Inflammatory Response In Patients Research Articles

Effects of Omega-3 Fatty Acids on Postoperative Inflammatory Response: A Systematic Review and Meta-Analysis.

a literature search of Cochrane Library was conducted to identify all randomized controlled trials (RCTs) investigating the effects of preoperatively initiated omega-3 to standard care, placebo, or other immunonutrients excluding omega-3 FAs in patients undergoing abdominal surgery until the end of December 2022. a total of 296 articles were found during the initial search. Thirteen RCTs involving 950 patients were identified that met the search criteria. These were successively analyzed and included in this meta-analysis. There was no significant difference between the groups with respect to inflammatory markers IL-6: -0.55 [-1.22; 0.12] p = 0.10, CRP: -0.14 [-0.67; 0.40] p = 0.55, WBC: -0.58 [-3.05; 1.89] p = 0.42, or hospital stay -0.5 [-1.43; 0.41] p = 0.2. although reduced inflammatory markers were observed, preoperative administration of omega-3 FAs immunonutrients had no significant effect on the postoperative inflammatory response in patients undergoing abdominal surgeries. Yet, results obtained from this study are inconclusive, likely attributed to the limited number of trials and patients included. Further studies are required to obtain a better educated verdict.

Intravenous lidocaine improves postoperative cognition in patients undergoing laparoscopic colorectal surgery: a randomized, double-blind, controlled study

BackgroundThe risk of postoperative cognitive dysfunction(POCD) in laparoscopic surgery should not be overlooked. Intravenous lidocaine can reduce perioperative inflammatory response in patients undergoing laparoscopic surgery, while the effect of intraoperative intravenous lidocaine on postoperative cognitive function in patients undergoing laparoscopic colorectal cancer surgery has not been well studied. We investigated whether intraoperative lidocaine improves postoperative cognitive function after laparoscopic radical resection for colorectal cancer.MethodsWe conducted a prospective, randomized double blinded controlled trial to investigate the effect of intravenous lidocaine on rapid postoperative recovery in patients undergoing laparoscopic radical resection of colorectal cancer. The patients were randomly assigned to receive either intravenous lidocaine or saline. The primary outcome was cognitive dysfunction defined by a decrease from pre- to postoperative ≥ 2 of the Mini-Mental State Examination (MMSE) score, at the 3rd and the 7th postoperative days. Secondary outcomes were the MMSE raw score and parameters of the patients’ postoperative recovery such as agitation and length of stay in the post-anaesthesia care unit (PACU), length of hospital stay, markers of inflammation (white blood cell count and CRP), and incidence of complications.ResultsSeventy-three patients in the lidocaine group and 77 patients in the control group completed the trial. The rate of cognitive dysfunction was lower in the lidocaine group than that in the control group, both at the 3rd (18.57% vs. 63.64% for each group respectively; RR = 0.26, 95%CI = 0.19–0.32; p < 0.0001) and at the 7th postoperative day (12.33% vs. 53.25% for each group respectively; RR = 0.28, 95%CI = 0.22–0.35; P < 0.001). The postoperative MMSE scores were also higher in the lidocaine group than in the control group both at the 3rd (median 25 vs. 24 respectively) and at the 7th postoperative day (26 vs. 24 respectively). Also, patients in the lidocaine group displayed a lower white blood cell count than the control group at the 1st postoperative day (8.5 ± 2.7 vs. 10.4 ± 3.3; p < 0. 001). No differences were evidenced for the other secondary outcomes.ConclusionsIntraoperative intravenous lidocaine can significantly improve postoperative cognitive function in patients undergoing laparoscopic radical resection of colorectal cancer.Trial registrationChinese Clinical Trial Registry (16/1/2022, registration number: ChiCTR2200055683)

Effects of Cannabidiol (CBD) on the inflammatory response of patients with rheumatoid arthritis.

Abstract – With an increase in the understanding of rheumatoid arthritis (RA) in terms of genetic and environmental risk factors, the pathogenesis of the disease is still not entirely understood. Treatments focus on maintaining joint function, analgesia and immunosuppression, however, in some cases there is little to no response to therapeutic drugs, highlighting the need to explore further therapeutic treatments. Cannabidiol (CBD) has been studied for its potential anti-inflammatory properties with regards to inflammatory conditions, but with conflicting and limited research surrounding RA. The aim of this systematic review was to determine the effects of cannabidiol on the inflammatory response of patients with RA. Most recent findings, relevance and quality of available research has been analyzed following the principles of the preferred reporting items for systematic review and meta-analysis (PRISMA) guidelines. An electronic literature search was conducted through PubMed, Google Scholar, ScienceDirect. The PICO framework, FINER, inclusion and exclusion criteria were considered to identify specific components within the studies. Four studies were identified as relevant after being assessed through the critical appraisal tool CASP. Two qualitative in vivo experiments on 58 humans and 54 rats. One in vivo study analyzed qualitative and quantitative data from 133 mice and a final study giving quantitative data from an in vitro experiment on macrophages. All participants were diagnosed with either acute or chronic rheumatoid arthritis, whilst receiving a variation of dosages and routes of administration, with a collation of data and observations from both before and after administration of the CBD treatment. The reviewed studies highlighted no significant adverse reactions from the use of the CBD therapeutics in the varying dosages and routes of administration. From these four studies there is evidence to suggest that there are benefits of CBD as a therapeutic in terms of inflammation, three of the studies specifically found a reduction in the inflammatory marker TNF-α caused by RA after administration of the various therapeutic interventions and dosages. There is a requirement for more human clinical trials to determine the anti- inflammatory properties, the safety, dosage, route of administration and efficacy of CBD in humans with RA.

Network Meta-analysis of efficacy of Chinese patent medicine in treatment of inflammatory response in diabetic nephropathy

This study aimed to evaluate the efficacy and safety of various Chinese patent medicines in the treatment of inflammatory response in diabetic nephropathy(DN) based on network Meta-analysis. Randomized controlled trial(RCT) of oral Chinese patent medicines for improving inflammatory response in patients with DN was retrieved from CNKI, Wanfang, VIP, SinoMed, PubMed, Cochrane Library, EMbase, Web of Science, and other databases from database inception to October 2022. All investigators independently screened the literature, extracted data, and evaluated the quality. Stata 16.0 software and RevMan 5.4.1 were used to analyze the data of the literature that met the quality standards. Finally, 53 RCTs were included, involving 6 Chinese patent medicines. The total sample size was 4 891 cases, including 2 449 cases in the test group and 2 442 cases in the control group. The network Meta-analysis showed that(1) in terms of reducing TNF-α, the top 3 optimal interventions according to the surface under the cumulative ranking curve(SUCRA) were Shenshuaining Capsules/Granules/Tablets + conventional western medicine, Jinshuibao Capsules + conventional western medicine, and Niaoduqing Granules + conventional western medicine.(2) In terms of reducing hs-CRP, the top 3 optimal interventions according to SUCRA were Bailing Capsules + conventional western medicine, Tripterygium Glycosides Tablets + conventional western medicine, and Shenshuaining Capsules/Granules/Tablets + conventional western medicine.(3) In terms of reducing IL-6, the top 3 optimal interventions according to SUCRA were Bailing Capsules + conventional western medicine, Tripterygium Glycosides Tablets + conventional western medicine, and Jinshuibao Capsules + conventional western medicine.(4) In terms of reducing UAER, the top 3 optimal interventions according to SUCRA were Shenshuaining Capsules/Granules/Tablets + conventional western medicine, Huangkui Capsules + conventional western medicine, and Jinshuibao Capsules + conventional western medicine.(5) In terms of reducing Scr, the top 3 optimal interventions according to SUCRA were Jinshuibao Capsules + conventional western medicine, Niaoduqing Granules + conventional wes-tern medicine, and Tripterygium Glycosides Tablets + conventional western medicine.(6) In terms of reducing BUN, the first 3 optimal interventions according to SUCRA were Niaoduqing Granules + conventional western medicine, Tripterygium Glycosides Tablets + conventional western medicine, and Huangkui Capsules + conventional western medicine.(7) In terms of improving the clinical total effective rate, the first 3 optimal interventions according to SUCRA were Jinshuibao Capsules + conventional western medicine, Niaoduqing Granu-les + conventional western medicine, and Huangkui Capsules + conventional western medicine. The results showed that the combination of western medicine and Chinese patent medicine could reduce the expression of serum inflammatory factors TNF-α, hs-CRP, and IL-6 and inhibit the inflammatory response. The combination of western medicine and Chinese patent medicine was superior to western medicine alone in reducing Scr, BUN, and UAER, and improving the total effective rate of treatment. Due to the limitation of the quantity and quality of literature included, the above conclusions need to be validated by more high-quality studies.

Erroneous presentation of respiratory-hemodynamic disturbances and postsurgical inflammatory responses in patients having undergone abdominal cavity cancer surgery.

In this letter to the editor, the authors discuss the findings and shortcomings of a published retrospective study, including 120 patients undergoing surgery for gastric or colon cancer under general anesthesia. The study focused on perioperative dynamic respiratory and hemodynamic disturbances and early postsurgical inflammatory responses.

Effects of S-ketamine on Postoperative Recovery Quality and Inflammatory Response in Patients Undergoing Modified Radical Mastectomy.

S-ketamine plays an important role in reducing postoperative pain, but its impact on the quality of recovery in breast cancer has not been clarified. We designed this trial to explore the effects of s-ketamine on the quality of postoperative recovery and inflammatory response in modified radical mastectomy. A total of 138 patients were randomly assigned to group C (group control), group K1 (group of s-ketamine dose 1) and group K2 (group of s-ketamine dose 2). Groups K1 and K2 were given 0.1mg/kg, 0.2mg/kg s-ketamine intravenous (IV) after induction, followed by 0.1mg/kg/h or 0.2mg/kg/h continuous intravenous infusion, respectively. Group C received the same volume of saline. A 40-item Quality of Recovery Questionnaire (QoR-40) was used to assess the quality of recovery at 24h postoperatively. Changes in inflammatory markers, nociceptive thresholds, and the occurrence of adverse events were recorded at 24h postoperatively. The QoR-40 scores at 24h postoperatively were higher in group K2 [182.00 (179.00-185.00)] compared to group K1 [174.00 (169.50-180.50)] and group C [169.00 (163.75-174.25)] (group K2 vs. group K1, P < 0.001; group K2 vs. group C, P < 0.001). At 24h postoperatively, the neutrophil count, NLR (neutrophil-lymphocyte ratio), and CRP (C-creative protein) were all significantly lower in group K2 than group C(P < 0.05), no differences were observed between group K1 and C(P > 0.05), group K1 and K2(P > 0.05), respectively. There was no significant difference in the incidence of adverse effects among the three groups (P > 0.05). A high dose of s-ketamine improved the quality of recovery at 24h after surgery, as well as alleviated the inflammatory response without increasing the incidence of adverse effects.

Nausea Predicts Bacteremia in Immunocompetent Patients with Pneumococcal Community-Acquired Pneumonia: Secondary Data Analysis from a Prospective Cohort.

In pneumococcal community-acquired pneumonia (CAP), bacteremia is associated with increased mortality, but initial clinical severity scores frequently fail to identify bacteremic patients at risk. We have previously shown that gastrointestinal symptoms are common among patients admitted to the hospital with pneumococcal bacteremia. The aim of this study was to examine gastrointestinal symptoms and inflammatory responses in bacteremic and non-bacteremic pneumococcal CAP in a prospective cohort of immunocompromised and immunocompetent patients hospitalized with CAP. Logistic regression analysis was used to estimate the predictive value of gastrointestinal symptoms for pneumococcal bacteremia in patients with CAP. The Mann-Whitney test was used to compare inflammatory responses in patients with bacteremic vs. non-bacteremic pneumococcal CAP. Eighty-one patients with pneumococcal CAP were included, of whom 21 (26%) had bacteremia. Immunocompetent patients with pneumococcal CAP had an odds ratio of 16.5 (95% CI 3.0-90.9, p = 0.001) for bacteremia if nausea was present, whereas no such association was found in the immunocompromised patients (OR 0.22, 95% CI 0.02-2.05, p = 0.18). The serum levels of C-reactive protein, procalcitonin and interleukin 6 were significantly higher in the patients with bacteremic pneumococcal CAP compared to non-bacteremic pneumococcal CAP patients (p < 0.001, p = 0.005, and p = 0.019, respectively). In immunocompetent patients hospitalized with pneumococcal CAP, nausea may be a predictor of bacteremia. Bacteremic pneumococcal CAP patients display an increased inflammatory response compared to non-bacteremic pneumococcal CAP patients.

Relationship between systemic inflammatory response and hypercoagulation in patients with immuno-inflammatory rheumatic diseases

The relationship between the processes of coagulation and inflammation protects the organism from potentially dangerous biological agents. However, hyperinflammation leads to an increase in the procoagulation potential, and activation of hemostasis factors maintains the inflammatory process. This phenomenon is called “immunothrombosis” or “ thromboinflammation”. The study of thromboinflammatory mechanisms is an actual problem of modern medicine, because in the future it will help to improve the therapy of diseases, in the pathogenesis of which thromboinflammation plays a significant role. The aim: to carry out a comparative analysis of the severity of the systemic inflammatory response in patients with immuno- inflammatory rheumatic diseases depending on the manifestations of hypercoagulation.To achieve the aim, a comparative analysis of proinflammatory markers (IL-6, IL-8, IL-10, TNFα, sIL-2R, CRP, ECP, β2-microglobulin) in the blood of patients with immune-inflammatory rheumatic diseases (systemic lupus erythematosus, rheumatoid arthritis, reactive arthritis, ankylosing spondylitis, psoriatic arthritis, rheumatic heart disease) was performed. Based on these inflammatory markers according to the authors' original methodology, the integral index of systemic inflammatory response (SIR) — Reactivity Level (RL) — was calculated. The cohort was divided into 2 groups: with the presence of signs of hypercoagulation and without signs of hypercoagulation according to the presence of elevated D-dimer level (&gt; 500 ng/mL). Control group — healthy blood donors.The results of the study showed that SIR develops in patients with immuno-inflammatory rheumatic diseases regardless of the blood hemostatic potential. Patients with signs of hypercoagulation were characterized by higher values of most proinflammatory molecular markers, as well as increased integral level of SIR, which indicates a strong relationship between coagulation processes and inflammation at the systemic level. In addition, the probability of hypercoagulation increases with increasing severity of SIR (assessed by means of the integral index — RL). Thus, there is a transition of quantitatively more pronounced signs to a new qualitative level of pathological process development.The pathogenesis of immuno-inflammatory rheumatic diseases is characterized by the development of SIR (hypercytokinemia, acute phase response, intravascular leukocyte activation), the severity of which is closely related to intravascular microthrombosis.

Identification of the relationship between biomarkers of autophagy, apoptosis and inflammation in the acute period of atherothrombotic ischemic stroke

The postischemic inflammatory response plays a significant role in the pathogenesis of acute ischemic stroke (IS). It has been established that acute IS is accompanied by aseptic inflammation, which induces the activation of costimulatory molecules in the process of innate immunity response to brain tissue damage. The constantly progressive destruction of neuronal antigens contributes to an increase in the volume of the ischemic lesion. Evidence continues to accumulate indicating an important role of NLRP3-mediated inflammation in the pathogenesis of IS. It has been shown that autophagy is involved in the inflammatory cascade in acute IS. Many of the anti-inflammatory mechanisms mediated by autophagy in acute IS involve the key autophagic proteins Beclin-1, LC3, and p62. Experimental studies have shown that autophagy suppresses the activation of NLRP3 inflammation. Data on cross interactions between apoptosis and autophagy in the pathogenesis of IS are still controversial. The aim of the study was to evaluate the relationship between biomarkers of autophagy, inflammation, and apoptosis in the dynamics of the acute period of atherothrombotic IS. The article presents the results of a dynamic study of the serum concentration of the key autophagy biomarkers Beclin-1, LC3 and p62, apoptosis indicators Bcl-2 and p53, pro-inflammatory cytokines IL-1β, TNFα, IL-8, IL-18 which are involved in postischemic neuroinflammation. A statistically significant increase in the studied parameters was established in comparison with the control group. The maximum increase in the studied biomarkers is noted on the 1st day after the development of ischemia in patients with a severe course of the disease. The relationship between autophagy activity, apoptosis biomarkers, and some indicators of the systemic inflammatory response in patients with moderate and severe atherothrombotic stroke was revealed. The results obtained confirm the literature data on the involvement of autophagy in the regulation of the postischemic inflammatory response.

Effect of Postoperative Self-Controlled Intravenous Analgesia Using Nalbuphine Hydrochloride Mixed with Sufentanil on Inflammatory Response in Patients Undergoing Laparoscopic Myomectomy

Effect of Postoperative Self-Controlled Intravenous Analgesia Using Nalbuphine Hydrochloride Mixed with Sufentanil on Inflammatory Response in Patients Undergoing Laparoscopic Myomectomy

Effects of vitamin D supplementation on inflammatory response in patients with cancer and precancerous lesions: Systematic review and meta-analysis of randomized trials

Inflammation plays a key role in tumor development and progression. Vitamin D has potential tumor suppressing effects through modulation of inflammatory processes. The aim of this systematic review and meta-analysis of randomized controlled trials (RCTs) was to summarize and evaluate the effects of vitamin D3 supplementation (VID3S) on serum inflammatory biomarkers among patients with cancer or pre-cancerous lesions. We searched PubMed, Web of Science and Cochrane databases until November 2022. The effects of VID3S were estimated from pooled standardized mean differences (SMDs) with their 95% confidence intervals (CIs) for inflammatory biomarker follow-up levels between intervention and control groups. Meta-analysis of eight RCTs (total of 592 patients with cancer or pre-cancerous conditions) showed that VID3S significantly lowered levels of serum tumor necrosis factor (TNF)-α (SMD [95%CI]:-1.65 [-3.07;-0.24]). VID3S also resulted in statistically non-significantly lower serum levels of interleukin (IL)-6 (SMD [95%CI]:-0.83, [-1.78; 0.13]) and C-reactive protein (CRP) (SMD [95%CI]:-0.09, [-0.35; 0.16]), whereas IL-10 levels were unaltered (SMD [95%CI]:-0.00, [-0.50; 0.49]). Our study shows evidence of a significant reduction of TNF-α levels by VID3S for patients with cancer or precancerous lesions. Patients with cancer or precancerous lesions may benefit from personalized VID3S in suppressing tumour-promoting inflammatory response. CRD42022295694.

Impact of endoprosthesis type on inflammatory response in patients undergoing endoscopic drainage of pancreatic fluid collections.

To study the impact of endoprosthesis type on inflammatory response in patients undergoing endoscopic ultrasound (EUS)-guided drainage of pancreatic fluid collections (PFC). Patients undergoing EUS-guided PFC drainage and treated using lumen-apposing metal stents (LAMS) or plastic endoprostheses constituted the study cohort. The primary outcome was the presence of systemic inflammatory response syndrome (SIRS) after index intervention. Secondary outcomes were persistent organ failure, new onset organ failure, duration of hospitalization, and treatment success. In all, 303 patients were treated using LAMS (n = 247) or plastic stents (n = 56). At 48 h postintervention, the presence of SIRS (25.0 vs. 14.2%, P = 0.047), new onset SIRS (10.0 vs. 1.8%, P = 0.017), and new organ failure (5.4 vs. 0.4%, P = 0.003) were significantly higher in the plastic stent cohort compared to LAMS. On multivariable logistic regression analysis, the use of plastic stents (odds ratio [OR] 2.7, 95% confidence interval [CI] 1.2-6.0, P = 0.014), patients receiving high-acuity care (OR 5.1, 95% CI 2.5-10.4, P < 0.001) and the presence of ≥33% of necrosis (OR 4.5, 95% CI 2.0-10.0, P < 0.001) were significantly associated with the presence of SIRS or new organ failure. While there was no significant difference in treatment success (96.4 vs. 95.5%, P = 0.77), duration of hospitalization was significantly longer for the plastic stent cohort (mean [standard deviation] 12.5 [17.8] vs. 7.9 [10.1] days, P = 0.009). Use of plastic stents as compared to LAMS was associated with a higher proportion of SIRS and new organ failure that prolonged hospital stay. Therefore, placement of LAMS is recommended in sick patients and those with ≥33% necrosis to minimize inflammatory response.

Infusion of GMSCs relieves autoimmune arthritis by suppressing the externalization of neutrophil extracellular traps via PGE2-PKA-ERK axis

IntroductionRheumatoid arthritis (RA) is a systemic autoimmune disease with limited treatment success, characterized by chronic inflammation and progressive cartilage and bone destruction. Accumulating evidence has shown that neutrophil extracellular traps (NETs) released by activated neutrophils are important for initiating and perpetuating synovial inflammation and thereby could be a promising therapeutic target for RA. K/B × N serum transfer-induced arthritis (STIA) is a rapidly developed joint inflammatory model that somehow mimics the inflammatory response in patients with RA. Human gingival-derived mesenchymal stem cells (GMSCs) have been previously shown to possess immunosuppressive effects in arthritis and humanized animal models. However, it is unknown whether GMSCs can manage neutrophils in autoimmune arthritis. ObjectivesTo evaluate whether infusion of GMSCs can alleviate RA by regulating neutrophils and NETs formation. If this is so, we will explore the underlying mechanism(s) in an animal model of inflammatory arthritis. MethodsThe effects of GMSCs on RA were assessed by comparing the symptoms of the K/B × N serum transfer-induced arthritis (STIA) model administered either with GMSCs or with control cells. Phenotypes examined included clinical scores, rear ankle thickness, paw swelling, inflammation, synovial cell proliferation, and immune cell frequency. The regulation of GMSCs on NETs was examined through immunofluorescence and immunoblotting in GMSCs-infused STIA mice and in an in vitro co-culture system of neutrophils with GMSCs. The molecular mechanism(s) by which GMSCs regulate NETs was explored both in vitro and in vivo by silencing experiments. ResultsWe found in this study that adoptive transfer of GMSCs into STIA mice significantly ameliorated experimental arthritis and reduced neutrophil infiltration and NET formation. In vitro studies also showed that GMSCs inhibited the generation of NETs in neutrophils. Subsequent investigations revealed that GMSCs secreted prostaglandin E2 (PGE2) to activate protein kinase A (PKA), which ultimately inhibited the downstream extracellular signal-regulated kinase (ERK) pathway that is essential for NET formation. ConclusionOur results demonstrate that infusion of GMSCs can ameliorate inflammatory arthritis mainly by suppressing NET formation via the PGE2-PKA-ERK signaling pathway. These findings further support the notion that the manipulation of GMSCs is a promising stem cell-based therapy for patients with RA and other autoimmune and inflammatory diseases.

Linking platelet lipidome and inflammatory response in septic patients

Sepsis is characterized by major endothelial dysfunction, microvascular alterations, and coagulopathy. Platelets are important players in sepsis as they promote thrombo-inflammation and generate lipidic mediators of inflammation. Previously, we observed that platelet acetyl-CoA carboxylase 1 (ACC1), responsible for de novo lipid synthesis, is phosphorylated and thus inhibited by AMP-activated protein kinase (AMPK) upon thrombin stimulation, leading to platelet lipidome changes. The role of the AMPK-ACC signaling in the regulation of platelet lipidome during sepsis, and its potential impact on inflammation, has never been investigated. To investigate whether changes in ACC phosphorylation can influence the platelet lipidome and the inflammatory response of patients during sepsis. Platelets and plasmas were isolated from 48 septic and 48 control patients. In parallel, WT and DKI mice injected intraperitoneally with lipopolysaccharides were used as a model of endotoxemia. Platelets ACC1 phosphorylation/expression levels were measured by western blot. Lipidomics analysis was carried out by untargeted liquid chromatography–mass spectrometry or on the commercial Lipidyzer platform. Plasma factors were measured by Enzyme-linked immunosorbent assays (ELISA). Platelet ACC1 expression and phosphorylation were increased both in septic patients and in septic mice. Lipidomics analysis highlighted significant changes of lipids in human and murine platelets during sepsis, with a substantial reduction in phosphatidylcholines and phosphatidylethanolamines containing long polyunsaturated fatty acid chains (ω3 and ω6), which are key phospholipids for the generation of pro- and anti-inflammatory lipid mediators. Our preliminary data obtained in humans and mice, suggest that elevated ACC phosphorylation in sepsis is associated with a higher content of these phospholipids as well as a plasma reduction in myeloid inflammatory parameters. Our data reveal that critical changes in the platelet lipidome occur during sepsis and may contribute to the pathophysiology of the disease. Our results also suggest that ACC can influence the platelet lipid content and/or composition.

Effect of nitric oxide synthase gene polymorphism on inflammatory response in patients with chronic obstructive pulmonary disease

This study aimed to investigate the association between nitric oxide synthase gene polymorphisms and the inflammatory responses in patients with ‘fast-’ and ‘slow-’ developing chronic obstructive pulmonary disease (COPD). In the main process, 190 patients with slow-developing COPD, 94 patients with fast-developing COPD and 105 healthy volunteers were selected for inclusion. Endothelial nitric oxide synthase (eNOS) was detected using western-blot eNOS sites, and inducible nitric oxide synthase (iNOS) was detected through SNPshot. T helper 17 cells (Th17) and regulator T (Treg) cells were detected via flow cytometry, and interferon-gamma, tumour necrosis factor-alpha, interleukin (IL)-17, IL-10, IL-6, IL-4 and IL-2 were detected using a cytometric bead array. The final results and conclusions drawn from the tests suggest that Th17/Treg-mediated immune inflammation plays an important role in the pathogenesis of COPD, but whether it affects the development of COPD needs further investigation. Overall, COPD patients with a young age of onset, young age of smoking initiation and small body mass index, as well as COPD patients with CC at rs3729508 in the iNOS gene and non-GG at rs7830 in the eNOS gene, may be more likely to contract fast-developing COPD.

ABCG2 plays a central role in the dysregulation of 25-hydrovitamin D in Crohn's disease

Vitamin D (VD) deficiency, as indicated by the main circulating form of VD metabolite 25-hydrovitamin D3 (25(OH)D3), in patients with Crohn's disease (CD) has been well documented, but the reasons for this remain unclear. In this study, 367 patients with CD and 57 healthy individuals who were enrolled, and the association between 25 (OH)D3 level and clinical biochemical characteristics including hepatic and renal functions, inflammatory response was analyzed with binary logistic regression models. VD metabolic enzymes and transporters were screened with bioinformatical analysis and identified with qRT-PCR and western blot. Compared to the healthy controls, serum 25(OH)D3 was significantly reduced in patients with CD, but the protein level of adenosine triphosphate (ATP)-binding cassette efflux transporter G2 (ABCG2) was evidently increased in the ileum and colon. Meanwhile, in lipopolysaccharide (LPS)-treated CaCO2 cells, the mRNA and protein levels of ABCG2 were significantly increased, and the overexpression of ABCG2 obviously promoted 25(OH)D3 efflux, but, Ko143, an ABCG2 inhibitors, substantially prevented the efflux of 25(OH)D3. In addition, in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced CD model mice, the ABCG2 protein levels were significantly increased in the ileum, colon, kidney and liver, and administration of Ko143 significantly inhibited the efflux of 25 (OH) D3in vivo. All of these findings suggest that VD deficiency in patients with CD may be associated with an abnormal increase in ABCG2 expression, but not directly implicated in hepatic and renal function, and inflammatory response in patients with CD.

Clinical value of the systemic immune-inflammation index in moyamoya disease.

Moyamoya disease (MMD) is a rare cerebrovascular disorder with unknown etiology. The underlying pathophysiological mechanism of moyamoya disease remains to be elucidated, but recent studies have increasingly highlighted that abnormal immune response may be a potential trigger for MMD. Neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII) are inflammatory markers that can reflect the immune-inflammation state of the disease. The purpose of this study was to investigate SII, NLR, and PLR in patients with moyamoya disease. A total of 154 patients with moyamoya disease (MMD group) and 321 age- and sex-matched healthy subjects (control group) were included in this retrospective case-control study. Complete blood count parameters were assayed to calculate the SII, NLR, and PLR values. The SII, NLR, and PLR values in the moyamoya disease group were significantly higher than those in the control group [754 ± 499 vs. 411 ± 205 (P < 0.001), 2.83 ± 1.98 vs. 1.81 ± 0.72 (P < 0.001), and 152 ± 64 vs. 120 ± 42 (P < 0.001), respectively]. The SII in the medium-moyamoya vessels of moyamoya disease was higher than that in the high-moyamoya vessels and low-moyamoya vessels (P = 0.005). Using the receiver operating characteristic (ROC) curve analysis to predict MMD, the highest area under the curve (AUC) was determined for SII (0.76 for SII, 0.69 for NLR, and 0.66 for PLR). Based on the results of this study, patients with moyamoya disease admitted for inpatient care due to acute or chronic stroke have significantly higher SII, NLR, and PLR when compared to blood samples drawn from completely healthy controls in a non-emergent outpatient setting. While the findings may suggest that inflammation plays a role in moyamoya disease, further studies are warranted to corroborate such an association. In the middle stage of moyamoya disease, there may be a more intense imbalance of immune inflammation. Further studies are needed to determine whether the SII index contributes to the diagnosis or serves as a potential marker of an inflammatory response in patients with moyamoya disease.

Arterial wall inflammation assessed by 18F-FDG-PET/CT is higher in individuals with Type 1 diabetes and associated with circulating inflammatory proteins.

The article investigates whether chronic hyperglycaemia in Type 1 diabetes (T1D) is associated with a proinflammatory immune signature and with arterial wall inflammation, driving the development of atherosclerosis. Patients with T1D (n = 41), and healthy age-, sex-, and body mass index-matched controls (n = 20) were recruited. Arterial wall inflammation and haematopoietic activity were measured with 2'-deoxy-2'-(18F)-fluoro-D-glucose (18F-FDG) positron emission tomography/computed tomography. In addition, flow cytometry of circulating leucocytes was performed as well as targeted proteomics to measure circulating inflammatory markers. 18F-FDG uptake in the wall of the abdominal aorta, carotid arteries, and iliac arteries was higher in T1D compared with that in the healthy controls. Also, 18F-FDG uptake in the bone marrow and spleen was higher in patients with T1D. CCR2 and CD36 expressions on circulating monocytes were higher in patients with T1D, as well as several circulating inflammatory proteins. In addition, several circulating inflammatory markers (osteoprotegerin, transforming growth factor-alpha, CX3CL1, and colony-stimulating factor-1) displayed a positive correlation with FDG uptake. Within T1D, no differences were found between people with a high and low HbA1c. These findings strengthen the concept that chronic hyperglycaemia in T1D induces inflammatory changes that fuel arterial wall inflammation leading to atherosclerosis. The degree of hyperglycaemia appears to play a minor role in driving this inflammatory response in patients with T1D.

The pleiotropic effects of statins in rheumatoid arthritis.

Rheumatoid arthritis (RA) is an inflammatory and autoimmune disease. Studies over the past two decades suggest that statins have a beneficial impact on the complications associated with RA. These complications include RA disease activity and risk for cardiovascular diseases (CVD). This review aims to discuss the efficacy of statin therapy in RA. The current evidence suggests that statins' immunomodulatory and antioxidant properties significantly reduce disease activity and inflammatory response in patients with RA. In RA patients, the risk of CVD is reduced by statin treatment, and statin discontinuation is associated with an increased cardiovascular disease risk. The combined effect of statins on improving vascular function, lowering lipid levels, and reducing inflammation in RA patients is responsible for the decreased all-cause mortality in statin users. Further clinical studies are needed to ensure the therapeutic efficacy of statins in patients with RA.

Evaluation of preclinical efficacy of human umbilical cord mesenchymal stem cells in ankylosing spondylitis.

Umbilical cord mesenchymal stem cells (UCMSCs) have significant regenerative, tissue repair, and immunomodulatory properties that can help reduce inflammatory responses in patients with ankylosing spondylitis (AS). In this study, we used a combination of bovine proteoglycan and dimethyldioctadecylammonium (DDA) to establish a mouse model of proteoglycan-induced spondylitis (PGISp). To evaluate the therapeutic effects of UCMSCs, we treated PGISp mice with different doses of hUCMSCs via tail vein injection. At week 13, the PGISp mice exhibited thickened, erythematous paws, erythema in the extremities, and lameness. CT scans revealed necrotic lysis of chondrocytes, formation of fissures, visible hemorrhage, connective tissue hyperplasia, and focal infiltration of lymphocytes in the intervertebral discs. At week 14, the PGISp mice were randomly divided into three groups and administered different doses of hUCMSCs (0.25, 0.5, and 1.0×107 cells/kg, iv, QOW×2, n=10). To assess the therapeutic effects of hUCMSCs, we evaluated Th cell subsets in the spleen, spleen and thymus coefficients, peripheral blood inflammatory factors, and pathological and imaging observations of the spines and lumbar spines in the PGISp mice. The results demonstrated that injection of hUCMSCs shifted the balance axis between Th1 and Th2 cells in the spleen towards Th2 cells. Moreover, the spleen coefficient and levels of inflammatory cytokines (TNF-α and CCL-2) in the serum decreased after hUCMSC injection. CT imaging and pathological analysis indicated that hUCMSC treatment inhibited ectopic osteogenesis and maintained clear small joint gaps, which slowed down the progression of structural lesions in the disc, nucleus pulposus, fibrous ring, and cartilage in PGISp mice. Administering hUCMSCs at the 14th week after modeling proved to be an effective treatment for PGISp mice. This experiment offers a valuable reference for the pre-clinical use of hUCMSCs in the treatment of AS.