noses) has shown promise in identifying disease-specific volatile organic compound (VOC) patterns (“breathprints”). Our aim was to evaluate the ability of an e-nose to differentiate between COPD and BCO patients, and to assess its utility in detecting inflammatory endotypes (neutrophilic vs. eosinophilic). In a monocentric, prospective, real-life study, 98 patients were enrolled over nine months. Forty-two patients had radiologically confirmed BCO, while fifty-six had COPD without bronchiectasis. Exhaled breath samples were analyzed using the Cyranose 320 e-nose. Principal component analysis (PCA) and discriminant analysis were used to identify group-specific breathprints and inflammatory profiles. PCA revealed significant breathprint differences between BCO and COPD (p = 0.021). Discriminant analysis yielded an overall accuracy of 69.6% (AUC 0.768, p = 0.037). The highest classification performance (76.8%) was achieved when distinguishing eosinophilic COPD from neutrophilic BCO. These findings suggest distinct inflammatory profiles that may be captured non-invasively. E-nose technology holds potential for the non-invasive endotyping of COPD, especially in identifying neutrophilic BCO as a unique inflammatory entity. Breathomics may support early, personalized treatment strategies. Full article

There is growing interest in the use of natural plant-derived compounds, such as polyphenols (including curcumin), flavonoids, silymarin, anthocyanins, lutein, and zeaxanthin, for the treatment of age-related macular degeneration (AMD). These substances exhibit antioxidant, anti-inflammatory, and protective effects on retinal cells, contributing to the preservation of retinal integrity by modulating the key pathogenic mechanisms of AMD, including oxidative stress, chronic inflammation, and pathological neovascularization. Consequently, they hold potential to support conventional therapeutic approaches and slow disease progression. Current studies highlight their promising role as adjunctive agents in AMD management. This literature review provides a comprehensive analysis of the potential role of the aforementioned natural plant-derived compounds in the prevention and supportive treatment of age-related macular degeneration. It also discusses their natural sources, modes of administration and supplementation, and highlights the importance of a nutrient-rich diet as a key factor in maintaining ocular health. Furthermore, the review synthesizes current scientific knowledge on the ability of natural antioxidants to slow the progression of AMD and outlines future research directions aimed at improving diagnostic methods and developing more effective preventive and therapeutic strategies. Full article

Ozone pollution is a significant public health problem due to its association with chronic diseases. This study examines the effects of repeated exposure to low doses of ozone on intestinal barrier function in rats. Seventy-two male Wistar rats were divided into six groups. The control group was exposed to normal air, while the ozone groups received a dose of 0.25 ppm for four hours daily for periods of 7, 15, 30, 60, and 90 days, respectively. After treatment, the duodenum, jejunum, and colon were removed and analyzed by biochemical assays, Western blot, immunohistochemistry, and histological techniques. The results indicated an increase in oxidized lipids and structural alterations in the duodenum and jejunum after 7 days of ozone exposure. The result showed changes in haptoglobin, IL-1β, and IL-6. In addition, increased immunoreactivity varied according to intestinal structure and the duration of ozone exposure in the duodenum, jejunum, and colon. In conclusion: Ozone exposure causes an increase in proinflammatory cytokines that leads to a loss of regulation of the immune response in the duodenum, jejunum, and colon of rats, as well as structural changes that alter the intestinal barrier and perpetuate a state of chronic inflammation characteristic of inflammatory bowel diseases. Full article

Atherosclerosis is a multifactorial, chronic inflammatory disorder characterized by the progressive accumulation of plaque within the arterial wall. Recent research has highlighted the pivotal role of bioactive peptides in modulating vascular homeostasis and inflammation. Among these, salusin-α and salusin-β have emerged as critical regulators of atherogenesis. These peptides are generated via differential proteolytic processing of preprosalusin: an amino acid precursor encoded by the torsin family 2 member A gene. Despite their common origin, salusin-α and salusin-β exhibit divergent biological activities. Salusin-β promotes vascular inflammation by enhancing oxidative stress, activating the nuclear factor kappa B signaling pathway, and upregulating proinflammatory cytokines as well as adhesion molecules, and it also facilitates foam cell formation by increasing the expression of acyl-CoA/cholesterol acyltransferase 1 and scavenger receptors, thereby contributing to plaque progression. In contrast, salusin-α appears to exert protective, anti-inflammatory, and anti-atherogenic effects by increasing the expression of the interleukin-1 receptor antagonist and inhibiting key proinflammatory mediators. Additionally, these peptides modulate the proliferation of vascular smooth muscle cells and fibroblasts, with salusin-β promoting cellular proliferation and fibrosis via calcium and 3′,5′-cyclic adenosine monophosphate-mediated pathways, while the role of salusin-α in these processes is less well defined. Altered plasma levels of salusins have been correlated with the presence and severity of atherosclerotic lesions, suggesting their potential as diagnostic biomarkers and therapeutic targets. This review provides a comprehensive overview of biosynthesis, tissue distribution, and dual roles of salusins in vascular inflammation and remodeling, emphasizing their significance in the pathogenesis and early detection of atherosclerotic cardiovascular disease. Full article

Osteoarthritis (OA) is a multifactorial joint disease traditionally characterized by cartilage degradation, while growing evidence underscores the critical role of synovial fibrosis in driving disease progression. The synovium exhibits pathological remodeling in OA, primarily due to the phenotypic transition of fibroblast-like synoviocytes (FLSs) into myofibroblasts. This fibroblast–myofibroblast transition (FMT) results in excessive deposition of extracellular matrix (ECM) and increased tissue stiffness and contractility, collectively contributing to chronic inflammation and fibrotic stiffening of the joint capsule. These fibrotic changes not only impair synovial function but also exacerbate cartilage degeneration, nociceptive sensitization, and joint dysfunction, thereby amplifying OA severity. Focusing on the frequently overlooked role of the FMT of synovial fibroblasts in OA, this review introduces the biological characteristics of FLSs and myofibroblasts and systematically examines the key molecular pathways implicated in OA-related FMT, including TGF-β, Wnt/β-catenin, YAP/TAZ, and inflammatory signaling cascades. It also discusses emerging therapeutic strategies targeting synovial fibrosis and FMT and considers their implications for the clinical management of OA. By highlighting recent advances and unresolved challenges, this review provides critical insights into the fibroblast–myofibroblast axis as a central contributor to OA progression and a promising therapeutic target for modifying disease trajectory. Full article

Background/Objectives: Vitamin C is frequently used in several dietary supplements due to its proposed health-promoting properties, while phenolic compounds and especially flavonoids have been suggested to provide synergistic antioxidant and cardiovascular benefits. However, the specific interactions between these compounds and their individual contributions to biological activity remain underexplored. This study aimed to evaluate the antioxidant potential and anti-inflammatory and antiplatelet biological effects of a high-dose (1 g) vitamin C–low-dose (50 mg) bioflavonoid (VCF)-based supplement using both in vitro and in vivo approaches in human platelets. Methods: Total phenolic content was quantified and antioxidant capacity was assessed using DPPH, FRAP, and ABTS assays and compared to individual phenolic standard compounds, including (simple phenolics like gallic acid, flavonoids like quercetin and catechin, and polyphenols like curcumin and tannin), and a standard supplement containing only high-dose vitamin C (VC). ATR-FTIR spectroscopy was used to assess molecular interactions between vitamin C and flavonoids. In vitro anti-inflammatory and antiplatelet activities of all supplements and standards were assessed by quantifying their IC₅₀ values against ADP, PAF, and thrombin-induced platelet aggregation. The in vivo evaluation of the efficacy and synergy of VCF supplement versus VC was achieved by a two-arm clinical study in healthy volunteers by quantifying their platelet reactivity, which was measured via EC₅₀ values on the aforementioned platelet agonists (PAF, ADP, and Thrombin) before (t = 0) and after receiving either solely VC or VCF supplementation for four weeks. Results: From all phenolic standards, the flavonoids and especially a mixture of flavonoids (catechin + quercetin) showed higher in vitro antioxidant capacity and anti-inflammatory and antiplatelet efficacy, followed by polyphenols and then simple phenolics. The VCF supplement showed the most potent antioxidant capacity, but also the strongest anti-inflammatory and antiplatelet activities too, in comparison to the VC and the mixture of flavonoids, suggesting higher synergy and thus bio-efficacy as a result of the co-presence of flavonoids and vitamin C in this supplement. Platelet reactivity decreased over time for PAF and thrombin in both arms of the trial, but no significant differences were observed between treatment groups, suggesting that the number of flavonoids used was not sufficient to translate the in vitro findings to the in vivo setting. Conclusions: VC-containing supplements provide antioxidant, anti-inflammatory, and antiplatelet benefits, while the incorporation of flavonoids may provide synergistic health benefits, but more in vivo assessment is needed to fully evaluate the dose efficacy. Full article

Background/Objectives: The potential of probiotics and postbiotics as adjunctive or alternative therapies for periodontal disease, which is characterized by chronic inflammation and alveolar bone loss, is gaining increasing attention. In this study, we aimed to elucidate the impact of postbiotic Lactococcus lactis HY449 and Streptococcus thermophilus HY9012 on key cellular processes implicated in the pathogenesis of periodontitis. Methods: THP-1 cells were polarized into M1 macrophages by exposure to Porphyromonas gingivalis lipopolysaccharide in the presence of postbiotics, i.e., heat-killed forms of HY449 or HY9012. The effect of postbiotics on the differentiation of bone marrow-derived macrophages into osteoclasts was analyzed using tartrate-resistant acid phosphatase staining. An in vivo mouse model of ligature-induced periodontitis was used to assess changes in periodontal tissues. Results: The combination of postbiotic L. lactis HY449 and S. thermophilus HY9012 synergistically modulated macrophage polarization by significantly suppressing pro-inflammatory M1 markers and enhancing anti-inflammatory M2 markers. Additionally, postbiotic HY449 and HY9012 inhibited osteoclast differentiation, downregulating the expression of key osteoclastogenic genes and master transcription factors of osteoclast differentiation. In a mouse model of ligature-induced periodontitis, co-treatment with postbiotic HY449 and HY9012 demonstrated synergistic effects in reducing alveolar bone loss. Conclusions: The present findings support the use of postbiotic HY449 or HY9012 as adjunct treatments for the management of periodontitis. Full article

Ankylosing spondylitis (AS) is a chronic inflammatory disease characterized by axial skeletal involvement and systemic metabolic changes. While inflammation is central to its pathophysiology, the potential role of thyroid hormones, particularly free triiodothyronine (FT3), in disease risk and activity remains underexplored. The objective of this study is to evaluate the relationship between serum FT3 levels and both the presence and clinical activity of AS, while also examining other endocrine-metabolic parameters. In this cross-sectional study, 120 AS patients and 117 healthy controls were assessed. Demographic, anthropometric, hematologic, and biochemical parameters were recorded. Disease activity was determined using the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), with BASDAI ≥ 4 indicating active disease. Logistic regression models adjusting for age, sex, BMI, and other relevant covariates were applied to identify independent predictors. FT3 levels were significantly lower in AS patients compared to controls (3.25 [3.01–3.58] vs. 3.44 [3.16–3.69] pg/mL, p = 0.037) and in patients with BASDAI ≥ 4 versus BASDAI < 4 (3.20 [2.94–3.48] vs. 3.44 [3.19–3.83] pg/mL, p = 0.004). The reduction was more evident in women, where it reflected disease presence, whereas in men it was associated with high disease activity. Low FT3 independently predicted both AS (OR 0.50, 95% CI 0.28–0.92, p = 0.026) and active disease (OR 0.48, 95% CI 0.24–0.99, p = 0.047). Lower HDL-C, BMI, and creatinine, and higher leukocyte counts were also associated with AS, but not with disease activity. Low-normal FT3 is independently associated with both the presence and activity of AS, reflecting disease presence in women and disease activity in men. This is the first study to demonstrate this sex-specific association after adjusting for metabolic parameters and multiple covariates, highlighting FT3’s potential as a marker of inflammation-driven metabolic dysregulation. Full article

Background: Chronic eosinophilic pneumonia (CEP) is a rare inflammatory lung disease typically responsive to glucocorticoids, but is prone to relapse and, in some cases, progressive deterioration. A subset of patients develops fibrosing CEP, a distinct phenotype characterized by irreversible parenchymal remodeling and declining lung function, for which no standard treatment exists. Although biologic therapies targeting interleukin-5 (IL-5) are effective in relapsing CEP, their role in fibrosing forms remains unclear. Case Presentation: We report the case of a 43-year-old man with idiopathic CEP initially treated with systemic glucocorticoids, which were discontinued due to severe adverse effects. Despite subsequent therapy with inhaled steroids and azathioprine, the disease relapsed and progressed to a fibrosing phenotype, as confirmed by radiologic and functional assessments. An off-label treatment with subcutaneous mepolizumab, 100 mg, every 4 weeks was started. After eight months of therapy, the patient achieved clinical stability, improved lung function, and the radiologic stabilization of fibrotic changes, without the need for any further treatment with a corticosteroid. Conclusions: This is, to the best of our knowledge, the first documented case of fibrosing CEP treated with an anti-IL-5 monoclonal antibody, highlighting its potential role as a steroid-sparing agent and immunomodulator even in the fibrotic phase of disease. Further research is warranted to define the place of biologics in the management of CEP with a fibrosing evolution and possible combinations with antifibrotic drugs. Full article

We describe the first use of phage therapy in Canada for the treatment of a life-threatening periprosthetic joint infection (PJI), with successful outcome. PJI is a devastating complication of joint replacement surgery, with high morbidity and mortality. Our patient presented with early sepsis from a chronic recalcitrant multidrug-resistant (MDR) Staphylococcus epidermidis hip PJI which had repeatedly failed standard therapy. She had previously undergone 10 operations of the right hip, and only three weeks after completing a prolonged course of daptomycin following her most recent hip revision, she developed a draining sinus tract. Given the high burden of disease, inability to achieve surgical source control, and lack of antibiotic treatment options for long-term suppressive therapy, bacteriophage (phage) therapy was pursued. The patient underwent irrigation and debridement with complex flap reconstruction: intraoperative tissue cultures again yielded MDR S. epidermidis. We developed a novel phage therapy protocol for this patient, with twice daily, intra-articular and intravenous (7 × 10⁹ PFU/dose) phage delivery over a planned 14-day course. Complete healing of the wound with cessation of drainage occurred within one month after treatment. A marked improvement in right hip pain and mobility occurred within three months after treatment. Twelve months following phage treatment, there is normalization of serum inflammatory markers with diminished pain, increased mobility, and no recurrent surgery. Our patient continues to improve and is currently living independently at home, with sustained clinical control of infection. Full article

Background/Objectives: Cardiovascular disease (CVD) remains one of the leading causes of death worldwide, with several well-established risk factors. Among dermatological conditions, psoriasis is a well-known contributor to cardiometabolic risk, while lichen planus (LP) remains an underexplored chronic inflammatory disorder in this context. This study aimed to comparatively assess the prevalence and clinical patterns of metabolic syndrome (MetS) components in patients with LP versus psoriasis and healthy controls, focusing on the intrinsic inflammatory burden in patients not receiving systemic therapy. We also examined whether specific clinical subtypes of LP carry distinct metabolic profiles. Methods: We conducted a cross-sectional observational study at a tertiary dermatology center between January 2020 and December 2024. A total of 236 adult patients were included: 78 with LP, 79 with psoriasis, and 79 controls with minor dermatological conditions. Demographic, clinical, and laboratory data were collected. LP subtypes (cutaneous, mucocutaneous, reticular oral, erosive oral) were evaluated using the Lichen Planus Activity Index (LPAI) and Oral Lichen Planus Clinical Index (OLP-CI); psoriasis severity was assessed using the Psoriasis Area and Severity Index (PASI). Cardiometabolic comorbidities were assessed according to established guidelines. Results: LP patients showed significantly higher prevalence of hypertension (OR 1.94, p = 0.044) and type 2 diabetes mellitus (OR 3.09, p = 0.015) compared to controls. Compared to psoriasis, LP was associated with a higher prevalence of mixed dyslipidemia (OR 3.41, p = 0.033), while psoriasis showed more abdominal obesity (OR 0.35, p = 0.003). Mucosal LP subtypes, especially erosive and reticular oral LP, were linked to elevated cardiometabolic risk. Conclusions: LP, particularly its oral subtypes, is associated with a distinct cardiometabolic risk profile comparable to or exceeding that of psoriasis. These findings support the need for systematic metabolic screening in LP patients as part of comprehensive care. Full article