The anti-inflammatory effects of exercise on autoimmune diseases:A 20-year systematic review

Background:The anti-inflammatory effect of exercise may be an underlying factor in improving several autoimmune diseases.The aim of this systematic review was to examine the evidence on the role of exercise training in mitigating inflammation in adolescents and adults with autoimmune disease.Methods:PubMed,Web of Science,and Embase databases were systematically reviewed for related studies published between January 1,2003,and August 31,2023.All randomized and non-randomized controlled trials of exercise interventions with autoimmune disease study participants that evaluated inflammation-related biomarkers were included.The quality of evidence was assessed using the Tool for the assEssment of Study qualiTy and reporting in EXercise scale and Cochrane bias risk tool.Results:A total of 14,565 records were identified.After screening the titles,abstracts,and full texts,87 were eligible for the systematic review.These studies were conducted in 25 different countries and included a total of 2779 participants(patients with autoimmune disease,in exercise or control groups).Overall,the evidence suggests that inflammation-related markers such as C-reactive protein,interleukin 6,and tumor necrosis factor a were reduced by regular exercise interventions.Regular exercise interventions combined with multiple exercise modes were associated with greater benefits.Conclusion:Regular exercise training by patients with autoimmune disease exerts an anti-inflammatory influence.This systematic review provides support for the promotion and development of clinical exercise intervention programs for patients with autoimmune disease.Most patients with autoimmune disease can safely adopt moderate exercise training protocols,but changes in inflammation biomarkers will be modest at best.Acute exercise interventions are ineffective or even modestly but transiently pro-inflammatory.

Glucagon-like peptide 1 receptor activation:anti-inflammatory effects in the brain

The glucagon-like peptide 1 is a pleiotropic hormone that has potent insulinotropic effects and is key in treating metabolic diseases such as diabetes and obesity.Glucagon-like peptide 1 exerts its effects by activating a membrane receptor identified in many tissues,including diffe rent brain regions.Glucagon-like peptide 1 activates several signaling pathways related to neuroprotection,like the support of cell growth/survival,enhancement promotion of synapse formation,autophagy,and inhibition of the secretion of proinflammatory cytokines,microglial activation,and apoptosis during neural morphogenesis.The glial cells,including astrocytes and microglia,maintain metabolic homeostasis and defe nse against pathogens in the central nervous system.After brain insult,microglia are the first cells to respond,followed by reactive astrocytosis.These activated cells produce proinflammato ry mediators like cytokines or chemokines to react to the insult.Furthermore,under these circumstances,mic roglia can become chro nically inflammatory by losing their homeostatic molecular signature and,consequently,their functions during many diseases.Several processes promote the development of neurological disorders and influence their pathological evolution:like the formation of protein aggregates,the accumulation of abnormally modified cellular constituents,the formation and release by injured neurons or synapses of molecules that can dampen neural function,and,of critical impo rtance,the dysregulation of inflammato ry control mechanisms.The glucagonlike peptide 1 receptor agonist emerges as a critical tool in treating brain-related inflammatory pathologies,restoring brain cell homeostasis under inflammatory conditions,modulating mic roglia activity,and decreasing the inflammato ry response.This review summarizes recent advances linked to the anti-inflammato ry prope rties of glucagon-like peptide 1 receptor activation in the brain related to multiple sclerosis,Alzheimer’s disease,Parkinson’s disease,vascular dementia,or chronic migraine.

T cell interactions with microglia in immune-inflammatory processes of ischemic stroke

The primary mechanism of secondary injury after cerebral ischemia may be the brain inflammation that emerges after an ischemic stroke,which promotes neuronal death and inhibits nerve tissue regeneration.As the first immune cells to be activated after an ischemic stroke,microglia play an important immunomodulatory role in the progression of the condition.After an ischemic stroke,peripheral blood immune cells(mainly T cells)are recruited to the central nervous system by chemokines secreted by immune cells in the brain,where they interact with central nervous system cells(mainly microglia)to trigger a secondary neuroimmune response.This review summarizes the interactions between T cells and microglia in the immune-inflammatory processes of ischemic stroke.We found that,during ischemic stroke,T cells and microglia demonstrate a more pronounced synergistic effect.Th1,Th17,and M1 microglia can co-secrete proinflammatory factors,such as interferon-γ,tumor necrosis factor-α,and interleukin-1β,to promote neuroinflammation and exacerbate brain injury.Th2,Treg,and M2 microglia jointly secrete anti-inflammatory factors,such as interleukin-4,interleukin-10,and transforming growth factor-β,to inhibit the progression of neuroinflammation,as well as growth factors such as brain-derived neurotrophic factor to promote nerve regeneration and repair brain injury.Immune interactions between microglia and T cells influence the direction of the subsequent neuroinflammation,which in turn determines the prognosis of ischemic stroke patients.Clinical trials have been conducted on the ways to modulate the interactions between T cells and microglia toward anti-inflammatory communication using the immunosuppressant fingolimod or overdosing with Treg cells to promote neural tissue repair and reduce the damage caused by ischemic stroke.However,such studies have been relatively infrequent,and clinical experience is still insufficient.In summary,in ischemic stroke,T cell subsets and activated microglia act synergistically to regulate inflammatory progression,mainly by secreting inflammatory factors.In the future,a key research direction for ischemic stroke treatment could be rooted in the enhancement of anti-inflammatory factor secretion by promoting the generation of Th2 and Treg cells,along with the activation of M2-type microglia.These approaches may alleviate neuroinflammation and facilitate the repair of neural tissues.

Metabolic reprogramming of the inflammatory response in the nervous system:the crossover between inflammation and metabolism

Metabolism is a fundamental process by which biochemicals are broken down to produce energy(catabolism) or used to build macromolecules(anabolism). Metabolism has received renewed attention as a mechanism that generates molecules that modulate multiple cellular responses. This was first identified in cancer cells as the Warburg effect, but it is also present in immunocompetent cells. Studies have revealed a bidirectional influence of cellular metabolism and immune cell function, highlighting the significance of metabolic reprogramming in immune cell activation and effector functions. Metabolic processes such as glycolysis, oxidative phosphorylation, and fatty acid oxidation have been shown to undergo dynamic changes during immune cell response, facilitating the energetic and biosynthetic demands. This review aims to provide a better understanding of the metabolic reprogramming that occurs in different immune cells upon activation, with a special focus on central nervous system disorders. Understanding the metabolic changes of the immune response not only provides insights into the fundamental mechanisms that regulate immune cell function but also opens new approaches for therapeutic strategies aimed at manipulating the immune system.

Development and validation of a prognostic immunoinflammatory index for patients with gastric cancer

BACKGROUND Studies have demonstrated the influence of immunity and inflammation on the development of tumors.Although single biomarkers of immunity and inflam-mation have been shown to be clinically predictive,the use of biomarkers integrating both to predict prognosis in patients with gastric cancer remains to be investigated.AIM To investigate the prognostic and clinical significance of inflammatory biomarkers and lymphocytes in patients undergoing surgical treatment for gastric cancer.METHODS Univariate COX regression analysis was performed to identify potential prognostic factors for patients with gastric cancer undergoing surgical treatment.Least absolute shrinkage and selection operator-COX(LASSO-COX)regression analysis was performed to integrate these factors and formulate a new prognostic immunoinflammatory index(PII).The correlation between PII and clinical charac-teristics was statistically analyzed.Nomograms incorporating the PII score were devised and validated based on the time-dependent area under the curve and decision curve analysis.RESULTS Patients exhibiting elevated neutrophil-to-lymphocyte ratio,platelet-to-lymphocyte ratio,and systemic immune inflammatory index displayed inferior progression-free survival(PFS)and overall survival(OS).Conversely,low levels of CD3(+),CD3(+)CD8(+),CD4(+)CD8(+),and CD3(+)CD16(+)CD56(+)T lymphocytes were associated with improved PFS and OS,while high CD19(+)T lymphocyte levels were linked to worse PFS and OS.The PII score demonstrated associations with tumor characteristics(primary tumor site and tumor size),establishing itself as an independent prognostic factor for both PFS and OS.Time-dependent area under the curve and decision curve analysis affirmed the effectiveness of the PII-based nomogram as a robust prognostic predictive model.CONCLUSION PII may be a reliable predictor of prognosis in patients with gastric cancer undergoing surgical treatment,and it offers insights into cancer-related immune-inflammatory responses,with potential significance in clinical practice.

Antimicrobial,antibiofilm,angiogenesis,anti-inflammatory,and wound healing activities of zinc nanoparticles green synthesized using Ferula macrecolea extract

Objective:To assess the antimicrobial,antibiofilm,anti-inflammatory,angiogenic,and wound healing activities of zinc nanoparticles(ZNPs)green synthesized using Ferula macrecolea extract.Methods:The green synthesis was conducted using the precipitation method.Then,the minimum inhibitory concentration(MIC),minimum bactericidal concentration(MBC),and minimum biofilm inhibition concentration 50%(MBIC50)of ZNPs against Staphylococcus aureus(S.aureus)and Pseudomonas aeruginosa(P.aeruginosa)were evaluated.The effects of ZNPs on the gene expressions of Staphylococcus spp.[intracellular adhesion A(icaA)and D(icaD)]and P.aeruginosa(rhlI and rhlR)were investigated using quantitative real-time PCR.In addition,the effects of ZNPs on wound healing,angiogenesis,and anti-inflammatory markers were assessed.Results:The green-synthesized ZNPs demonstrated significant antimicrobial efficacy against S.aureus and P.aeruginosa.The biofilm formation in S.aureus and P.aeruginosa was also inhibited by ZNPs with MBIC50 values of 3.30μg/mL and 2.08μg/mL,respectively.Additionally,ZNPs downregulated the expression of biofilm-related genes icaA,icaD,rhlI,and rhlR in the tested bacteria.They also demonstrated promising in vitro wound healing effects by promoting fibroblast cell proliferation and wound closure in a dose-dependent manner.A significant increase in the expression of HLA-G5 and VEGF-A genes as well as a marked decrease in the expression of NF-κB,IL-1β,and TNF-αgenes were observed in cells treated with ZNPs compared to the control group(P<0.05).Conclusions:ZNPs display promising antibacterial effects against S.aureus and P.aeruginosa and wound-healing effects by inhibiting biofilm formation,inducing angiogenesis,and reducing inflammation.However,further studies must be conducted to specify the accurate mechanisms of action and toxicity of ZNPs.

FK506 contributes to peripheral nerve regeneration by inhibiting neuroinflammatory responses and promoting neuron survival

FK506(Tacrolimus)is a systemic immunosuppressant approved by the U.S.Food and Drug Administration.FK506 has been shown to promote peripheral nerve regeneration,however,its precise mechanism of action and its pathways remain unclear.In this study,we established a rat model of sciatic nerve injury and found that FK506 improved the morphology of the injured sciatic nerve,increased the numbers of motor and sensory neurons,reduced inflammatory responses,markedly improved the conduction function of the injured nerve,and promoted motor function recovery.These findings suggest that FK506 promotes peripheral nerve structure recovery and functional regeneration by reducing the intensity of inflammation after neuronal injury and increasing the number of surviving neurons.

Mechanistic research:Selenium regulates virulence factors,reducing adhesion ability and inflammatory damage of Helicobacter pylori

BACKGROUND The pathogenicity of Helicobacter pylori is dependent on factors including the environment and the host.Although selenium is closely related to pathogenicity as an environmental factor,the specific correlation between them remains unclear.AIM To investigate how selenium acts on virulence factors and reduces their toxicity.METHODS H.pylori strains were induced by sodium selenite.The expression of cytotoxin-associated protein A(CagA)and vacuolating cytotoxin gene A(VacA)was determined by quantitative PCR and Western blotting.Transcriptomics was used to analyze CagA,CagM,CagE,Cag1,Cag3,and CagT.C57BL/6A mice were infected with the attenuated strains subjected to sodium selenite induction,and H.pylori colonization,inflammatory reactions,and the cell adhesion ability of H.pylori were assessed.RESULTS CagA and VacA expression was upregulated at first and then downregulated in the H.pylori strains after sodium selenite treatment.Their expression was significantly and steadily downregulated after the 5th cycle(10 d).Transcriptome analysis revealed that sodium selenite altered the levels affect H.pylori virulence factors such as CagA,CagM,CagE,Cag1,Cag3,and CagT.Of these factors,CagM and CagE expression was continuously downregulated and further downregulated after 2 h of induction with sodium selenite.Moreover,CagT expression was upregulated before the 3rd cycle(6 d)and significantly downregulated after the 5th cycle.Cag1 and Cag3 expression was upregulated and downregulated,respectively,but no significant change was observed by the 5th cycle.C57BL/6A mice were infected with the attenuated strains subjected to sodium selenite induction.The extent of H.pylori colonization in the stomach increased;however,sodium selenite also induced a mild inflammatory reaction in the gastric mucosa of H.pylori-infected mice,and the cell adhesion ability of H.pylori was significantly weakened.CONCLUSION These results demonstrate that H.pylori displayed virulence attenuation after the 10th d of sodium selenite treatment.Sodium selenite is a low toxicity compound with strong stability that can reduce the cell adhesion ability of H.pylori,thus mitigating the inflammatory damage to the gastric mucosa.

Levisticum officinale extract protects against CCl4-induced hepatotoxicity through anti-inflammatory,anti-fibrotic,and antioxidant properties in rats

Objective:To investigate the hepatoprotective effects of Levisticum officinale extract on CCl4-induced hepatotoxicity.Methods:Different doses of Levisticum officinale extract were given orally to rats for 10 days,then rats received a single dose of CCl4(2.5 mL/kg,50%v/v in liquid paraffin).Biochemical and histopathological assays were performed to assess the effects of the extract on liver function and architecture.Moreover,antioxidant and oxidative markers as well as inflammatory and fibrotic indicators were measured.Results:Pretreatment with Levisticum officinale extract significantly mitigated CCl4-induced damage to liver structure,improved serum levels of alanine aminotransferase,aspartate aminotransferase,alkaline phosphatase,urea,total bilirubin,and total protein,enhanced glutathione content and superoxide dismutase and catalase activities in the liver,as well as decreased plasma and hepatic malondialdehyde levels.Immunohistochemical results demonstrated that the extract reduced Ki-67 andα-SMA expression and Masson’s trichrome staining revealed decreased liver collagen in rats treated with Levisticum officinale extract.Moreover,Levisticum officinale extract markedly decreased the gene expressions of TNF-α,IL-6,TGF-β1,MCP-1,and COX-2.Conclusions:Levisticum officinale extract exerts hepatoprotective effects on CCl4-induced hepatotoxicity through antioxidant,anti-inflammatory,and anti-fibrotic activities.

Capsosiphon fulvescens suppresses LPS-stimulated inflammatory responses by suppressing TLR4/NF-κB activation in RAW264.7 murine macrophages

Objective:To evaluate the effects of Capsosiphon fulvescens(C.fulvescens)ethanolic extract on inflammation in lipopolysaccharide(LPS)-induced RAW296.7 macrophages.Methods:The protective effects of C.fulvescens ethanolic extract on LPS-induced inflammation in RAW264.7 macrophages were assessed using biochemical analysis,including enzyme-linked immunosorbent assay,quantitative reverse transcription-polymerase chain reaction,and Western blot analysis.To examine reactive oxygen species(ROS)production,flow cytometry analysis,and immunofluorescence staining were used.Furthermore,the modulatory effect of C.fulvescens ethanolic extract on NF-κB activation was investigated.Results:C.fulvescens ethanolic extract significantly attenuated LPS-induced levels of pro-inflammatory cytokines and notably reduced the secretion and mRNA levels of LPS-mediated matrix metalloproteinases.In addition,C.fulvescens ethanolic extract decreased ROS production and suppressed the TLR4/NF-κB signaling pathway.Conclusions:C.fulvescens ethanolic extract alleviates inflammation as well as oxidative stress by modulating the TLR4/NF-κB signaling in LPS-induced RAW264.7 macrophages.C.fulvescens can be used as a potential therapeutic agent to suppress inflammation and oxidative stress-associated diseases.

Combining systemic inflammatory response index and albumin fibrinogen ratio to predict early serious complications and prognosis after resectable gastric cancer

BACKGROUND Gastric cancer has a high incidence and fatality rate,and surgery is the preferred course of treatment.Nonetheless,patient survival rates are still low,and the incidence of major postoperative complications cannot be disregarded.The systemic inflammatory response,nutritional level,and coagulation status are key factors affecting the postoperative recovery and prognosis of gastric cancer patients.The systemic inflammatory response index(SIRI)and the albumin fibrinogen ratio(AFR)are two valuable comprehensive indicators of the severity and prognosis of systemic inflammation in various medical conditions.AIM To assess the clinical importance and prognostic significance of the SIRI scores and the AFR on early postoperative outcomes in patients undergoing radical gastric cancer surgery.METHODS We conducted a retrospective analysis of the clinicopathological characteristics and relevant laboratory indices of 568 gastric cancer patients from January 2018 to December 2019.We calculated and compared two indicators of inflammation and then examined the diagnostic ability of combined SIRI and AFR values for serious early postoperative complications.We scored the patients and categorized them into three groups based on their SIRI and AFR levels.COX analysis was used to compare the three groups of patients the prognostic value of various preoperative SIRI-AFR scores for 5-year overall survival(OS)and disease-free survival(DFS).RESULTS SIRI-AFR scores were an independent risk factor for prognosis[OS:P=0.004;hazards ratio(HR)=3.134;DFS:P<0.001;HR=3.543]and had the highest diagnostic power(area under the curve:0.779;95%confidence interval:0.737-0.820)for early serious complications in patients with gastric cancer.The tumor-node-metastasis stage(P=0.001),perioperative transfusion(P=0.044),positive carcinoembryonic antigen(P=0.014)findings,and major postoperative complications(P=0.011)were factors associated with prognosis.CONCLUSION Preoperative SIRI and AFR values were significantly associated with early postoperative survival and the occurrence of severe complications in gastric cancer patients.

Identification of a novel inflammatory-related gene signature to evaluate the prognosis of gastric cancer patients

BACKGROUND Gastric cancer(GC)is a highly aggressive malignancy with a heterogeneous nature,which makes prognosis prediction and treatment determination difficult.Inflammation is now recognized as one of the hallmarks of cancer and plays an important role in the aetiology and continued growth of tumours.Inflammation also affects the prognosis of GC patients.Recent reports suggest that a number of inflammatory-related biomarkers are useful for predicting tumour prognosis.However,the importance of inflammatory-related biomarkers in predicting the prognosis of GC patients is still unclear.AIM To investigate inflammatory-related biomarkers in predicting the prognosis of GC patients.was constructed using the least absolute shrinkage and selection operator Cox regression model based on the GEO database.GC patients from the GSE26253 cohort were used for validation.Univariate and multivariate Cox analyses were used to determine the independent prognostic factors,and a prognostic nomogram was established.The calibration curve and the area under the curve based on receiver operating characteristic analysis were utilized to evaluate the predictive value of the nomogram.The decision curve analysis results were plotted to quantify and assess the clinical value of the nomogram.Gene set enrichment analysis was performed to explore the potential regulatory pathways involved.The relationship between tumour immune infiltration status and risk score was analysed via Tumour Immune Estimation Resource and CIBERSORT.Finally,we analysed the association between risk score and patient sensitivity to commonly used chemotherapy and targeted therapy agents.RESULTS A prognostic model consisting of three inflammatory-related genes(MRPS17,GUF1,and PDK4)was constructed.Independent prognostic analysis revealed that the risk score was a separate prognostic factor in GC patients.According to the risk score,GC patients were stratified into high-and low-risk groups,and patients in the high-risk group had significantly worse prognoses according to age,sex,TNM stage and Lauren type.Consensus clustering identified three subtypes of inflammation that could predict GC prognosis more accurately than traditional grading and staging.Finally,the study revealed that patients in the low-risk group were more sensitive to certain drugs than were those in the high-risk group,indicating a link between inflammation-related genes and drug sensitivity.CONCLUSION In conclusion,we established a novel three-gene prognostic signature that may be useful for predicting the prognosis and personalizing treatment decisions of GC patients.

Synchronous gastric and colon cancers:Important to consider hereditary syndromes and chronic inflammatory disease associations

In this editorial we comment on the manuscript,describing management and surveillance strategies in synchronous and metachronous,gastric and colon cancers.Synchronous or metachronous primary malignancies at different sites of the gastrointestinal tract pose a unique diagnostic and therapeutic challenge.Multidisciplinary services and strategies are required for the management of multiple site primary malignancies,to provide the best oncological outcomes.Although this study highlights the dual cancers in 76 sporadic cases,the authors excluded 55 patients due to combination of factors which includes;incomplete clinical data,genetic syndrome,gastric stump cancers.In addition,the authors did not elaborate if any patients presented with signet ring cell morphology,E-cadherin mutations or presence of inflammatory bowel disease.Genetic and mutational errors and epithelial field defects from chronic inflammatory diseases of the gastrointestinal tract are important when considering synchronous gastric and colonic cancers.We will briefly discuss these in this editorial.

Interactions between myoblasts and macrophages under high glucose milieus result in inflammatory response and impaired insulin sensitivity

BACKGROUND Skeletal muscle handles about 80% of insulin-stimulated glucose uptake and become the major organ occurring insulin resistance(IR).Many studies have confirmed the interactions between macrophages and skeletal muscle regulated the inflammation and regeneration of skeletal muscle.However,despite of the decades of research,whether macrophages infiltration and polarization in skeletal muscle under high glucose(HG)milieus results in the development of IR is yet to be elucidated.C2C12 myoblasts are well-established and excellent model to study myogenic regulation and its responses to stimulation.Further exploration of macrophages'role in myoblasts IR and the dynamics of their infiltration and polarization is warranted.AIM To evaluate interactions between myoblasts and macrophages under HG,and its effects on inflammation and IR in skeletal muscle.METHODS We detected the polarization status of macrophages infiltrated to skeletal muscles of IR mice by hematoxylin and eosin and immunohistochemical staining.Then,we developed an in vitro co-culture system to study the interactions between myoblasts and macrophages under HG milieus.The effects of myoblasts on macrophages were explored through morphological observation,CCK-8 assay,Flow Cytometry,and enzyme-linked immunosorbent assay.The mediation of macrophages to myogenesis and insulin sensitivity were detected by morphological observation,CCK-8 assay,Immunofluorescence,and 2-NBDG assay.RESULTS The F4/80 and co-localization of F4/80 and CD86 increased,and the myofiber size decreased in IR group(P<0.01,g=6.26).Compared to Mc group,F4/80+CD86+CD206-cells,tumor necrosis factor-α(TNFα),inerleukin-1β(IL-1β)and IL-6 decreased,and IL-10 increased in McM group(P<0.01,g>0.8).In McM+HG group,F4/80+CD86+CD206-cells,monocyte chemoattractant protein 1,TNFα,IL-1βand IL-6 were increased,and F4/80+CD206+CD86-cells and IL-10 were decreased compared with Mc+HG group and McM group(P<0.01,g>0.8).Compered to M group,myotube area,myotube number and E-MHC were increased in MMc group(P<0.01,g>0.8).In MMc+HG group,myotube area,myotube number,E-MHC,GLUT4 and glucose uptake were decreased compared with M+HG group and MMc group(P<0.01,g>0.8).CONCLUSION Interactions between myoblasts and macrophages under HG milieus results in inflammation and IR,which support that the macrophage may serve as a promising therapeutic target for skeletal muscle atrophy and IR.

Dietary inflammatory index and its impact on severity and recurrence of Tourette syndrome in children

BACKGROUND Tourette syndrome(TS)is a neurodevelopmental disorder characterized by the presence of motor and vocal tics,typically beginning in childhood.Despite signifi-cant research efforts,the exact pathophysiology of TS remains incompletely understood.Recent studies suggest that inflammation may play a role in the severity and progression of TS,pointing to the potential influence of dietary and lifestyle factors on the condition.Currently,research on the specific connection between dietary inflammatory index(DII)and TS is still in its early stages,requir-ing additional clinical and epidemiological studies to validate the strength and specific mechanisms of this connection.METHODS A total of 207 children diagnosed with TS in the pediatric department of Qingdao Chengyang People’s Hospital from January 2022 to January 2023 were selected.They were divided into stable and unstable groups based on follow-up condi-tions.Before enrollment,general information of the children[age,gender,body mass index(BMI),guardian’s education level,DII score,medical history,family history,academic stress,electronic device usage,medication,and disease progression]was assessed,and serum inflammatory levels were measured during follow-up visits.DII scores and Yale Global Tic Severity Scale(YGTSS)scores were calculated.Furthermore,based on YGTSS scores,the children were classified into mild,moderate,and severe groups.The DII,interleukin-6(IL-6),C-reactive protein(CRP),and tumor necrosis factor-alpha(TNF-α)levels in each group were compared.RESULTS Follow-up surveys were completed by 207 children and their guardians.Among them,117 children were in the stable group,and 90 were in the recurrent group.We found no statistically significant differences in age,gender,comorbidities,BMI,and disease duration between the two groups(P>0.05).However,academic stress,electronic device usage,medication,guardian’s education level,and DII scores showed statistically significant differences between the groups(P<0.05).Multifactorial regression analysis revealed that guardian’s anxiety level,DII score,medication,academic stress,and family history were statistically significant factors(P<0.05)affecting the recurrence of TS in children.Therefore,anxiety level,DII score,medication status,electronic device usage,and academic stress were identified as factors influencing the recurrence of TS in children.Among them,DII score,academic stress,and family history had odds ratios(OR)greater than 1,indicating risk factors,whereas medication status and guardian’s education level had OR values less than 1,indicating protective factors.According to the YGTSS scores,children were categorized into mild,moderate,and severe groups.Comparative analysis of DII and inflammatory levels in children with different degrees of tic disorders revealed that the severe group had the highest DII and inflammatory levels,followed by the moderate group,and the mild group had the lowest levels.The trend of TS progression was consistent with the DII results.Receiver operating characteristic curves were plotted to predict disease progression in patients with TS via inflammatory markers.The areas under the curve for IL-6,CRP,and TNF-αwere 0.894(95%CI:0.817-0.969),0.793(95%CI:0.694-0.893),and 0.728(95%CI:0.614-0.843)respectively,with statistically significant differences(P<0.05).According to the Youden index,the optimal cutoff values were IL-6=3.775 ng/L(sensitivity 68.1%and specificity 68.4%),CRP=6.650 mg/L(sensitivity 60.6%and specificity 68.4%),and TNF-α=0.666(sensitivity 60.6%and specificity 71.1%).CONCLUSION We found a certain correlation between DII and the severity,recurrence,and inflammatory levels of TS in children.Reasonable reduction in the intake of pro-inflammatory foods may be beneficial in reducing the risk of disease progression in children with TS.

Link between periodontitis and diabetic retinopathy:Inflammatory pathways and clinical implications

The bidirectional relationship between periodontitis and type 2 diabetes mellitus has been well-established.However,the underlying molecular mechanisms remain unclear.Diabetic retinopathy(DR)is an important complication of diabetes,but there are few studies on the relationship between DR and periodontitis,especially on the intrinsic inflammatory pathway mechanism.This article reviews the latest clinical data on how diabetes promotes susceptibility to periodontitis from the epidemiological and molecular perspectives,with a special focus on the key roles of systemic inflammation and endothelial dysfunction in the interplay between DR and periodontitis.Comprehension of the intertwined pathogenesis of DR and periodontitis can better guide the development of comprehensive management strategies for glycemic control and periodontal health,with the aim of mitigating the progression of DR and enhancing overall well-being.

Prognostic impact of preoperative nutritional and immune inflammatory parameters on liver cancer

The immune response to tissue damage or infection involves inflammation,a multifaceted biological process distinguished by immune cell activation,mediator secretion,and immune cell recruitment to the site of injury.Several blood-based immune-inflammatory biomarkers with prognostic significance in malignancies have been identified.In this issue of the World Journal of Gastrointestinal Surgery,they examined the prognosis of liver cancer radical resection in relation to pre-operative systemic immune-inflammation and nutritional risk indices.Comparing older and younger individuals often reveals compromised nutritional and immu-nological statuses in the former.Therefore,performing preoperative evaluations of the nutritional status and immunity in geriatric patients is critical.In addition to being a primary treatment modality,radical resection is associated with a sig-nificant mortality rate following surgery.Insufficient dietary consump-tion and an elevated metabolic rate within tumor cells contribute to the increased proba-bility of malnutrition associated with the ailment,consequently leading to a sub-stantial deterioration in prognosis.Recent studies,reinforce the importance of nu-tritional and immune-inflammatory biomarkers.Prior to surgical intervention,geriatric nutritional risk and systemic immune-inflammatory indices should be prioritized,particularly in older patients with malignant diseases.

Polygenic Profile and Magnitude Impact of Inflammatory Response in Soccer Athletes

The practice of soccer involves carrying-out actions of high intensity, which demand a great generation of eccentric strength, which in turn results in an increase in the inflammatory response after training practice and game matches. The study aimed to investigate, in combination and individually, the association of 28 polymorphisms with the inflammatory responses of soccer athletes. The sample consisted of 47 male under-20 soccer athletes who belong to clubs in the first division of Brazilian soccer. Blood samples were collected at Pre, and 03, 24, and 48 hours after the training session to evaluate the inflammatory responses (hematological analyzes (hemogram), creatine phosphokinase (CK), high sensitivity quantitative C-reactive protein (CRP), tumor necrosis factor-alpha, (TNFα), interleukin 6 (IL-6) and insulin-like growth factor 1 (IGF-1)). DNA was obtained through scraping of buccal cells, where a sterile swab was rubbed on the inner side of the mouth of each participant 06 times. The database was built using the TruSeq DNA PCRFree kit (Illumina®) and the Covaris equipment for shearing genomic DNA (gDNA) by ultrasound. Of the analyzed SNPs, 09 (ACTN3 rs1815739, COL5A1 rs12722, COL5A1 rs3196378, HGF rs5745697, IGF1 rs35767, IL-6 rs1800795, MMP3 rs679620, SLC30A8 rs13266634, SOX15 rs4227) were individually associated with biomarkers and 07 SNPs, (COL5A1 rs12722, COL5A1 rs3196378, COL5A1 rs1800012, HGF rs5745697, IGF1 rs35767, IL-6 rs1800795 and MMP3 rs679620) analyzed in combination, explained 16% to 40% of the variation of inflammatory responses in soccer athletes. The results suggest that the genotypic profile can be taken into account for a more individualized distribution of the training load, along with the elaboration of recovery strategies for high-level athletes between training sessions and games of high physical and physiological demand.

Research progress of TCM monomer in treating diabetic kidney disease based on inflammatory mechanism

With the increasing morbidity of diabetes mellitus (DM), diabetic kidney disease (DKD) has become the major reason causing chronic kidney disease (CKD) and end-stage renal disease (ESRD) over the world. However, current treating strategy is aiming at blood glucose controlling and renin-angiotensin system (RAS) restricting which can’t effectively preventing the development of DKD. Recent research indicating that low level of inflammatory and activation of immune system play a significant role in occurrence and progression of DKD. Understanding of inflammatory cascade and its mechanism is conducive to discern novel target of DKD and contributing to design new treating strategy based on anti-inflammatory. For the past few years, an increasing number of evidences proved that Tradit Chin Med (TCM) could delay the progression of ESRD on the basis of inflammatory. In this review, we overview the protective effect against DKD-based renal injury of TCM monomer, offering novel ideas in drug discovery and in mechanism-related research.sd.

Performance of nutritional and inflammatory markers in patients with pancreatic cancer

BACKGROUND Systemic inflammation and nutrition play pivotal roles in cancer progression and can increase the risk of delayed recovery after surgical procedures.AIM To assess the significance of inflammatory and nutritional indicators for the prognosis and postoperative recovery of patients with pancreatic cancer(PC).METHODS Patients who were diagnosed with PC and underwent surgical resection at our hospital between January 1,2019,and July 31,2023,were enrolled in this retrospective observational cohort study.All the data were collected from the electronic medical record system.Seven biomarkers-the albumin-to-globulin ratio,prognostic nutritional index(PNI),systemic immune–inflammation index(SII),neutrophil-to-lymphocyte ratio(NLR),platelet-to-lymphocyte ratio(PLR),nutritional risk index(NRI),and geriatric NRI were assessed.RESULTS A total of 446 patients with PC met the inclusion criteria and were subsequently enrolled.Patients with early postoperative discharge tended to have higher PNI values and lower SII,NLR,and PLR values(all P<0.05).Through multivariable logistic regression analysis,the SII value emerged as an independent risk factor influencing early recovery after surgery.Additionally,both univariable and multivariable Cox regression analyses revealed that the PNI value was the strongest prognostic marker for overall survival(OS;P=0.028)and recurrence-free survival(RFS;P<0.001).The optimal cutoff PNI value was established at 47.30 using X-tile software.Patients in the PNI-high group had longer OS(P<0.001)and RFS(P=0.0028)times than those in the PNI-low group.CONCLUSION Preoperative systemic inflammatory-nutritional biomarkers may be capable of predicting short-term recovery after surgery as well as long-term patient outcomes.