Journal of Inflammation Research最新文献

Purpose: Benign prostatic hyperplasia (BPH) is a common condition in older men, but treatment is often associated with complications and high recurrence rates. Previous clinical studies have shown that Brain Awakening and Mind Opening (BAMO) acupuncture and Simiao Pill can improve lower urinary tract symptoms in patients with BPH. This study explores the potential mechanisms behind these treatment methods for BPH using a mice model.

Methods: Six-week-old ICR male mice were divided into 5 groups (n=10). The Mice were injected subcutaneously with TP (5mg/kg/d) / corn oil (equal volume) for 28 days to establish a BPH model and a control group. After successful modelling, the mice were treated with distilled water for 21 days, while the BAMO acupuncture group, the Simiao pill group, and the mixed group were treated accordingly (BAMO acupuncture at Neiguan (PC6), Sanyinjiao (SP6), and Guanyuan (CV4) acupoints for 30 minutes every other day, or Simiao pill once a day).

Results: BAMO acupuncture, Simiao pills, and their combination effectively reduced prostate hyperplasia in mice. The observed therapeutic effects likely involve multiple mechanisms: suppression of dihydrotestosterone (DHT) synthesis via reduced testosterone levels and downregulated SRD5A2 expression (P<0.01), promotion of prostate cell apoptosis (indicated by an increased BAX/BCL-2 ratio, P<0.05), and mitigation of inflammation through decreased levels of pro-inflammatory cytokines IL-6 and TNF-α (P<0.05).

Conclusion: BAMO acupuncture and Simiao pill can restore normal prostate tissue structure in mice through multiple mechanisms: (1) reducing DHT production; (2) promoting apoptosis; (3) reducing inflammatory responses. Future studies could further investigate the hormonal regulation and apoptosis of BAMO acupuncture in mice.

With 13% of global tumorigenesis related to pathogens and 2.2 million new tumour cases related to viral infections every year, the role played by viruses in tumorigenesis cannot be ignored. At present, the viruses that have been identified as carcinogenic substances are EB virus, hepatitis B virus, hepatitis C virus, Kaposi's sarcoma virus, human immunodeficiency virus type 1, human T-cell lymphotropic virus type 1, human papillomavirus, Merkel cell polyomavirus, and BK virus. There are also a number of viruses which have not been designated as carcinogens, but which are also closely related to the tumours' development, such as Simian virus 40, JC virus and human cytomegalovirus. Human oncolytic viruses are divided into DNA oncolytic viruses and RNA oncolytic viruses, which are highly diverse and have different tumorigenic mechanisms. This article focuses on these confirmed DNA tumor viruses and RNA tumor viruses, delving into the various tumor types they cause and the mechanisms behind them. Based on the comparative analysis of their oncogenic pathways, we conclude that common mechanisms, such as the disruption of tumor suppressor proteins, chronic inflammation, and immune evasion, presenting actionable targets for both prophylactic intervention and precision therapy against virus-associated cancers.

Background and purpose: Chronic atrophic gastritis (CAG), affecting approximately 20-30% in high-risk populations, contributes to significant morbidity and mortality due to its progression to gastric cancer. Despite two decades of research into its pathogenesis, the vast body of literature has not yet been systematically mapped. A comprehensive bibliometric analysis mapping the field's evolution, collaborative networks, and knowledge gaps remains lacking. Therefore, we conduct a 20-year bibliometric analysis (2005-2024) of research on the mechanism of CAG to identify seminal works, emerging themes, evaluate global collaboration networks, and highlight translational challenges and opportunities.

Patients and methods: Data were retrieved from the Web of Science Core Collection (WoSCC) spanning from January 1, 2005, to December 31, 2024. Bibliometric analysis was performed using CiteSpace and VOSviewer to analyze publication trends, influential authors and institutions, keyword clusters, and citation bursts.

Results: A total of 954 papers were identified, with China leading in publication output (41.51%), followed by the USA (15.20%). The USA demonstrated high centrality in international collaboration. Key journals included WORLD J GASTROENTERO and GASTROENTEROLOGY. Prolific authors such as Liu Yuetao and co-cited authors like CORREA P were identified. Keyword analysis revealed "Helicobacter pylori" as the most prominent term, with clusters focusing on traditional Chinese medicine, macrophage biology, and gastric intestinal metaplasia.

Conclusion: The study highlights the significant research output and collaboration in CAG, emphasizing the importance of interdisciplinary approaches and international partnerships. Future research should focus on integrating traditional knowledge with modern mechanistic studies and addressing emerging themes such as microbiome dysbiosis and precision medicine.

Purpose: Chronic low-grade inflammation is increasingly recognized as a contributing factor in the development of cardiovascular events. This study aimed to evaluate the association between time-weighted cumulative exposure to high-sensitivity C-reactive protein (cumhsCRP) and the risk of new-onset cardiac conduction block (CCB).

Patients and methods: A total of 48,703 participants from a prospective community-based cohort were included. The average exposure time for cumhsCRP was 6.36 years. Participants were stratified into two groups: cumhsCRP < 2 mg/L and cumhsCRP ≥ 2 mg/L. The incidence of new-onset cardiac conduction block and its subtypes was identified through standard 12-lead electrocardiograms. Cox proportional hazards models were used to assess the relationship between cumhsCRP levels and incident CCB risk, adjusting for potential confounders. A restricted cubic spline curve further explored the dose-response pattern.

Results: During a mean follow-up period of 9.24 years, 803 cases of new-onset CCB were documented (incidence rate: 1.65%). After full multivariable adjustment, individuals in the cumhsCRP ≥ 2 mg/L group exhibited a significantly higher risk of CCB compared to those with cumhsCRP < 2 mg/L (HR: 1.24, 95% CI: 1.07-1.44). The RCS analysis suggested a linear association between log-transformed cumhsCRP and CCB risk (p for non-linearity = 0.294).

Conclusion: Elevated cumulative exposure to high-sensitivity C-reactive protein is independently associated with an increased risk of developing CCB, especially left bundle branch block and left anterior fascicular block. This study will provide new insights into the prevention of CCB.

Purpose: To explore the mechanism of cuprotosis in psoriasis, screen cuprotosis related genes (PDCRGs) in psoriasis, and provide new targets for precise diagnosis and treatment of psoriasis.

Material and methods: Integrate bioinformatics analysis and experimental validation. Firstly, based on the GEO database (GSE161683, GSE166388, GSE277173), differentially expressed genes (DEGs) and weighted gene co-expression network analysis (WGCNA) in psoriasis were screened; Identification of differential cuprotosis related genes (PDCRGs) in psoriasis using a self built cuprotosis gene database (1098 CRGs); Screen key PDCRGs through PPI network, machine learning, and ROC analysis. Subsequently, a mouse model of psoriasis induced by imiquimod (IMQ) was constructed, and gene expression, copper ion levels, inflammatory factors, and oxidative stress factors were validated using qPCR, Western blot, immunohistochemistry, fluorescence, and ELISA.

Results: Thirty-four PDCRGs were identified, among which STAT1, DLD, GBP1, CXCL10, PDHB, and LIAS are Hub genes. Machine learning and ROC analysis further identified APOL6, CD274, and LIAS as key diagnostic biomarkers. PDCRGs are significantly enriched in the TCA cycle, copper ion transport, and glucose metabolism pathways. The levels of FDX1 and serum copper ions were increased in the skin lesions of psoriasis mice, accompanied by upregulation of TCA cycle key proteins and PDCRGs expression; Copper overload triggers oxidative stress and inflammation cascade.

Conclusion: APOL6, CD274, and LIAS were screened as cuprotosis markers in psoriasis. Overexpression of these PDCRGs in psoriasis model mice can promote copper ion accumulation and interfere with the TCA cycle, increase oxidative stress and inflammation levels, and ultimately lead to the occurrence of psoriasis. Therefore, targeted intervention of cuprotosis is of great significance for the clinical treatment of psoriasis.

Background: Acute pancreatitis (AP) is a common abdominal emergency, often associated with severe complications such as infected pancreatic necrosis (IPN) and the need for surgical intervention. Platelet count dynamics during the course of AP may be linked to disease progression and outcomes.

Purpose: This study aimed to identify clinically meaningful longitudinal platelet count patterns in AP.

Methods: Longitudinal platelet count patterns were derived using group-based trajectory modeling (GBTM). Generalized additive models were used to demonstrate the association between platelet counts and outcomes.

Results: 2225 AP patients are enrolled in the analysis and classified into 5 subclasses using GBTM. Class 1 (n=269) had a low initial platelet count, which increased slowly; Class 2 (n=983) and Class 4 (n=597) had different initial platelet count levels, but fluctuated within the normal range; Class 3 (n=225) and Class 5 (n=151) had different initial platelet count levels, but both increased beyond the normal range. A significantly decreased risk of infected pancreatic necrosis (IPN) is observed in classes 2 (OR 0.3, CI 0.16-0.55) and 4 (OR 0.14, CI 0.06-0.33), but the risk was comparable among classes 1 (ref), 3 (OR 1.25, CI 0.66-2.41), and 5 (OR 0.69, CI 0.28-1.56). The risks of the surgical interventions were similar. However, the 30-day and 90-day mortality rates were significantly lower in classes 2, 3, 4, and 5 than in class 1. Generalized additive models also demonstrated the lowest risk of IPN, surgical intervention, and in-hospital mortality as platelet counts remained within the normal range.

Conclusion: Patients with platelet counts within the normal range had the lowest risk of IPN, surgical intervention, and mortality. Both thrombocytopenia and thrombocytosis indicate an increased risk of IPN and surgical intervention; however, mortality is significantly increased only in patients with thrombocytopenia.

Purpose: Dihydromyricetin (DMY) is known for its wide range of pharmacological effects and has been approved as a dietary supplement. This study aimed to investigate the therapeutic effects of DMY on dextran sulfate sodium (DSS)-induced disruption of intestinal homeostasis in mice and to explore the underlying molecular mechanisms.

Methods: To establish a model of colitis, mice were treated with a 3% DSS solution, followed by gavage administration of DMY for therapeutic intervention. Techniques such as histomorphology, RT-qPCR, 16S rRNA sequencing, and Western blot analysis were used.

Results: DMY alleviated several physiological symptoms in colitis mice, including a reduction in the disease activity index (DAI) and spleen index, as well as decreases in the numbers of white blood cells, lymphocytes, and monocytes. Additionally, DMY helped repair the intestinal mucosal barrier function, reshaped the composition of gut microbiota, and regulated intestinal immune responses. These effects collectively contributed to the partial restoration of intestinal homeostasis in colitis mice. Furthermore, experiments with NLRP3^-/- mice and pseudo-germ-free mice confirmed that DMY exerts its anti-colitis effects through the gut microbiota-NLRP3 inflammasome axis.

Conclusion: DMY helps regulate intestinal homeostasis in colitis mice by suppressing the NLRP3 inflammasome via the gut microbiota. Our study provides new evidence supporting DMY as a potential therapeutic agent for colitis.

Background: Acute pancreatitis (AP) is a common gastrointestinal disease. Systemic inflammatory response syndrome (SIRS), a severe complication of AP, increases the risk of organ failure and progression to severe AP (SAP). Gut microbiota dysbiosis is linked to AP pathogenesis. The aim of this study is to investigate the gut microbiota characteristics of AP patients and their association with SIRS and organ failure.

Methods: Rectal swabs from 19 healthy controls (HC) and 88 AP patients (stratified into non_SIRS, SIRS, low/med/high_sequential organ failure assessment (SOFA) groups) were analyzed using 16S rRNA gene sequencing. Microbiota diversity, composition, and function were evaluated, and random forest diagnostic models were constructed.

Results: Compared with HC, AP (SIRS/non_SIRS) patients had altered clinical indices, reduced gut microbial richness and diversity. As SOFA scores increased, the high_SOFA group exhibited further reductions in richness and diversity. Barplots analysis showed that there were differences in the mainly dominant microbiota between HC and AP (SIRS/non_SIRS) patients. Some differentially abundant genera such as Faecalibacterium, Parabacteroides, Megasphaera, and Fusicatenibacter may be closely associated with the occurrence of AP, development of SIRS, and severity of organ failure. Furthermore, functional pathways like L-isoleucine biosynthesis, lysine biosynthesis, AMPK signaling, and glycogen biosynthesis may also play significant roles in diseases. The random forest models constructed for distinguishing between HC and non_SIRS, as well as for distinguishing between HC and SIRS, showed extremely diagnostic accuracy.

Conclusion: Gut microbiota dysbiosis is correlated with the occurrence of AP, development of SIRS, and severity of organ failure. Specific microbiota taxa and functional pathways may serve as potential therapeutic targets or diagnostic biomarkers for AP, providing a microbial perspective for personalized management of this disease.

Acute myocardial infarction (AMI) remains one of the leading causes of mortality and disability worldwide, involving complex immune and inflammatory responses. Among these, macrophages play a pivotal role as key immune cells. The polarization state of macrophages determines their function in both myocardial injury and repair. In the early phase of AMI, M1 macrophages promote inflammation and facilitate the clearance of necrotic tissue by releasing pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6). However, excessive or prolonged M1 polarization may contribute to myocardial fibrosis and further deterioration of cardiac function. In contrast, M2 macrophages promote tissue repair and anti-inflammatory responses in the later phase by secreting anti-inflammatory cytokines such as interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β), thereby reducing fibrosis and facilitating myocardial remodeling. This review summarizes the dynamic changes in macrophage polarization during AMI and elaborates on their roles in myocardial injury, inflammation, and tissue repair. Furthermore, it highlights recent advances in therapeutic strategies aimed at modulating macrophage polarization to improve AMI outcomes, including mTOR inhibitors, sodium-glucose co-transporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, and gene-editing technologies such as CRISPR/Cas9. Overall, this review underscores the importance of regulating macrophage polarization, particularly the transition from M1 to M2, as a promising therapeutic target for AMI. Modulating macrophage function may provide novel insights into enhancing myocardial repair and preventing adverse cardiac events.

Background: Corynebacterium striatum (CS) is an uncommon but potentially fatal pathogen of infective endocarditis (IE). The literature on the patterns and clinical progression of Corynebacterium striatum infective endocarditis (CSIE) is limited. This article aims to provide insights into the clinical presentation and management of CSIE through a retrospective analysis of documented cases.

Methods: An electronic search was conducted across various databases including PubMed, China National Knowledge Infrastructure (CNKI), China Science and Technology Journal Database, and Wanfang database to identify relevant articles in both English and Chinese literature documenting CSIE. Subsequently, patient-level data were extracted and subjected to analysis.

Results: The systematic search yielded 38 patients from 35 articles. The median age was 68 [IQR 54, 73] years, and 63.2% of patients were men. A history of heart disease was present in 55.3% of cases, while 15.8% had a history of cardiovascular electronic device implantation. The mitral valve was the most commonly affected site, accounting for 52.8%. The misdiagnosis or missed diagnosis rate of CSIE was 28.9%. Microbiological confirmation by 16S ribosomal ribonucleic acid (16S rRNA) or metagenomic next-generation sequencing (mNGS) was present in 13.2% of cases. Vancomycin was the most effective antibiotic, with 41.7% of the CS isolates showing resistance to multiple drugs. Surgical intervention was performed in 55.3% of the CSIE patients, and the overall fatality rate was 37.8%, both of which were higher than those reported in standard IE due to common pathogens such as Staphylococcus aureus (surgical intervention rate 37.8%, fatality rate 22.4%) and viridans streptococci (surgical intervention rate 29.5%, fatality rate 36.6%).

Conclusion: CSIE often presents with nonspecific symptoms, making it prone to misdiagnosis or underdiagnosis. Echocardiography and blood cultures remain the primary diagnostic tools, but advanced approaches such as 16S rRNA and mNGS improve accuracy in pathogen identification. Compared to IE caused by common microorganisms (eg, Staphylococcus aureus, viridans streptococci), CSIE is associated with higher rates of surgical intervention and mortality, underscoring the urgent need for increased clinical vigilance and prompt, targeted management.