Search Results (10,616)

Background: Excess adiposity induces low-grade inflammation, including increased C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α). Green tea contains epigallocatechin gallate (EGCG), with anti-inflammatory potential. EGCG metabolism is influenced by individual variations in catechol-O-methyltransferase (COMT) genotypes. Objectives: To evaluate the effect of green tea extract (GTE) supplementation on circulating inflammatory cytokines among postmenopausal women with overweight or obesity and differing COMT genotypes. Methods: This study is a secondary analysis of a random subset (N = 97) from the Minnesota Green Tea Trial (MGTT), a randomized double-blinded placebo-controlled trial. The intervention was a high-dose GTE supplement (843 ± 44 mg EGCG/day) or placebo for 1 year. Serum CRP, TNF-α, and IL-6 were measured at 0, 6, and 12 months. Absolute changes in inflammatory cytokines from baseline to month 12 were evaluated using linear mixed-effects models adjusted for age, body mass index (BMI), smoking history, physical activity, and vitamin supplement use. Results: The changes from month 0 to month 12 were not statistically different between the groups for any of the inflammatory cytokines measured. The overall treatment effect was not statistically significant for CRP (p = 0.24), IL-6 (p = 0.59), TNF-α (p = 0.36), nor for the interaction between treatment group and time (all Ps > 0.40). There was no significant interaction between treatment group and COMT genotype for the stated markers. Conclusions: A high-dose GTE supplement consumed daily for one year did not significantly decrease inflammatory cytokines among postmenopausal women with overweight or obesity. The COMT genotype did not modify the effects of GTE supplementation on inflammatory cytokines. Future studies with a larger sample size among those at high risk of systemic inflammation are warranted. Full article

Foot-and-mouth disease virus (FMDV) infection elicits sustained, high-level interleukin-10 (IL-10) secretion in cattle and pigs, which correlates with lymphopenia and immunosuppression. We previously showed that macrophages are the principal source of IL-10 during FMDV infection in mice, but the viral trigger and host pathways remained unknown. In the present study, we examined whether the FMDV structural protein VP3 regulates IL-10 expression. To this end, a eukaryotic VP3 expression vector was transfected into porcine alveolar macrophages (3D4/21 cells), and IL-10 expression together with related signaling pathways was interrogated by qRT-PCR, ELISA, Western blot, co-immunoprecipitation (Co-IP), confocal microscopy, and luciferase reporter assays. The results showed that VP3 significantly increased IL-10 mRNA and protein levels (p < 0.001) in a time-dependent manner. Mechanistically, VP3 promoted phosphorylation of PI3K, AKT, and mTOR; this effect was abolished by the PI3K inhibitor LY294002, which also abrogated VP3-induced IL-10 secretion (p < 0.05). Furthermore, VP3 upregulated mRNA expression of STAT3, ATF1, and CREB (p < 0.05) and enhanced IL-10 promoter activity. The STAT3 inhibitor Stattic reduced IL-10 secretion by 22% (p < 0.05). Co-IP and confocal microscopy confirmed direct binding of VP3 to PI3K in the cytoplasm. In conclusion, FMDV VP3 induces IL-10 overexpression by directly activating the PI3K/AKT-mTOR signaling pathway, thereby elucidating a key mechanism of FMDV-induced immunosuppression. Full article

Background/Objectives: Chronic obstructive pulmonary disease (COPD) remains a major global health problem, affecting over 300 million people worldwide. Its high morbidity and mortality rates impose substantial psychosocial and financial burdens on patients and healthcare systems. In the emergency setting, managing acute exacerbations of COPD (AECOPD) poses a major clinical challenge, as these patients often present with multi-organ dysfunction secondary to hypoxia and hypercapnia. Identifying reliable prognostic biomarkers could improve early risk stratification, guide therapeutic decisions, and enhance patient outcomes. Methods: This multicenter, prospective, observational study aims to evaluate the prognostic significance of several novel biomarkers—resistin, club cell secretory protein 16 (CC16), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), S100β protein—alongside conventional markers such as N-terminal-pro–B-type-Natriuretic-Peptide (NT-proBNP), D-dimer, high-sensitivity troponin I (hs-cTnI), C-reactive protein (CRP), and procalcitonin in patients with AECOPD admitted to the Emergency Department (ED). Blood samples will be collected at admission. The novel biomarkers (resistin, CC16, IL-6, TNF-α, S100β) will be measured using standardized ELISA kits, while conventional biomarkers (NT-proBNP, troponin I, CRP, procalcitonin) will be analyzed using routine automated clinical laboratory methods. Correlations between biomarker levels, clinical and imaging data, severity scores (GCS, SOFA, CFS, Ottawa COPD Risk Scale, DECAF, BAP-65), and short-term outcomes (hospital discharge status and 28-day survival) will be assessed. The study has received approval from the Ethics Committee of the “Iuliu-Hatieganu” University of Medicine and Pharmacy, Cluj-Napoca, and all participating hospitals. Written informed consent will be obtained from all participants or their legal representatives. Results: This study protocol does not report results, as data collection and analysis are ongoing. Conclusions /Expected Impact: By identifying novel biomarkers with prognostic and pathophysiological relevance, this research aims to inform the development of early risk stratification tools and support future evidence-based approaches to the management of critically ill COPD patients in the ED. Full article

Obesity plays a crucial role in the progression of insulin resistance and type 2 diabetes which are related to inflammation and liver disease. GATA-3 is a transcription factor that is involved in adipogenesis and inflammation. Therefore, it could be a potential therapeutic target for obesity-associated metabolic disorders. This study aimed to examine the effects of GATA-3 suppression on body weight, fat depot redistribution, liver histopathology, and inflammatory markers in transgenic db/db obese mice. Male db/db mice received subcutaneous injections of GATA-3-specific DNAzyme (hgd40; 10 or 100 µg/mL), pioglitazone (as a positive control), or vehicle only (as a negative control), twice weekly for two weeks. Body weight, organ weights, liver histopathology, mRNA expression of selected genes and serum cytokine levels were assessed. GATA-3 expression was not region specific, and its suppression did not significantly affect fat depot distribution or organ weights. However, the low dose of hgd40 accelerated body weight gain transiently. It also increased Il10 mRNA expression in the liver and significantly increased IL-10 protein concentration in the serum. In addition, a high dose of hgd40 resulted in a marked decrease in hepatocyte ballooning degeneration. These findings suggest that GATA-3 suppression may modulate inflammation and liver injury in obesity, warranting further investigation into its therapeutic potential for obesity-related metabolic disorders. Full article

Inflammation plays a pivotal role in the pathogenesis of acute coronary syndromes (ACS), contributing to plaque instability, thrombosis, and myocardial injury. This review aims to comprehensively examine the inflammatory mechanisms underlying ACS and evaluate current and emerging anti-inflammatory therapeutic strategies. We conducted a comprehensive literature review examining the role of inflammatory pathways in ACS pathophysiology, including innate and adaptive immune responses, key inflammatory mediators, and cellular mechanisms. We analyzed current evidence for anti-inflammatory therapies and their clinical outcomes in ACS management. Inflammatory processes in ACS involve complex interactions between innate immune cells (neutrophils, macrophages, monocytes) and adaptive immune cells (T lymphocytes, B cells). Key mechanisms include neutrophil extracellular trap (NET) formation, macrophage polarization, T cell subset imbalances (Th1/Th17 predominance with regulatory T cell dysfunction), and complement activation. Inflammatory biomarkers such as C-reactive protein, interleukin-6, and NET-specific markers demonstrate prognostic value. Anti-inflammatory therapies including colchicine, canakinumab (IL-1β inhibition), and methotrexate have shown cardiovascular benefits in clinical trials. Emerging targets include NET inhibition, T cell modulation, and precision inflammatory profiling approaches. Inflammation represents a critical therapeutic target in ACS beyond traditional risk factor modification. While colchicine and IL-1β inhibition have demonstrated clinical efficacy, future strategies should focus on precision medicine approaches targeting specific inflammatory pathways based on individual patient profiles. Integration of anti-inflammatory therapy with lipid management and antithrombotic strategies offers promise for improving ACS outcomes through comprehensive targeting of the multifactorial pathophysiology underlying coronary artery disease. Full article

Background/Objectives: There is no definitive consensus regarding the effects of melatonin on cardiometabolic risk factors (CMRFs). This systematic review and dose–response meta-analysis of randomized controlled trials (RCTs) evaluated the impacts of melatonin supplementation on CMRFs, including anthropometric, lipid, glycemic, inflammatory, oxidative, and liver function parameters. Methods: A systematic search across multiple databases retrieved 63 eligible RCTs published up to October 2025. Results: This random-effects meta-analysis indicated that melatonin supplementation significantly reduced hip circumference (weighted mean difference (WMD): −1.18 cm, 95% confidence interval (CI): −2.28, −0.08), systolic blood pressure (WMD: −2.34 mmHg, 95% CI: −4.13, −0.55), fasting blood glucose (WMD: −11.63 mg/dL, 95% CI: −19.16, −4.10), low-density lipoprotein cholesterol (WMD: −6.28 mg/dL, 95% CI: −10.53, −2.03), total cholesterol (WMD: −6.97 mg/dL, 95% CI: −12.20, −1.74), C-reactive protein (WMD: −0.59 mg/L, 95% CI: −0.94, −0.23), malondialdehyde (WMD: −1.54 μmol/L, 95% CI: −2.07, −1.01), tumor necrosis factor-alpha (WMD: −1.61 pg/mL, 95% CI: −2.31, −0.90), interleukin-6 (WMD: −6.43 pg/mL, 95% CI: −10.72, −2.15), and alanine aminotransferase (WMD: −2.61 IU/L, 95% CI: −4.87, −0.34). Supplementation with melatonin substantially increased serum total antioxidant capacity (WMD: 0.15 mmol/L, 95% CI: 0.08, 0.22) and high-density lipoprotein cholesterol (WMD: 2.04 mg/dL, 95% CI: 0.50, 3.57). No significant effects of melatonin were observed on body weight, waist circumference, body fat percentage, body mass index, fasting insulin, homeostasis model assessment of insulin resistance, hemoglobin A1c, triglycerides, diastolic blood pressure, aspartate aminotransferase, or gamma-glutamyl transferase. Conclusions: Melatonin supplementation significantly ameliorated multiple CMRFs. Full article

Chronic HBV infection remains a global health challenge, driving liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Liver injury is primarily mediated by host immune responses rather than direct viral cytotoxicity. Macrophages, including Kupffer cells, play dual roles in antiviral defense and disease progression. HBV skews macrophages toward an M2-like, immunosuppressive phenotype, promoting viral persistence and fibrogenesis via cytokines such as Interleukin (IL)-10 and Transforming growth factor-beta (TGF-β). Therapeutic strategies targeting macrophage polarization, including Toll-like receptor (TLR) agonists, immune checkpoint inhibitors, and nanoparticle-based systems, are under investigation. Addressing macrophage heterogeneity and the immunosuppressive hepatic microenvironment using advanced models is essential. Modulating macrophages offers a promising avenue to control HBV, restore immune balance, and mitigate liver injury. This review highlights the central role of macrophages in chronic HBV infection and explores emerging therapeutic strategies. Full article

Background/Objectives: This study aimed to evaluate the pharmacokinetics (PK), effectiveness, and safety of the direct interleukin-6 (IL-6) inhibitor olokizumab (OKZ) in adolescent patients with active polyarticular juvenile idiopathic arthritis (pJIA) who had an inadequate response or intolerance to methotrexate (MTX). Methods: We analyzed results from an open-label, single-arm trial of OKZ therapy at a dose of 64 mg every 4 weeks for 24 weeks. We evaluated pharmacokinetic (PK) parameters, clinical effectiveness, serum C-reactive protein (CRP) dynamics, and adverse events (AEs). Results: Sixteen patients were included in the study, of whom 13 (81.2%) received OKZ through Week 24. The PK profile was consistent with observations in adults with rheumatoid arthritis (RA). By Week 16, 12 (80%) patients achieved an ACRpedi30 response, 11 (73.3%) achieved an ACRpedi50 response, and 2 (13.3%) reached inactive disease status. This response was sustained through Week 24, and no disease flares were observed. A trend toward a better response was noted among patients with baseline CRP > 10 mg/L, higher baseline IL-6, and those naïve to biologic DMARDs. Twelve patients (75.0%) experienced twenty-three mild or moderate AEs. Infections were the most frequent AEs (in 6 patients, 37.5%). No serious AEs or deaths occurred. Conclusions: OKZ treatment reduced pJIA disease activity and was well tolerated. The safety profile was consistent with that of other IL-6 inhibitors, and the PK profile matched that seen in adult RA patients. Full article

Nanoemulsions (NEs) offer a promising strategy for delivering lipophilic cannabidiol (CBD) to protect skin from particulate matter (PM)-induced damage. In this study, CBD-loaded oil-in-water NEs based on Brij^® O10 (polyoxyethylene (10) oleyl ether) and olive oil were prepared by the phase inversion temperature (PIT) method and characterized. A 20% w/w Brij^® O10 formulation (B20) remained clear and stable for 30 days. CBD solubility was markedly enhanced in Brij^® O10 micelles and further increased in NEs, exceeding theoretical predictions and indicating synergistic solubilization in the oil–surfactant system. CBD incorporation lowered the PIT and induced nonlinear changes in droplet size with oil content. All formulations exhibited nanoscale droplets by dynamic light scattering and transmission electron microscopy, moderately low zeta potentials consistent with nonionic steric stabilization, and maintained physical stability despite increased turbidity at higher oil levels. In a full-thickness human ex vivo skin model exposed to PM, both blank and CBD-loaded NEs reduced interleukin-6 (IL-6) and matrix metalloproteinase-1 (MMP-1) in PM-exposed skin, with CBD-loaded NEs providing additional reductions and uniquely restoring procollagen type I C-peptide (PIP) relative to their blanks. Overall, PIT-based CBD NEs enhance CBD solubilization and protect human ex vivo skin from PM-induced inflammation and extracellular matrix degradation. Full article

Background/Objectives: Acetaminophen (paracetamol or APAP) overdose is a major cause of acute liver injury mediated by oxidative stress, inflammation, and hepatocellular necrosis. The present study investigates the in vivo hepatoprotective potential of morin (M), lignin nanoparticles (LN), and morin-encapsulated lignin nanoparticles (LMN) against APAP-induced hepatotoxicity in mice. The specific goal was to determine whether LMN could strengthen hepatic antioxidant and anti-inflammatory defenses prior to toxic insult, which aligns with a prophylactic model rather than a post-injury clinical rescue approach. This study was guided by the primary hypothesis that LMN pretreatment would markedly reduce APAP-induced hepatic injury. Methods: Experimental groups included control, APAP, M, LN, LMN, M+APAP, LN+APAP, and LMN+APAP treatments. Serum hepatic biomarkers, oxidative stress parameters, and inflammatory cytokines were analyzed to assess protective responses. Results: APAP exposure markedly elevated aspartate aminotransferase (AST) and alkaline phosphatase (ALP) levels, indicating severe hepatic dysfunction, accompanied by increased lipid peroxidation and pro-inflammatory cytokine production. LMN+APAP treatment significantly restored hepatic enzyme levels to approximately normal values and suppressed malondialdehyde (MDA) formation, while enhancing superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities. LMN also downregulated interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), and interleukin 1β (IL-1β), while upregulating interleukin 10 (IL-10), suggesting effective attenuation of inflammatory signaling. Correlation analyses demonstrated positive interactions between MDA, cytokines, and hepatic enzymes, whereas antioxidant enzyme levels were inversely correlated with liver injury markers. Histopathological analysis revealed that treatment with LMN enhanced hepatoprotection, demonstrating predominantly mild, reversible lesions and suggesting a synergistic antioxidant and immunomodulatory effect. Conclusions: It could be concluded that LMN provided superior hepatoprotection compared to M or LN. These findings establish LMN as a promising bio-based nanotherapeutic agent for mitigating drug-induced hepatotoxicity through coordinated antioxidant and anti-inflammatory mechanisms. Full article

Atopic dermatitis (AD) is a chronic inflammatory skin disease in which barrier impairment, immune dysregulation, and gut–skin dysbiosis intersect, prompting growing interest in probiotics as microbiota-modulating adjuncts. We conducted a narrative review of peer-reviewed articles indexed in PubMed, Scopus, and Google Scholar, restricted to publications from 1 January 2018 to 31 October 2025 (searches last run in December 2025). Eligible evidence included randomized controlled trials (RCTs), observational studies, and mechanistic or conceptual reviews addressing microbiome alterations and microbiota-modulating interventions in AD. Most pediatric RCTs using multistrain, Lactobacillus-dominant formulations (often combined with Bifidobacterium) reported modest improvements in AD severity and pruritus and in selected barrier- and inflammation-related biomarkers. However, direct cutaneous microbiome “restoration” outcomes were reported in a minority of studies, and most clinical evidence relies on clinical endpoints and gut–skin axis plausibility rather than longitudinal skin microbiome readouts. Single-strain regimens showed inconsistent effects, and evidence in adolescents and adults remained heterogeneous. Mechanistically, probiotics may enhance short-chain fatty acid (SCFA) signaling, dampen toll-like receptor 2/4 (TLR2/4)-nuclear factor kappa B (NF-κB) activation, and promote interleukin-10 (IL-10)- and transforming growth factor-β (TGF-β)-driven tolerance. Probiotics are a biologically plausible adjunct targeting the gut–skin axis in AD and are generally well tolerated; however, heterogeneity across trials, limited follow-up, inconsistent adverse-event reporting, and scarce skin microbiome endpoints preclude firm clinical recommendations. Full article

This study evaluated the protective effects of naringin (NG) against intestinal injury in 7-day-old piglets infected with porcine epidemic diarrhea virus (PEDV). Eighteen piglets (Duroc × Landrace × Large, body weight = 2.58 ± 0.05 kg) were divided into three treatment groups based on similar body weights and equal numbers of males and females: the blank control group (CON group), the PEDV infection group (PEDV group), and the NG intervention + PEDV infection group (NG + PEDV group) (n = 6 per group). The experiment lasted for 11 days, comprising a pre-feeding period from days 0 to 3 and a formal experimental period from days 4 to 10. On days 4–10 of the experiment, piglets in the NG + PEDV group were orally administered NG (10 mg/kg). On Day 8 of the experiment, piglets in the PEDV and NG + PEDV groups were inoculated with PEDV (3 mL, 10⁶ 50% tissue culture infective dose (TCID₅₀) per milliliter). On day 11 of the experiment, piglets were euthanized for sample collection. PEDV infection caused significant intestinal damage, including a decreased (p < 0.05) villus height in the duodenum and ileum and an increased (p < 0.05) crypt depth in all intestinal segments. This intestinal damage was accompanied by an impaired absorptive function, as indicated by reduced (p < 0.05) serum D-xylose. Further results showed that PEDV compromised the intestinal antioxidant capacity by decreasing (p < 0.05) glutathione peroxidase and catalase activities, and it stimulated the intestinal inflammatory response by upregulating (p < 0.05) the expression of key inflammatory genes, including regenerating family member 3 gamma (REG3G; duodenum, jejunum, colon), S100 calcium binding protein A9 (S100A9; ileum, colon), interleukin 1 beta (IL-1β; ileum, colon), and S100 calcium binding protein A8 (S100A8; colon). PEDV also suppressed the intestinal lipid metabolism pathway by downregulating (p < 0.05) the ileal expression of Solute Carrier Family 27 Member 4 (SLC27A4), Microsomal Triglyceride Transfer Protein (MTTP), Apolipoprotein A4 (APOA4), Apolipoprotein C3 (APOC3), Diacylglycerol O-Acyltransferase 1 (DGAT1), and Cytochrome P450 Family 2 Subfamily J Member 34 (CYP2J34). Moreover, PEDV suppressed the intestinal antiviral ability by downregulating (p < 0.05) interferon (IFN) signaling pathway genes, including MX dynamin like GTPase 1 (MX1) and ISG15 ubiquitin like modifier (ISG15) in the duodenum; weakened intestinal water and ion transport by downregulating (p < 0.05) aquaporin 10 (AQP10) and potassium inwardly rectifying channel subfamily J member 13 (KCNJ13) in the duodenum, aquaporin 7 (AQP7) and transient receptor potential cation channel subfamily V member 6 (TRPV6) in the ileum, and TRPV6 and transient receptor potential cation channel subfamily M member 6 (TRPM6) in the colon; and inhibited intestinal digestive and absorptive function by downregulating (p < 0.05) phosphoenolpyruvate carboxykinase 1 (PCK1) in the duodenum and sucrase-isomaltase (SI) in the ileum. Notably, NG effectively counteracted these detrimental effects. Moreover, NG activated the IFN signaling pathway in the jejunum and suppressed PEDV replication in the colon. In conclusion, NG alleviates PEDV-induced intestinal injury by enhancing the antioxidant capacity, suppressing inflammation, normalizing the expression of metabolic and transport genes, and improving the antiviral ability. Full article

Breast cancer remains the most common malignancy worldwide and the leading cause of cancer-related mortality. Recently, extracellular vesicles (EVs) derived from adipose tissue-derived stem cells (ADSCs) have attracted increasing attention for their potential to modulate inflammatory signaling and influence tumor cell behavior. This in vitro study was designed to investigate the effects of ADSC-EVs on MCF-7 breast cancer cells. EVs were isolated from ADSC culture supernatants and applied to MCF-7 cells at concentrations ranging from 0 to 80% (v/v). Cell viability, migration, and expression of IL-6/STAT3 pathway-related genes were evaluated using MTT, scratch assays, and qRT-PCR. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test, with significance set at p < 0.05. The results showed that 20% EV treatment markedly inhibited MCF-7 cell activity, significantly reducing viability and almost completely blocking migration, with wound closure rates of 35.4% ± 3.80 at 24 h and 47.6% ± 4.2 at 48 h, compared with 48% ± 4.6 and 67% ± 4.2 in the control group, respectively. Notably, expression levels of IL-6, IL-6RST, and STAT3 were significantly downregulated (fold changes 0.155 ± 0.02 and 0.258 ± 0.012, p < 0.01), accompanied by severe disruption of the microtubule network. Immunofluorescence imaging revealed a disorganized microtubule architecture and irregular filament distribution in EV-treated cells, corresponding with decreased expression of TubA1 and CALR genes. These findings indicate that ADSC-EVs not only suppress IL-6/STAT3 inflammatory signaling but also destabilize the intracellular microtubule system, collectively contributing to the inhibition of MCF-7 breast cancer cell migration and survival. This provides an important molecular basis for developing novel EV-based therapeutic strategies in breast cancer treatment. Full article

Cytokines are a diverse group of signaling proteins that regulate immune responses by mediating cell communication. Among them, interleukins (ILs) play essential roles in immune regulation, influencing diverse cell processes through tightly controlled signaling networks. Dysregulation of interleukin signaling could lead to chronic inflammation, contributing to the development of autoimmune and inflammatory diseases as well as cancer. IL-26, a cytokine of the IL-10 family, has emerged as a unique modulator of immune function. Although structurally related to IL-10 and sharing one of its receptor subunits, IL-26 exerts distinct biological effects, particularly in promoting inflammatory responses and interacting with extracellular DNA to activate immune pathways. Increasing evidence implicates IL-26 in the development of several chronic conditions, such as psoriasis, rheumatoid arthritis, inflammatory bowel disease, asthma, and various types of cancer. This review summarizes current knowledge on IL-26’s biology, including its structural and receptor characteristics, immunomodulatory functions, and roles in inflammation and disease. Understanding IL-26’s dual functions in normal and inflammatory states may provide insights into novel therapeutic strategies targeting IL-26-mediated pathways in pathological conditions. Full article

Avian pathogenic Escherichia coli (E. coli) impairs poultry production and causes substantial economic losses. This study investigated the effects of Lactobacillus reuteri postbiotics (LR) on growth performance and intestinal health of broiler chickens challenged with E. coli. A total of 180 one-day-old Arbor Acres+ broilers were allocated into three groups (six replicates per group and 10 chicks each replicate): CTR, control group; E. coli-infected group, orally challenged with a mixture of E. coli O₁, O₂, and O₇₈ at a dose of 10⁹ CFU/mL; LR + E. coli-infected group, challenged with E. coli and fed a basal diet supplemented with 100 mg/kg LR. The results showed that dietary LR significantly improved the average daily gain (ADG) in the LR + E. coli group compared to the E. coli-infected group from days 1 to 18 (p < 0.05). However, no significant differences in average daily feed intake (ADFI) or feed conversion ratio (FCR) were observed among the CTR, E. coli, and LR + E. coli groups. Infection with E. coli led to lower total antioxidant capacity in jejunum and activity of total superoxide dismutase in ileum. Moreover, dietary LR significantly alleviated the down-regulation of Mucin2 and Aquaporin-3 gene expression in jejunum and ileum caused by E. coli infection and up-regulated the gene expression of Claudin-1 and Zonula occludens 1 in the ileum. In addition, dietary LR treatment led to the up-regulation of interleukin-10 mRNA transcripts in the jejunum. Further analysis demonstrated that dietary supplementation with LR reshaped the ileal flora of birds challenged with E. coli via elevating the relative abundance of Romboutsia and Bacteroidota, while reducing the abundance of Candidatus_Arthromitus and Escherichia-Shigella. In conclusion, dietary LR supplementation improved the expression of intestinal barrier and anti-inflammatory genes and reshaped the intestinal flora in E. coli-infected broilers. Full article