Chronic Autoimmune Disease Research Articles

Rice Husk Silica Liquid Enhances Autophagy and Reduces Overactive Immune Responses via TLR-7 Signaling in Lupus-Prone Models.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder characterized by widespread inflammation and multi-organ damage. Toll-like receptor 7 (TLR-7) and autophagy have been implicated in SLE pathogenesis. Rice husk silica liquid (RHSL) has shown potential for modulating inflammatory responses, but its effects on SLE have not been thoroughly investigated. This study aims to evaluate the impact of RHSL on immune responses and autophagy in cell culture experiments, focusing on its effects on TLR-7 signaling, cytokine production, and autophagy modulation. RAW264.7 cells and human peripheral blood mononuclear cells (PBMCs) from healthy donors and SLE patients were used. Cells were stimulated with LPS or TLR-7 agonists and treated with RHSL. Cell viability was assessed, and cytokine levels (TNF-α and IL-6) were measured by ELISA. Autophagy-related proteins (LC3II, ATG5-ATG12) were analyzed by Western blotting. The effect of autophagy inhibition was studied using 3-methyladenine (3-MA). A concentration of 100 μg/mL RHSL did not affect cell viability but significantly reduced the TNF-α production in TLR-7 agonist-stimulated RAW264.7 cells (compared to TLR-7 alone, 3.41 ± 0.54 vs. 6.72 ± 0.07 folds) and PBMCs (compared to TLR-7 alone, 0.97 ± 0.19 vs. 1.40 ± 0.33 folds). RHSL enhanced autophagy, as evidenced by increased LC3II (4.35 ± 1.08 folds) and ATG5-ATG12 (7.07 ± 1.30 folds) conjugation in both RAW264.7 cells and SLE patient-derived PBMCs. The reduction in TNF-α production by RHSL was attenuated by 3-MA, indicating that autophagy plays a role in this process. RHSL also inhibited the translocation of phosphorylated NF-κB into the nucleus, suggesting a mechanism for its anti-inflammatory effects. RHSL exhibits potential as an immunomodulatory agent in SLE by enhancing autophagy and modulating TLR-7 signaling pathways. These findings suggest that RHSL could offer therapeutic benefits for managing inflammatory responses in SLE and warrant further investigation into its clinical applications.

Major clinical evidence on the use of low-dose naltrexone in the treatment of cancer: a systematic review

Introduction: Opioid receptors are groups of receptors (γ-, κ-, δ-, and ζ-opioid receptors) that are widely distributed in nerve cells in the brain, spinal cord, and digestive tract. Naltrexone is a type of general opioid receptor antagonist. It has been used to treat chronic pain syndrome, autoimmune diseases, and cancer at a dose of 5 mg/day, which is generally called low-dose naltrexone (LDN). Objective: It was to analyze the pharmacological functions of low-dose naltrexone, especially in anti-inflammation and immunoregulation, and its therapeutic potential against cancer. Methods: The research and development of the work were carried out from June to July 2024 in the Scopus, PubMed, Science Direct, and Scielo databases, using scientific articles from the last 15 years, following the PRISMA rules. The quality of the studies was based on the GRADE and AMSTAR2 instruments, and the risk of bias was assessed using the Cochrane instrument (Funnel Plot). Results and Conclusion: Fifteen studies were included in the systematic review out of 30. Most studies showed homogeneity in their results, with X2=94.5%>50%. Low-dose naltrexone has immunomodulatory and therapeutic effects. Low-dose naltrexone regulates the production of inflammatory cytokines, influencing the level of endogenous opioid peptides in the body. Furthermore, low-dose naltrexone has an antitumor effect and can modulate the neuroblastoma tumor response, delaying the onset and reducing the incidence rate of tumors, significantly decreasing tumor volume and weight, and DNA synthesis in cancer.

Current Landscape and Evolving Therapies for Primary Biliary Cholangitis

Primary Biliary Cholangitis (PBC) is a chronic autoimmune liver disorder characterized by progressive cholestatic that, if untreated, can progress to liver fibrosis, cirrhosis and liver decompensation requiring liver transplant. Although the pathogenesis of the disease is multifactorial, there is a consensus that individuals with a genetic predisposition develop the disease in the presence of specific environmental triggers. A dysbiosis of intestinal microbiota is increasingly considered among the potential pathogenic factors. Cholangiocytes, the epithelial cells lining the bile ducts, are the main target of a dysregulated immune response, and cholangiocytes senescence has been recognized as a driving mechanism, leading to impaired bile duct function, in disease progression. Bile acids are also recognized as playing an important role, both in disease development and therapy. Thus, while bile acid-based therapies, specifically ursodeoxycholic acid and obeticholic acid, have been the cornerstone of therapy in PBC, novel therapeutic approaches have been developed in recent years. In this review, we will examine published and ongoing clinical trials in PBC, including the recently approved peroxisome-proliferator-activated receptor (PPAR) agonist, elafibranor and seladelpar. These novel second-line therapies are expected to improve therapy in PBC and the development of personalized approaches.

Endophytic Fungi: A Treasure Trove of Antifungal Metabolites.

Emerging and reemerging fungal infections are very common in nosocomial and non-nosocomial settings in people having poor immunogenic profiles either due to hematopoietic stem cell transplants or are using immunomodulators to treat chronic inflammatory disease or autoimmune disorders, undergoing cancer therapy or suffering from an immune weakening disease like HIV. The refractory behavior of opportunistic fungi has necessitated the discovery of unconventional antifungals. The emergence of black fungus infection during COVID-19 also triggered the antifungal discovery program. Natural products are one of the alternative sources of antifungals. Endophytic fungi reside and co-evolve within their host plants and, therefore, offer a unique bioresource of novel chemical scaffolds with an array of bioactivities. Hence, immense possibilities exist that these unique chemical scaffolds expressed by the endophytic fungi may play a crucial role in overcoming the burgeoning antimicrobial resistance. These chemical scaffolds so expressed by these endophytic fungi comprise an array of chemical classes beginning from cyclic peptides, sesquiterpenoids, phenols, anthraquinones, coumarins, etc. In this study, endophytic fungi reported in the last six years (2018-2023) have been explored to document the antifungal entities they produce. Approximately 244 antifungal metabolites have been documented in this period by different groups of fungi existing as endophytes. Various aspects of these antifungal metabolites, such as antifungal potential and their chemical structures, have been presented. Yet another unique aspect of this review is the exploration of volatile antifungal compounds produced by these endophytic fungi. Further strategies like epigenetic modifications by chemical as well as biological methods and OSMAC to induce the silent gene clusters have also been presented to generate unprecedented bioactive compounds from these endophytic fungi.

Systemic lupus erythematosus: an unusual presentation of stroke - a case report from Azal hospital, Sana'a, Yemen

Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder characterized by various clinical manifestations and potential multi-organ involvement. It predominantly affects women, with peak incidence during middle age. Case report: This case report describes a 36-year-old female patient who presented with right-sided body weakness, fever, and headache but maintained normal speech. The patient, with a known history of SLE, was diagnosed with an ischemic stroke. Following appropriate fluid resuscitation and medical management, the patient improved. Notably, the patient had a previous ischemic stroke four years ago while on warfarin but without antiplatelet therapy. Conclusion: Our findings suggest that stroke may be an initial presentation of SLE and that warfarin alone may not adequately protect against stroke in this patient population.

Impact of perception of illness on quality of life in juvenile systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that affects multiple organs, notably the skin, joints, and kidneys. The primary goal in managing SLE is to enhance patients' quality of life (QoL). Illness perception can influence QoL in patients with chronic disease. We assessed illness perception in juvenile SLE (jSLE) patients and its effect on patient's and parental QoL. Patients diagnosed with jSLE according to the SLICC 2012 criteria between January and November 2023 were included. Patients' illness perceptions were gaged using the brief illness perception questionnaire (B-IPQ), while patient's and parental QoL were evaluated using PedsQL and WHOQOL- BREF, respectively. The study comprised 32 patients and 32 parents, predominantly female (78.1%). Musculoskeletal involvement was the most common (65.6%), followed by mucocutaneous (59.4%), renal, and hematological involvement (50% each). Neuropsychiatric involvement was absent. The median SLEDAI-2K score at the last outpatient clinic visit, which was documented in the patient's file was 2 (0-18) and was not correlated with the B-IPQ score (r = 0.121, p = .51). A significant negative correlation was found between B-IPQ and patient QoL, indicating poorer QoL in patients with negative illness perceptions (r = -0.576, p < .001). No correlation was observed between parental QoL and B-IPQ (p => .05). Of note, 56.3% of patients had poor QoL, scoring below the PedsQL cut-off, while 43.8% of parents had poor QoL for general health, scoring below the WHOQOL-BREF cut-off for general health. Although disease perception did not correlate with disease activation in jSLE, it significantly impacted patient QoL. Enhancing patients' perceptions of jSLE may improve their overall QoL.

Changes and significance of Th1/Th2 and Treg/Th17 cells and their cytokines in patients with alopecia areata

BackgroundAlopecia areata (AA) is a chronic autoimmune disease. Th1/Th2 and Treg/Th17 cells and their cytokines are implicated in AA, and we explored their clinical significance in AA. MethodsAA patients and healthy people (controls) were enrolled, with their Th1/Th2/Th17/Treg cell proportion changes and serum Th1 (INF-γ)/Th2 (IL-5, IL-6)/Th17 (IL-17, IL-22)/Treg (IL-35) cytokine levels assessed. AA patients were assigned into mild, moderate and severe alopecia according to Severity of Alopecia Tool (SALT). The relationship between alopecia severity and initial onset age, disease course, family/smoking/drinking history and sleep disorders was explored. Th1/Th2 and Treg/Th17 cells and their cytokine levels in AA patients with different severity levels were compared. The correlation between cytokine levels and SALT scores was analyzed using Spearman. Additionally, the changes of serum cytokine levels in inactive/active AA patients were compared. ResultsAA patients differed from controls in family history/smoking history/drinking history/sleep disorders. Peripheral blood Th1/Th2/Th17 cell proportions and INF-γ/IL-5/IL-6/IL-17/IL-22 levels increased, while Treg cell proportions and IL-35 level dropped. With higher alopecia severity, the proportions of Th1, Th2 and Th17 cells increased, and Treg cell proportion decreased. AA patients with mild/moderate alopecia had significant differences in IL-17 level. Serum INF-γ, IL-5, IL-17 and IL-22 levels were elevated, and IL-35 level dropped in severe AA patients versus moderate AA patients. ConclusionTh1/Th2/Th17 cell proportions and serum INF-γ/IL-5/IL-6/IL-17/IL-22 levels in AA patients were up-regulated, while Treg cell proportion and IL-35 level were repressed. SALT scores were positively-correlated with serum IL-5/IL-17 levels. SALT scores were negatively-correlated with serum IL-35.

The Role of Mesenchymal Stem Cells in Modulating Adaptive Immune Responses in Multiple Sclerosis.

Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system, leading to significant disability through neurodegeneration. Despite advances in the understanding of MS pathophysiology, effective treatments remain limited. Mesenchymal stem cells (MSCs) have gained attention as a potential therapeutic option due to their immunomodulatory and regenerative properties. This review examines MS pathogenesis, emphasizing the role of immune cells, particularly T cells, in disease progression, and explores MSCs' therapeutic potential. Although preclinical studies in animal models show MSC efficacy, challenges such as donor variability, culture conditions, migratory capacity, and immunological compatibility hinder widespread clinical adoption. Strategies like genetic modification, optimized delivery methods, and advanced manufacturing are critical to overcoming these obstacles. Further research is needed to validate MSCs' clinical application in MS therapy.

Cancer Stem Cell Marker CD147 Expression in Erosive Oral Lichen Planus Compared to Moderately and Severely Dysplastic Leukoplakia

Oral lichen planus is a frequent, chronic autoimmune disease that affects the oral mucosa and is characterized as an oral potentially malignant disorder. The aim of our study is to examine the presence of CSCs bearing CD147 (a marker related to local inflammation and associated with various cancers) through immunohistochemistry in oral lichen planus (OLP) compared to oral leukoplakia (OL) and healthy tissues. These findings could contribute to clinical practice by providing a marker for the prognostic assessment of OLP lesions with regards to their potentially malignant nature. The study sample consisted of paraffin-embedded oral mucosa specimens from the archives of the Department of Oral Medicine/Pathology, School of Dentistry, Aristotle University of Thessaloniki, Greece during the period 2009–2019. The study sample contained 24 cases of OLP (14 erosive and 10 reticular) and 30 cases of oral leukoplakia, which were compared to 5 normal oral epithelium samples derived from healthy epithelium adjacent to fibromas from other cases. Cell membrane staining of CD147 was observed mostly in the basal and parabasal cell layer. The statistically significantly higher expression of CD147 in the erosive lichen planus subgroup than in the moderately and severely dysplastic leukoplakia subgroup (p = 0.01) constituted the most important finding of this study. The characteristic expression of CD147 in erosive OLP suggests the presence of epithelial cells with CSC characteristics, but its lower expression in oral leukoplakias suggests a more intense relation of the CD147 marker with inflammation rather than with oral dysplastic progression.

Impact of Lifestyle Interventions on Multiple Sclerosis: Focus on Adipose Tissue.

Multiple sclerosis (MS) is a chronic autoimmune disorder characterized by demyelination in the central nervous system (CNS), affecting individuals globally. The pathological mechanisms underlying MS remain unclear, but current evidence suggests that inflammation and immune dysfunction play a critical role in the pathogenesis of MS disease. Adipose tissue (AT) is a dynamic multifunctional organ involved in various immune diseases, including MS, due to its endocrine function and the secretion of adipokines, which can influence inflammation and immune responses. Physical activity represents an efficacious non-pharmacological strategy for the management of a spectrum of conditions that not only improves inflammatory and immune functions but also directly affects the status and function of AT. Additionally, the exploration of nutritional supplementation represents an important field of MS research aimed at enhancing clinical symptoms and is closely tied to the regulation of metabolic responses, including adipokine secretion. This review, therefore, aims to elucidate the intricate relationship between lifestyle and MS by providing an overview of the latest published data about the involvement of AT and the main adipokines, such as adiponectin, leptin, and tumor necrosis factor α (TNFα) in the pathogenesis of MS. Furthermore, we explore whether physical activity and dietary management could serve as useful strategies to improve the quality of life of MS patients.

Endoplasmic reticulum's role in multiple sclerosis, exploring potential biomarkers, and pioneering therapeutic strategies: a comprehensive review of literature.

Multiple Sclerosis (MS) is a complex and chronic autoimmune disease that affects the central nervous system. Inflammation and demyelination characterize it, which results in a range of neurological impairments. The increasing worldwide occurrence of MS, affecting an estimated 2.8 million individuals in 2020, highlights the urgent requirement for further research to tackle the significant impact it has on individuals and healthcare systems globally. In this study, we wanted to explore the complex function of the endoplasmic reticulum (ER) in the origin, development, and resolution of MS, emphasizing its importance in neuroinflammatory illnesses. The ER has become a central focus in comprehending the pathogenesis of MS. Upon reviewing the literature, we observed a lack of thorough analysis that explores the involvement of endoplasmic reticulum stress in multiple sclerosis. Thus, we aimed through this research to examine the correlations between ER stress and its influence on immunological dysregulation, demyelination, and neurodegeneration in MS. Based on the latest clinical trials, we suggested theories that explore possible biomarkers linked to ER stress and the unfolded protein response. Identifying molecules that are suggestive of early stages of illness and can serve as prognostic tools for improving our understanding of the heterogeneity of MS and offering novel approaches for managing the disease. Finally, through our comprehensive search, we wanted to offer a plan for future research, suggesting new and creative methods for managing MS and encouraging the creation of specific treatments that aim to reduce the impact of MS on individuals worldwide.

Vitamin D in Primary Sjogren's Syndrome (pSS) and the Identification of Novel Single-Nucleotide Polymorphisms Involved in the Development of pSS-Associated Diseases.

Sjögren's syndrome (SS) is a chronic autoimmune disorder characterised by lymphocytic infiltration of the exocrine glands, which leads to dryness of the eyes and mouth; systemic manifestations such as arthritis, vasculitis, and interstitial lung disease; and increased risks of lymphoma and cardiovascular diseases. SS predominantly affects women, with a strong genetic component linked to sex chromosomes. Genome-wide association studies (GWASs) have identified numerous single-nucleotide polymorphisms (SNPs) associated with primary SS (pSS), revealing insights into its pathogenesis. The adaptive and innate immune systems are crucial to SS's development, with viral infections implicated as environmental triggers that exacerbate autoimmune responses in genetically susceptible individuals. Moreover, recent research has highlighted the role of vitamin D in modulating immune responses in pSS patients, suggesting its potential therapeutic implications. In this review, we focus on the recently identified SNPs in genes like OAS1, NUDT15, LINC00243, TNXB, and THBS1, which have been associated with increased risks of developing more severe symptoms and other diseases such as fatigue, lymphoma, neuromyelitis optica spectrum disorder (NMOSD), dry eye syndrome (DES), and adverse drug reactions. Future studies should focus on larger, multi-ethnic cohorts with standardised protocols to validate findings and identify new associations. Integrating genetic testing into clinical practise holds promise for improving SS management and treatment strategies, enabling personalised interventions based on comprehensive genetic profiles. By focusing on specific SNPs, vitamin D, and their implications, future research can lead to more effective and personalised approaches for managing pSS and its complications.

Enhanced Association of Novel Cardiovascular Biomarkers Fetuin-A and Catestatin with Serological and Inflammatory Markers in Rheumatoid Arthritis Patients.

Rheumatoid arthritis (RA) is a chronic autoimmune disease associated with increased cardiovascular disease (CVD) risk and mortality. This work aimed to evaluate the serum levels of the novel CV biomarkers fetuin-A (fet-A), Dickkopf-1 (DKK-1), galectin-3 (Gal-3), interleukin-32 (IL-32), and catestatin (CST) in RA patients and their associations with RA parameters and CVD markers. A cohort of 199 RA patients was assessed for traditional CVD risk factors, RA disease activity, and biomarker levels. Carotid ultrasound was used to measure carotid intima-media thickness (cIMT) and carotid plaque presence (cPP). Multivariate analyses examined correlations between biomarkers and RA parameters, serological markers, and CVD markers. Adjusted models showed that elevated CST expression levels were associated with rheumatoid factor (RF) and anti-citrullinated protein antibody (ACPA) positivity (OR = 2.45, p = 0.0001 and OR = 1.48, p = 0.04, respectively) in the overall cohort and for RF in men and women, respectively. In addition, fet-A concentration was inversely associated with the erythrocyte sedimentation rate (ESR) in the overall cohort (β = -0.15, p = 0.038) and in women (β = -0.25, p = 0.004). Fet-A levels were also negatively correlated with disease activity (DAS28-ESR) scores (β = -0.29, p = 0.01) and fibrinogen concentration (β = -0.22, p = 0.01) in women. No adjusted associations were observed for Gal-3, DKK-1 or IL32 concentration. The study revealed no significant associations between the biomarkers and cIMT or cPP. The measurement of CST and fet-A levels could enhance RA patient management and prognosis. However, the utility of biomarkers for evaluating CV risk via traditional surrogate markers is limited, highlighting the need for continued investigations into their roles in RA.

Non-coding RNA and its network in the pathogenesis of Myasthenia Gravis.

Myasthenia Gravis (MG) is a chronic autoimmune disease that primarily affects the neuromuscular junction, leading to muscle weakness in patients with this condition. Previous studies have identified several dysfunctions in thymus and peripheral blood mononuclear cells (PBMCs), such as the formation of ectopic germinal centers in the thymus and an imbalance of peripheral T helper cells and regulatory T cells, that contribute to the initiation and development of MG. Recent evidences suggest that noncoding RNA, including miRNA, lncRNA and circRNA may play a significant role in MG progression. Additionally, the network between these noncoding RNAs, such as the competing endogenous RNA regulatory network, has been found to be involved in MG progression. In this review, we summarized the roles of miRNA, lncRNA, and circRNA, highlighted their potential application as biomarkers in diagnosing MG, and discussed their potential regulatory networks in the abnormal thymus and PBMCs during MG development.

Assessment of hepcidin in Egyptian patients with rheumatoid arthritis and its relation to anemia: a single-center study

BackgroundRheumatoid arthritis (RA) is a chronic systemic autoimmune inflammatory disorder characterized by synovial inflammation that leads to joint damage, bony erosions, and related deformities. Between 30 and 70% of RA patients will experience anemia. Early detection of anemia is of great importance. This study aimed to evaluate the serum level of hepcidin (HEP) in RA patients and to assess its relation to disease activity and anemia. The current cross-sectional study included 44 cases with RA in addition to 44 healthy controls. The disease activity in the RA patient was assessed by using the disease activity score (DAS) 28 score-CRP. The serum levels of HEP and ferritin were assessed in both groups using enzyme-linked immunosorbent assay (ELISA) technique.ResultsHepcidin level in the RA group was statistically significantly higher as compared to the control group (p = 0.001). The prevalence of Anemia of chronic disease (ACD) was 40.9%, and iron deficiency anemia (IDA) was 27.3% which accounted for 68.2% of the total anemia cases. The HEP level was statistically significantly higher in the RA patients with ACD than those without anemia (P = 0.028), RA patients with IDA (P < 0.001), and control group (P < 0.001). There was a statistically significant positive correlation between HEP level and serum ferritin level (p = 0.005). HEP level was significantly and inversely correlated with hemoglobin (Hb) in patients with ACD. Serum HEP level is higher in RA patients with high disease activity than those with moderate activity, low activity, and patients in remission (p = 0.380). However, the difference was not statistically significant. The best cutoff point of HEP level to identify RA patients from healthy controls was > 355.5 Pg/ml. This point showed moderate sensitivity (70.5%) with moderate specificity (63.6%) with a statistically significant value.ConclusionsWe found the anemia, and particularly ACD, is more common in RA patients. In RA patients with ACD, serum HEP levels were considerably higher. Although serum HEP showed no diagnostic significance when it came to evaluating disease activity, it could be a dependable non-invasive biomarker for the diagnosis of various forms of anemia in RA patients.

Antirheumatic Drugs : Mechanisms, Therapeutic Efficacy, and Clinical Considerations in Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a chronic autoimmune disease that causes inflammation and damage to joints and other tissues. Antirheumatic drugs, including disease-modifying antirheumatic drugs (DMARDs), biologic agents, and non-steroidal anti-inflammatory drugs (NSAIDs), play a crucial role in the treatment and management of RA. This review examines the mechanisms of action, clinical efficacy, and adverse effects of these drugs. We also explore emerging therapies and future directions for RA management, highlighting the importance of individualized treatment strategies to improve patient outcomes while minimizing potential risks.

Chronic disease associated with bullous pemphigoid risk: A systematic review and meta-analysis

BackgroundBullous pemphigoid (BP) is a chronic autoimmune blistering disease prevalent in elderly, often accompanied by renal comorbidities. Immune dysregulation can lead to secondary BP and increased mortality rates in those already diagnosed. MethodsA literature review identified studies on the association between kidney disease and other comorbidities with BP. Pooled effect estimates were analyzed utilizing a random-effects model. ObjectiveTo assess comorbidity risks with BP and determine mortality risk among BP patients with comorbidities. ResultsAnalysis included 45,323 BP patients from 49 studies. Kidney diseases were significantly linked to higher BP incidence (SDHR 1.51, 95% CI: 1.10-2.07) and increased mortality (HR 1.62, 95% CI: 1.13-2.32). Cerebrovascular diseases, dementia, and diabetes also showed significant associations with both increased BP incidence and mortality (p < 0.05). However, cardiovascular diseases and malignancy were only associated with increased mortality among BP patients (p < 0.001), without affecting BP incidence (p = 0.785 and p = 0.792, respectively). LimitationThe study comprises mostly case-control, prospective, and retrospective observational studies, alongside data heterogeneity. ConclusionThis study reveals the association of several chronic conditions including kidney diseases with BP, contributing to elevated mortality rates. The findings emphasize the importance of management targeting both BP and associated comorbidities to improve patient outcomes.

Dysregulation of miR-223, miR-146a, and miR-193a Expression Profile in Acute and Chronic Phases of Experimental Autoimmune Encephalomyelitis in C57BL/6 Mice.

Multiple sclerosis (MS) is a chronic autoimmune disease with an unknown etiology. The purpose of this research was to assess miR-223, miR-146a, and miR-193a in acute and chronic phases of experimental autoimmune encephalomyelitis (EAE) mice to consider the possible role of these genes in the pathogenesis of MS. EAE induction was given by myelin oligodendrocyte glycoprotein peptide on female C57BL/6 mice. Clinical scores and other criteria were followed daily until day 21 for the acute group and day 77 for the chronic group. At the end of the course, inflammation and demyelination of the central nervous system (CNS) were assessed by histological analysis. MicroRNA expression levels were assessed by real-time PCR. EAE development attenuated in the chronic group, and histological analysis showed less infiltration and demyelination in the chronic group compared to the acute group. The upper expression of miR-223 is demonstrated in the acute phase of EAE. Moreover, the expression levels of miR-146a and miR-193a decreased in the chronic phase of EAE. MiR-223 showed a highly coordinated elevation in the acute phase both in vivo and in vitro. MiR-146a shares a pathway with miR-223 through effecting IL-6 expression. Further studies are needed to reveal their impact on EAE and possible applications as drug targets and biomarkers.

Potential Application of Plant-Derived Compounds in Multiple Sclerosis Management.

Multiple sclerosis (MS) is a chronic autoimmune disorder characterized by inflammation, demyelination, and neurodegeneration, resulting in significant disability and reduced quality of life. Current therapeutic strategies primarily target immune dysregulation, but limitations in efficacy and tolerability highlight the need for alternative treatments. Plant-derived compounds, including alkaloids, phenylpropanoids, and terpenoids, have demonstrated anti-inflammatory effects in both preclinical and clinical studies. By modulating immune responses and promoting neuroregeneration, these compounds offer potential as novel adjunctive therapies for MS. This review provides insights into the molecular and cellular basis of MS pathogenesis, emphasizing the role of inflammation in disease progression. It critically evaluates emerging evidence supporting the use of plant-derived compounds to attenuate inflammation and MS symptomology. In addition, we provide a comprehensive source of information detailing the known mechanisms of action and assessing the clinical potential of plant-derived compounds in the context of MS pathogenesis, with a focus on their anti-inflammatory and neuroprotective properties.

Diagnostic Biomarkers of Microvascular Complications in Children and Adolescents with Type 1 Diabetes Mellitus-An Updated Review.

Type 1 diabetes mellitus (T1DM) is regarded as the most chronic autoimmune disease affecting children and adolescents that results from a destruction of pancreatic β-cell and leads to insulin insufficiency and persistent hyperglycemia (HG). Children and adolescents with T1DM are at an increased risk of developing microvascular complications, including diabetic nephropathy (DNE), diabetic retinopathy (DR), and diabetic neuropathy (DNU). The risk factors and prevalence of these complications differ greatly in pediatric studies. Screening for T1DM microvascular complications undergoes different stages and it is recommended to identify early symptoms and clinical signs. The identification of biomarkers in T1DM microvascular complications is needed to provide optimal treatment. Despite several studies on early biomarkers for DNE in children, the potential biomarkers for predicting DR and DNU have not been completely illustrated. This review fills this gap by identifying biomarkers of T1DM microvascular complications in children and adolescents through searches in the PubMed/Medline database.