Serum Levels Of Interleukin-1 Beta Research Articles

Serum Levels of Interleukin-1 Beta are Decreased in Patients with Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis at the Time of Hospitalization

BACKGROUND: Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe cutaneous adverse drug reactions. Some immunological and genetic factors are believed to be involved in the pathogenesis of the disease, including tumor necrotic factor-alpha, interferon-gamma, and interleukin (IL)-17. IL-1β is one of the most prominent cytokines associated with the innate immune response. AIMS: The study aimed to evaluate the serum level of IL-1β in SJS/TEN and the relation between it and the progress of SJS/TEN. METHODS: This was a cross-sectional descriptive study conducted at the National Hospital of Dermatology and Venereology, in Hanoi, Vietnam, from October 2017 to September 2019. 48 SJS/TEN patients, 43 erythema multiforme (EM) patients, and 20 healthy controls (HCs) participated. IL-1β levels were measured using the fluorescence covalent microbead immunosorbent assay (ProcartaPlex Immunoassay Panels kit, Thermo Fisher Scientific, USA). The Mann–Whitney U test was used to compare serum IL-1β levels. The Wilcoxon tests were used to compare quantitative variables before and after the treatment. Differences were considered to be statistically significant at p < 0.05. RESULTS: 19 SJS patients (39.5%) and 29 TEN patients (60.5%) participated in our study. The mean age was 49.3 years; the range was 19–77 years (47.9% males; 52.1% females). The most common causative drugs were traditional medicine (29.1%), carbamazepine (12.5%), and allopurinol (12.5%). On the day of hospitalization, the mean serum level of IL-1β of the SJS/TEN group was 26.4 ± 81.7 pg/mL, ranging from 0.5 pg/mL to 447 pg/mL. This level was significantly lower than that of the HCs group (p < 0.001) but not lower than that of the EM group. The mean serum level of IL-1β in the SJS/TEN patients on the day of hospitalization was 26.4 ± 81.7 pg/ml, higher than that on the day of re-epithelialization (1.9 ± 5.6 pg/mL) and the difference was statistically significant with p < 0.01. CONCLUSION: Serum IL-1β level in SJS/TEN patients is lower than in HCs. It is not a good biomarker to differentiate SJS/TEN from EM.

Free water alterations in different inflammatory subgroups in schizophrenia

BackgroundAccumulating evidence suggests that inflammatory dysregulation both in blood and the brain is implicated in the pathogenesis of schizophrenia. Alterations in peripheral cytokines are not evident in all patients and there may be discrete altered inflammatory subgroups in schizophrenia. Recent studies using a novel and in vivo free-water imaging to detect inflammatory processes, have shown increased free water in white matter in schizophrenia. However, no studies to date have investigated the free water alterations in different inflammatory subgroups in schizophrenia. MethodsForty-four patients with schizophrenia and 49 controls were recruited. The serum levels of interleukin-1 beta (IL-1β), IL-6, IL-10, and IL-12p70 were measured and used for cluster analysis with K-means and hierarchical algorithms. Diffusion tensor imaging (DTI) images were collected for all participants and voxel-wise free water and fractional anisotropy of tissue (FA-t) were compared between groups with Randomise running in FSL. Partial correlation analysis was employed to explore the association of the peripheral cytokine levels with free water. ResultsWe identified two statistically quantifiable discrete subgroups of patients based on the cluster analysis of cytokine measures. The peripheral levels of IL-1β (P < 0.001), IL-10 (P = 0.041), and IL-12p70 (P < 0.001) showed significant differences between the two different inflammatory subgroups. In the inflammatory subgroup with a predominantly higher IL-1β level, increased free water values in white matter were found mainly in the left posterior limb of the internal capsule, posterior corona radiata, and partly in the left sagittal stratum. These affected areas did not overlap with the regions that showed significant free water differences between patients and healthy controls. In the inflammatory subgroup with lower IL-1β levels, peripheral IL-1β was significantly associated with free water values in white matter while no such association was detected in the patient group. ConclusionsLocalized free water differences were demonstrated between the two identified inflammatory subgroups in our data, and free water appears to be a feasible in vivo neuroimaging biomarker guiding the target of inflammatory intervention and development of new therapeutic strategies in an individualized manner in schizophrenia.

Association of Long Non-Coding RNA Malat1 with Serum Levels of Interleukin-1 Beta and Vitamin D in Patients with Ischemic Stroke

Background:Previous studies have demonstrated the strong association of inflammatory cytokines and vitamin D (VitD) deficiency and ischemic stroke (IS) pathogenesis. Due to the negative correlation between long non-coding RNA (lncRNA) Malat1 and pro-inflammatory factors we decided to investigate the associations between Malat1 expression with serum interleukin-1β (IL-1β), and VitD levels in IS patients. Materials and Methods:In this cross-sectional study, 63 IS patients were included. We used enzyme-linked immunosorbent assays to evaluate the serum levels of VitD and IL-1β. Malat1 expression was evaluated by the real-time polymerase chain reaction test. The associations between Malat1expression with VitD and IL-1β were analysed with linear regression (Stepwise model) and Pearson’s correlation analysis. Results: The Malat1 expression was inversely correlated with stroke severity (r=-0.25, P=0.043). Stepwise regression analysis showed a significant positive relationship between VitD level and Malat1 expression (Beta=0.28, P=0.02), and also showed a non-significant negative relationship between IL-1β and stroke severity. VitD level showed a positive Pearson correlation with Malat1 (r=0.28, P=0.023) and a negative correlation with IL-1β (r=-0.29, P=0.018) while it could not detect a significantly negative correlation with stroke severity. Conclusion: For the first time the associations between Malat1 expression with IL-1β and VitD in IS patients was analyzed. We found a significant positive relationship between VitD and Malat1. This correlation needs to be investigated with a larger sample size to achieve a strong and reliable association between VitD and Malat1.[GMJ.2023;12:e2457]

Association of Long Non-Coding RNA Malat1 with Serum Levels of Interleukin-1 Beta and Vitamin D in Patients with Ischemic Stroke.

Previous studies have demonstrated the strong association of inflammatory cytokines and vitamin D (VitD) deficiency and ischemic stroke (IS) pathogenesis. Due to the negative correlation between long non-coding RNA (lncRNA) Malat1 and pro-inflammatory factors we decided to investigate the associations between Malat1 expression with serum interleukin-1β (IL-1β), and VitD levels in IS patients. In this cross-sectional study, 63 IS patients were included. We used enzyme-linked immunosorbent assays to evaluate the serum levels of VitD and IL-1β. Malat1 expression was evaluated by the real-time polymerase chain reaction test. The associations between Malat1expression with VitD and IL-1β were analysed with linear regression (Stepwise model) and Pearson's correlation analysis. The Malat1 expression was inversely correlated with stroke severity (r=-0.25, P=0.043). Stepwise regression analysis showed a significant positive relationship between VitD level and Malat1 expression (Beta=0.28, P=0.02), and also showed a non-significant negative relationship between IL-1β and stroke severity. VitD level showed a positive Pearson correlation with Malat1 (r=0.28, P=0.023) and a negative correlation with IL-1β (r=-0.29, P=0.018) while it could not detect a significantly negative correlation with stroke severity. For the first time the associations between Malat1 expression with IL-1β and VitD in IS patients was analyzed. We found a significant positive relationship between VitD and Malat1. This correlation needs to be investigated with a larger sample size to achieve a strong and reliable association between VitD and Malat1.

Evaluation of the therapeutic and the chemical effects of balneological treatment on clinical and laboratory parameters in knee osteoarthritis: a randomized, controlled, single-blinded trial.

The purpose of this study was to investigate the therapeutic and the chemical effects of balneological treatment (peloidotherapy + hydrotherapy), and its effects on serum levels of interleukin-1beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and insulin-like growth factor-1 (IGF-1) in patients with knee osteoarthritis (OA). Sixty-four (64) knee OA patients were randomly divided into study and control groups. Balneological treatment, consisting of hydrotherapy, and peloidotherapy were given to both groups. Unlike the study group, in the control group, the peloid was applied over a stretch film cover, preventing any contact between the skin and peloid. Clinical outcome measures of the study were pain degree, patient's and investigator's global assessment on visual analog scale (VAS-pain, VAS-PGA, VAS-IGA), and Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) (pain, stiffness, and physical function). Patients were evaluated at baseline, post-treatment (after 10th session), and 3 and 6 months after treatment. Blood samples were taken at baseline, post- treatment, and 6 months after treatment for analysis of IL-1β, TNF-α, and IGF-1 serum levels. When compared with the baseline, VAS measurements decreased significantly in almost all evaluation periods in both groups, and no difference was observed between the groups. In the study group, WOMAC scores showed significant improvement in all assessments. In the control group, pain and physical function subscores of WOMAC significantly decreased at post-treatment and 3 months after treatment. In group comparison, pain and stiffness subscores showed a significant difference in favor of the study group at 6 months after treatment. No clinically significant improvement was seen in levels of IL-1β and IGF-1 in both groups during the whole assessment period. Because of TNF-α kit failure, we could not evaluate the measurements. In conclusion, balneological treatment is an effective treatment option to improve the pain and functional capacity of patients with knee OA. The application of peloid by contact with the skin is superior in the long-term period, which means that in addition to the thermal effect, the chemical content of peloid can also contribute to the therapeutic effect.

Cerebral Structural Abnormalities and Their Associations With Peripheral Cytokine Levels in a Group of Untreated Patients With Nasopharyngeal Carcinoma.

The current study is to characterize the alterations of peripheral cytokines and anatomical brain changes, and their relationships in untreated nasopharyngeal carcinoma (NPC) patients with depressive symptoms. Twenty-nine newly diagnosed NPC patients without any treatment and 46 matched healthy comparisons were recruited, scanned with high-resolution T1 images and assessed psychologically using Hamilton Rating Scale for Depression (HAMD). Serum levels of interleukin-1 beta (IL-1β), IL-2, IL-6, IL-8, IL-10, interferon-gamma (IFN-γ) and transforming growth factor-beta (TGF-β) were measured by quantitative chemiluminescence assay. Inter-group comparisons of anatomical brain measures were performed, and regions with significant inter-group differences were correlated to HAMD scores and cytokines in NPC patients. A subgroup analysis especially within NPC patients with depression was conducted to precisely characterize the associations among serum cytokines, brain changes and depressive symptoms. Relative to healthy subjects, NPC patients showed significantly decreased cortical thickness in the left parahippocampal gyrus, increased surface area in the right superior parietal lobule and precentral gyrus, and increased gray matter volume in the right postcentral gyrus, bilateral caudate nucleus and right thalamus, as well as significantly elevated IL-1β, IL-2 and IL-10. The elevated IL-2 and IL-10 were negatively correlated with surface area in right superior parietal lobule, whilst IL-1β level was positively correlated to HAMD scores. In patients with depression, specific brain changes and evaluated IL-1β were identified, and the IL-1β interacted with right precentral gyrus to significantly affect the depressive symptoms. Our findings provide novel evidence indicating potential effects of inflammation on brain structure and behavior in NPC patients.

The effect of water-based intervention on sleep habits and two sleep-related cytokines in children with autism

ObjectivePrevious studies have shown that children with autism have sleep disturbances and elevated levels of pro-inflammatory cytokines. This study aimed to evaluate the effect of aquatic exercise on sleep habits and two certain sleep-related cytokines of children with autism spectrum disorders (ASD). MethodsForty boys with ASD (aged 6–14) were recruited and randomly assigned to an aquatic exercise (n = 20) or a control group (n = 20). Participants in aquatic exercise group performed water-based activities for 10 weeks/2 sessions per week/60 min, while control group didn't get any intervention. The serum levels of Interleukin-1 beta (IL-1β) and Tumor necrosis factor-α (TNF-α) and sleep quality were measured before and after the intervention. ResultsResults revealed that aquatic exercise may improve sleep quality and reduce the serum levels of IL-1β and TNF-α in children with ASD compared to control group. ConclusionsOverall, it is recommended that physicians and educators should provide a safe and effective exercise environment for ASD children to alleviate sleep issues and inflammatory biomarkers.

Blockade of anti-dsDNA ameliorates systemic lupus erythematosus in MRL/Faslpr mice through ameliorating inflammation via the PKCδ-NLRC4 axis.

Anti-double-stranded DNA (anti-dsDNA) is closely associated with the inflammatory burden in the brain after ischemic stroke. Here, we studied the inflammatory cascade and investigated the mechanisms behind the pro-inflammatory role of dsDNA in systemic lupus erythematosus (SLE). The serum levels of interleukin-1beta (IL-1β) and IL-6 in SLE patients and the corresponding controls were evaluated using ELISA, and the expression level of caspase-1 was evaluated using quantitative real-time polymerase chain reaction (qRT-PCR). We found that the serum levels of IL-1β and IL-6 were increased in the SLE patients. The expression of caspase-1 was upregulated and positively correlated with the levels of pro-inflammatory factors. The level of anti-dsDNA was also elevated and positively correlated with the results for the mean fluorescence intensity (MFI) of caspase-1. Additionally, we evaluated the functions of PRKCD encoding protein kinase c delta (PKCδ) and NLRC4, in vivo, in MRL/Faslpr mice. We found that renal injury was aggravated, and the levels of pro-inflammatory factors were increased in the MRL/Faslpr mice. We also found that increased levels of NLRC4 in the mice exacerbated renal injury and increased the levels of pro-inflammatory factors, whereas inhibition of PKCδ had the opposite results. These findings provide unique perspectives on pathogenesis of SLE and indicate that inhibition of anti-dsDNA could attenuate renal inflammatory burden, representing a promising therapeutic opportunity for SLE.

Central and peripheral immune responses to low-dose lipopolysaccharide in a mouse model of the 15q13.3 microdeletion

Carriers of the human 15q13.3 microdeletion (MD) present with a variable spectrum of neuropathological phenotypes that range from asymptomatic to severe clinical outcomes, suggesting an interplay of genetic and non-genetic factors. The most common 2 MB 15q13.3 MD encompasses six genes (MTMR10, FAN1, TRPM1, KLF13, OTUD7A, and CHRNA7), which are expressed in neuronal and non-neuronal tissues. The nicotinic acetylcholine receptor (nAChR) α7, encoded by CHRNA7, is a key player in the cholinergic anti-inflammatory pathway, and the transcription factor KLF13 is also involved in immune responses. Using a mouse model with a heterozygous deletion of the orthologous region of the human 15q13.3 (Df[h15q13]/+), the present study examined peripheral and central innate immune responses to an acute intraperitoneal (i.p.) injection of the bacteriomimetic, lipopolysaccharide (LPS) (100 μg/kg) in adult heterozygous (Het) and wildtype (WT) mice. Serum levels of inflammatory markers were measured 2 h post injection using a Multiplex assay. In control saline injected animals, all measured cytokines were at or below detection limits, whereas LPS significantly increased serum levels of interleukin 1beta (IL-1β), tumor necrosis factor alpha (TNF-α), IL-6 and IL-10, but not interferon-γ. There was no effect of genotype but a sexual dimorphic response for TNF-α, with females exhibiting greater LPS-induced TNF-α serum levels than males. In situ hybridization revealed similar increases in LPS-induced c-fos mRNA expression in the dorsal vagal complex in all groups. The hippocampal expression of the pro-inflammatory cytokines was evaluated by real-time quantitative PCR. LPS-treatment resulted in significantly increased mRNA expression for IL-1β, IL-6, and TNF-α compared to saline controls, with no effect of genotype, but a significant sex-effect was detected for IL-1β. The present study provided no evidence for interactive effects between the heterozygous 15q13.3 MD and a low-dose LPS immune challenge in innate peripheral or central immune responses, although, sex-differential effects in males and females were detected.

Association of peripheral cytokine levels with cerebral structural abnormalities in schizophrenia

A large body of evidence indicates that both the altered cytokines that mediate the immune-inflammatory process and abnormal gray matter are associated with schizophrenia. Whether peripheral cytokines are related to cerebral structural abnormality remains unclear. Therefore, we aimed to investigate the association of peripheral cytokine levels with gray matter abnormalities at the whole brain level in schizophrenia. Forty-four outpatients with schizophrenia and 44 controls were recruited. The serum levels of interleukin-1 beta (IL-1β), IL-2, IL-6, IL-8, interferon-gamma (IFN-γ), transforming growth factor-beta (TGF-β), and IL-10 were measured using a quantitative chemiluminescence assay. High-resolution T1 weighted images were acquired from all subjects and processed using FreeSurfer software to obtain the cortical thickness, surface area, and cortical and subcortical gray matter volumes. The cytokines and cerebral structures were compared between patients and controls using analysis of covariance (ANCOVA). The association between the cytokines and whole cerebral structures was performed using stepwise linear regression. Patients had higher levels of IL-2, IL-6, IL-8, and IL-10 than controls. In patients, the IL-6 level was significantly associated with the cortical thickness in the left pars opercularis, right pars triangularis, left superior temporal gyrus, and right middle temporal gyrus, which showed structural differences between the two groups. Altered cytokine levels may be associated with particular but not all cortical abnormalities in schizophrenia, especially IL-6, which was significantly associated with the abnormal cortical thickness of the bilateral Broca’s area and temporal gyrus, which provided neuroimaging evidence to support the relationship between peripheral cytokines and the cerebral cortex in schizophrenia.

Levels of cytokines and GADA in type I and II diabetic patients

BackgroundDiabetes Mellitus is described as a group of metabolic diseases in which the patient has higher blood glucose levels due to many causes. These include a defect in insulin secretion and failure of the body's cells to respond to the hormone. Cytokines and autoantibodies have a critical role in the pathogenesis of diabetes, especially type I. Aim of the studyThe aim of this study was to measure the serum levels of interleukin-1 beta (IL-1 β), interleukin-3 (IL-3), interferon-gamma (INF- γ), and glutamic acid decarboxylase autoantibody (GADA) in patients with type I and type II diabetes mellitus. Material and methodsIn this cross-sectional study, serum samples were taken from 250 individuals, including 100 samples from patients with type II diabetes mellitus, 100 samples from healthy controls, and 50 samples from patients with type I diabetes mellitus. Five milliliters of venous blood were taken from each individual and the samples were analyzed for cytokines (IL-1 β, IL-3, and INF- γ) and GABA using ELISA. ResultsIn the study, we found that the serum levels of IL-1 β were significantly higher in the healthy control group compared to the patients with type I and type II diabetes mellitus. The levels of IL-3 and INF- γ were significantly higher in type II diabetes mellitus, while GABA serum levels were higher in type I diabetes mellitus. ConclusionOur data showed that GADA is an important autoantibody, not only in type I but also in type II diabetes mellitus and can probably be used in the future for diagnosis of this disease. There was also a close association of GADA with systemic immunoregulation in type I and II diabetes mellitus. The relation of cytokines (IL-1 β, IL-3, and INF- γ) and GADA in patients with diabetes will also increase our understanding for the immunology of diabetes mellitus and to propose specific treatment on the basis of our findings. Our data also include correlation between age and the level of cytokines and GADA with different conclusion for each parameter.

Lemon-Peel extract ameliorates rheumatoid arthritis by reducing xanthine oxidase and inflammatory cytokine levels

Abstract We investigated the effect of a lemon-peel extract in a rat model of rheumatoid arthritis and SW1353 chondrocytes. The rats were divided into control (sham), rheumatoid arthritis (control), extract (150 mg/kg bwt) and extract (300 mg/kg bwt) groups. Pyrogallic acid, caffeic acid, eugenol, p-coumaric acid, p‑hydroxyl benzoic acid, resorcinol, salicylic acid, luteoline, quercetin, chrysin, and luteolin-3‑methoxy‑7-rutinoside were noted in the extracts. The extract was administered orally for five consecutive weeks, and antioxidant and inflammatory markers were investigated. Extracts markedly increased the plasma levels of catalase, superoxide dismutase, reduced glutathione, glutathione peroxidase and zinc, and reduced those of lipid peroxidation, nitric oxide, uric acid, ceruloplasmin, copper, matrix metalloproteinase-3 and prostaglandin E2. Moreover, the extracts reduced the serum levels of interleukin-1 beta, tumor necrosis factor-alpha and interleukin-6. Extracts at 50, 100 and 150 mg/L reduced chondrocyte proliferation by 20.9, 38.8, and 52.1%, respectively, and reduced the reactive oxygen species and NF-κB levels by > 40%. Furthermore, the lemon-peel extract at 50, 100 and 150 mg/L reduced the xanthine oxidase level by 0.26-, 0.55- and 0.89-fold, respectively. Taking all these data together, it is suggested the lemon peel extract ameliorated rheumatoid arthritis, reduced the SW1353 chondrocyte proliferation, ROS, inflammatory cytokines, and xanthine oxidase levels.

Nesfatin-1 Ameliorates Testicular Function Changes in Type 2 Diabetic Rats

Nesfatin-1 Ameliorates Testicular Function Changes in Type 2 Diabetic Rats

Effects of melatonin treatment on the spermatogenesis and serum inflammatory cytokine levels in diabetic rats

Aim: Diabetes mellitus (DM) is known to have side effects on sexual and reproductive functions in males. The aim of current study was to investigate the effect of melatonin treatment on spermatogenesis and serum inflammatory cytokine levels in diabetic rats. Material and Method: Eighteen adult Wistar albino male rats were divided randomly into three groups each containing 6 rats; control group (group 1), diabetic group (group 2), diabetic treated with melatonin group (group 3). Experimental diabetes was obtained by administrating 50 mg/kg streptozotocin. Melatonin treatment was administered intraperitoneally for 7 days at a dose of 20 mg, daily. Serum levels of interleukin-1 beta (IL-1β), interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were assayed. Spermatogenesis was evaluated according to Johnsen score at immunopathological examination.Results: The Johnsen scores in control, diabetic and treatment groups were 9.78, 8.91, and 9.61, respectively. Spermatogenesis was negatively affected in diabetic rats and significantly improved with melatonin therapy (p0.05). The serum levels of TNF-α in diabetic rats were observed to be increased compared to the control group (p0.05). The levels of serum IL-1β and TNF- α were significantly decreased with melatonin treatment. IL-6 levels were not different among the three groups (p=0.248). Conclusions: In the present study, intraperitoneal melatonin treatment was determined to have a positive effect of on spermatogenesis and caused a decrease in serum inflammatory cytokine levels in diabetic rats.Keywords: Cytokines; Diabetes Mellitus; Melatonin; Rats; Spermatogenesis.

Serum levels of interleukin-1 beta associate better with severity of simple steatosis than liver function tests in morbidly obese patients.

Background:In high-fat diet-fed mice, interleukin-1 beta (IL-1 beta) has been shown to play a key role in hepatic steatosis. However, it remains unknown whether IL-1 beta could be associated with different grades of steatosis in obese humans.Materials and Methods:Morbidly obese patients (n = 124) aged 18–65 years were divided into four groups: no steatosis (controls), mild steatosis, moderate steatosis, and severe steatosis using abdominal ultrasound. IL-1 beta serum levels and liver function tests were measured and significant differences were estimated by one-way ANOVA followed by Tukey test.Results:IL-1 beta serum levels significantly increased in morbidly obese patients with mild (11.38 ± 2.40 pg/ml), moderate (16.72 ± 2.47 pg/ml), and severe steatosis (23.29 ± 5.2 pg/ml) as compared to controls (7.78 ± 2.26 pg/ml). Liver function tests did not significantly change among different grades of steatosis.Conclusion:IL-1 beta serum levels associate better with steatosis degree than liver function tests in morbidly obese population.

Huanglian-Wendan Decoction Inhibits NF-κB/NLRP3 Inflammasome Activation in Liver and Brain of Rats Exposed to Chronic Unpredictable Mild Stress.

Depression is a common mental disorder in modern society. A traditional Chinese medicine Huanglian-Wendan decoction with potential anti-inflammation is used as a clinical antidepressant. Our previous study showed central and peripheral inflammatory responses in a rat model of depression developed by chronic unpredictable mild stress (CUMS). Here, we investigated the anti-inflammatory activity and mechanism of Huanglian-Wendan decoction in CUMS rats. LC-MS/MS and HPLC were performed to determine the major compounds in water extract of this decoction. This study showed that Huanglian-Wendan decoction significantly increased sucrose consumption and reduced serum levels of interleukin-1 beta (IL-1β), IL-6, and alanine aminotransferase (ALT) in CUMS rats. Moreover, this decoction inhibited nuclear entry of nuclear factor-kappa B (NF-κB) with the reduction of phosphorylated protein of NF-κB (p-NF-κB) and inhibitor of NF-κB alpha (p-IκBα) and downregulated protein of nod-like receptor family pyrin domain-containing 3 (NLRP3), apoptosis-associated speck-like protein containing CARD (ASC), cysteinyl aspartate-specific proteinase-1 (Caspase-1), and IL-1β in liver and brain regions of CUMS rats. These findings demonstrated that Huanglian-Wendan decoction had antidepressant activity with hepatoprotection in CUMS rats coinciding with its anti-inflammation in both periphery and central. The inhibitory modulation of NF-κB and NLRP3 inflammasome activation by Huanglian-Wendan decoction may mediate its antidepressant action.

Apolipoprotein M Protects Against Lipopolysaccharide-Induced Acute Lung Injury via Sphingosine-1-Phosphate Signaling.

It had been demonstrated that apolipoprotein M (apoM) is an important carrier of sphingosine-1-phosphate (S1P) in blood, and the S1P has critical roles in the pathogenesis of sepsis-induced acute lung injury (ALI). In the present study, we investigated whether apoM has beneficial effects in a mouse model after lipopolysaccharide (LPS)-induced ALI. Forty-eight mice were divided into two groups: male C57BL/6 wild-type (apoM+/+) group (n = 24) and apoM gene-deficient (apoM-/-) group (n = 24) and then randomly subdivided into four subgroups (n = 6 each) according to different intraperitoneal (i.p.) injection: control group, W146 group, LPS group, and LPS + W146 group. Serum levels of interleukin-1 beta (IL-1β) and mRNA levels of IL-1β, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), lung histology, wet/dry weight ratio, and immunohistochemistry were measured at 3h after the baseline and compared in each group. Our results clearly demonstrated that IL-1β mRNA levels and other inflammatory biomarkers were significantly increased in the lungs of LPS-induced ALI apoM-/- mice compared to those of the apoM+/+ mice. Moreover, when apoM+/+ mice were treated with W146, a S1P receptor (S1PR1) antagonist, these inflammatory biomarkers could be significantly upregulated by LPS-induced ALI. Therefore, it suggests that apoM-S1P-S1PR1 signaling might underlie the pathogenesis of ALI and apoM could have physiological benefits to alleviate LPS-induced ALI.

Delirium in patients with acute ischemic stroke admitted to the non-intensive stroke unit: Incidence and association between clinical features and inflammatory markers

BackgroundStroke patients with development of delirium have unfavorable outcomes, higher mortality, longer hospitalizations, and a greater degree of dependence after discharge. Studies suggest that delirium is associated with abnormal immunological responses and a resultant increase in inflammatory markers. ObjectiveOur aim was to determine whether there is an entity relationship between delirium, inflammation and acute ischemic stroke (AIS). MethodsSixty AIS patients admitted to the hospital were consecutively recruited. Delirium was diagnosed with the clinical assessment according to the Statistical Manual of Mental Disorders, Fifth Edition (DSM-V) criteria. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum levels of Interleukin-1 beta (IL-1 beta), Interleukin 18 (IL-18), Tumor Necrosis Factor-alpha (TNF-alpha), Brain-Derived Neurotrophic Factor (BDNF), and Neuron Specific Enolase (NSE) at admission. ResultsEleven (18.3%) of 60 patients were diagnosed with delirium, and the majority (n=8, 72.7%) was the hypoactive type. Delirious and non-delirious patients had similar demographic and clinical features. Delirious patients had significantly higher lengths of hospital stay, National Institutes of Health Stroke Scale (NIHSS) at admission and discharge compared to non-delirious patients. In addition, there was no significant statistical difference between delirious and non-delirious patients with AIS in respect of levels of TNF-alpha, IL-1 beta, IL-18, BDNF and NSE. This study suggests that delirium is not scarce in patients with AIS admitted to the non-intensive stroke unit, and that delirium developing after AIS seems not to be associated with serum TNF-alpha, IL-1 beta, IL-18, BDNF and NSE but is associated with length of hospital stay and stroke severity.

Serum levels of interleukin-1 beta, interleukin-6 and melatonin over summer and winter in kidney deficiency syndrome in Bizheng rats.

To observe the seasonal changes in serum levels of interleukin-1 beta (IL-1β), interleukin-6 (IL-6) and melatonin (MT) in Bizheng rat model, and explore the relationship between MT and the pathogenesis of rheumatoid arthritis. One hundred and sixty Sprague-Dawley rats were randomly divided into four groups in summer (n=80) and winter (n=80) respectively: normal group, collagen-induced arthritis (CIA) model group, operation group, and sham-operation group (n=20 in each group). The CIA model group was injected with collagen emulsion at the base of the tail to induce arthritis. The rats in the operation group received pineal gland resection, and 7 days after the first operation, underwent testectomy or oophorectomy. The rats in the sham-operation group were operated to ligature the sagittal sinus, without extracting the pineal gland. After the operations, the operation group and the sham-operation group both were immunized as the CIA group was. The serum levels of IL-1β, IL-6 and MT in different groups were measured by radioimmunoassay. Compared with the normal group, the serum levels of IL-1β and IL-6 increased in the CIA model, operation, and sham-operation groups both in summer and in winter (IL-1β in summer, P=0.008, P<0.01, P=0.012; IL-1β in winter, P=0.019, P<0.01, P=0.027; IL-6 in summer, P=0.028, P<0.01, P=0.024; IL-6 in winter, P=0.006, P<0.01, P=0.008). In the operation group, the serum levels of IL-1β and IL-6 in winter were higher than in summer, but with no statistically significant differences (P=0.844, 0.679). Compared with the normal group, the serum level of MT significantly increased in summer and winter in both the CIA model group (P=0.002, 0.008) and the sham-operation group (P=0.003, 0.007), while significantly decreased in the operation group (P=0.023, 0.003). There was no significant difference in MT level in the operation group between summer and winter (P=0.947). The increase of serum levels of IL-1β and IL-6 may exacerbate the inflammatory reaction and cause a more severe condition in the rheumatoid arthritis. The concentrations of IL-1β, IL-6, and MT correspond with the change of seasons, confirming that there are connections between nature and human body.

Potential Biomarkers for Intellectual Disability: A Gipsy Family Study

Intellectual disability (ID) is frequently due to the synergic action of environmental and genetic factors. Here we describe the particular case of three Gipsy Italian siblings, fifteen, twelve and eleven years old, with ID. Genetic analysis stated that the parents are not consanguineous, and no human leukocyte antigen (HLA) alleles related to autism and/or other neurological disorders are present in the 3 ID patients. Instead, a positive association of ID with brain derived neurotrophic factor (BDNF) (Val66Met and C270T), IL6 (-174) and interleukin 1receptor antagonist (IL1RA) mspa 11100 polymorphisms was demonstrated in these three ID patients. Moreover, serum levels of interleukin 1beta (IL1β), interleukin 6 (IL6) were significantly different between the three patients and controls.