scholarly journals The Role Of IL-6 In TMPD-Treated Lupus Arthritis Mice

2017 ◽  
Vol 3 (6) ◽  
pp. 468
Author(s):  
Niken Indriyanti
Keyword(s):  
Lupus Erythematosus ◽  
Severity Score ◽  
Treated Group ◽  
Preclinical Study ◽  
Knee Joints ◽  
Isolated Cells ◽  
Arthritis Severity ◽  
Naive Group ◽  
Severe Erosion

Lupus or systemic lupus erythematosus is a chronic autoimmune disease with systemic inflammation manifestations mainly in targeted organs. The appropriate animal model for lupus is necessary. The induction method by using 2,6,10,14 tetramethylpentadecane (TMPD) reveals more complex manifestations than other hydrocarbons. However, the autophagy of macrophages as an effect of TMPD makes differences to make the decision in lupus biomarker as a targeted therapy in lupus arthritis. Thus, this research focused on the role of CD68+IL-6 produced by macrophages and total IL-6 in lupus in correlation to the arthritis severity. The naïve and TMPD-treated groups (n=3) were induced by means of 0.5 ml TMPD i.p. After 6 months, the mice were sacrificed then the fresh spleens were prepared as isolated cells to be measured by using flow cytometry method. The knee joints were prepared for histology observation. The statistical analysis was performed by using T-test SPSS 22 version. The results showed the relative percentage of CD68+IL-6+ in the TMPD-treated group increased significantly (P<0.05) with the value of 62.38±9.97 %, compared to naïve group 49.70±2.34 %. Moreover, the total IL-6 did not increase significantly (P>0.05). Meanwhile, the arthritis severity score of the TMPD-treated group revealed severe erosion with the grade of 3.7±1.06, higher significantly (P<0.05) than the naïve group (0.5±0.71). The joint spaces in both groups were not significantly different. Finally, the observations gave the clear information that despite the autophagy potency, the CD68+IL-6 and the arthritis severity score were good markers in lupus preclinical study. Keywords: CD68+IL-6; inflammation; lupus arthritis; TMPD  

Tryptophan-Niacin Metabolism in Rat with Puromycin Aminonucleoside-Induced Nephrosis

2006 ◽  
Vol 76 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Yukari Egashira ◽  
Shin Nagaki ◽  
Hiroo Sanada
Keyword(s):  
Body Weight ◽  
Urinary Excretion ◽  
Enzyme Activities ◽  
Treated Group ◽  
Control Group ◽  
Puromycin Aminonucleoside ◽  
Low Level ◽  
Key Enzyme

We investigated the change of tryptophan-niacin metabolism in rats with puromycin aminonucleoside PAN-induced nephrosis, the mechanisms responsible for their change of urinary excretion of nicotinamide and its metabolites, and the role of the kidney in tryptophan-niacin conversion. PAN-treated rats were intraperitoneally injected once with a 1.0% (w/v) solution of PAN at a dose of 100 mg/kg body weight. The collection of 24-hour urine was conducted 8 days after PAN injection. Daily urinary excretion of nicotinamide and its metabolites, liver and blood NAD, and key enzyme activities of tryptophan-niacin metabolism were determined. In PAN-treated rats, the sum of urinary excretion of nicotinamide and its metabolites was significantly lower compared with controls. The kidneyα-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) activity in the PAN-treated group was significantly decreased by 50%, compared with the control group. Although kidney ACMSD activity was reduced, the conversion of tryptophan to niacin tended to be lower in the PAN-treated rats. A decrease in urinary excretion of niacin and the conversion of tryptophan to niacin in nephrotic rats may contribute to a low level of blood tryptophan. The role of kidney ACMSD activity may be minimal concerning tryptophan-niacin conversion under this experimental condition.

The role of microRNAs (MiR-125a and MiR-146a), RANTES, and IFN-γin systemic lupus erythematosus

2020 ◽  
Vol 23 (13) ◽  
Author(s):  
Ikram khazal Qasim Al- hasso ◽  
Aida Rashid Al- Derzi ◽  
Ahmed Abdul-hassan Abbas ◽  
Faiq I. Gorial ◽  
Ahmed Sameer Alnuimi
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Systemic Lupus

Inhibition of microRNA-155 Alleviates Neurological Dysfunction Following Transient Global Ischemia and Contribution of Neuroinflammation and Oxidative Stress in the Hippocampus

2020 ◽  
Vol 25 (40) ◽  
pp. 4310-4317 ◽  
Author(s):  
Lichao Sun ◽  
Shouqin Ji ◽  
Jihong Xing
Keyword(s):  
Oxidative Stress ◽  
Brain Edema ◽  
Severity Score ◽  
Global Ischemia ◽  
Signal Pathways ◽  
Neurological Severity Score ◽  
Tnf Α ◽  
Transient Global Ischemia ◽  
And Oxidative Stress

Background/Aims: Central pro-inflammatory cytokine (PIC) signal is involved in neurological deficits after transient global ischemia induced by cardiac arrest (CA). The present study was to examine the role of microRNA- 155 (miR-155) in regulating IL-1β, IL-6 and TNF-α in the hippocampus of rats with induction of CA. We further examined the levels of products of oxidative stress 8-isoprostaglandin F2α (8-iso PGF2α, indication of oxidative stress); and 8-hydroxy-2’-deoxyguanosine (8-OHdG, indication of protein oxidation) after cerebral inhibition of miR-155. Methods: CA was induced by asphyxia and followed by cardiopulmonary resuscitation in rats. ELISA and western blot analysis were used to determine the levels of PICs and products of oxidative stress; and the protein expression of NADPH oxidase (NOXs) in the hippocampus. In addition, neurological severity score and brain edema were examined to assess neurological functions. Results: We observed amplification of IL-1β, IL-6 and TNF-α along with 8-iso PGF2α and 8-OHdG in the hippocampus of CA rats. Cerebral administration of miR-155 inhibitor diminished upregulation of PICs in the hippocampus. This also attenuated products of oxidative stress and upregulation of NOX4. Notably, inhibition of miR-155 improved neurological severity score and brain edema and this was linked to signal pathways of PIC and oxidative stress. Conclusion: We showed the significant role of blocking miR-155 signal in improving the neurological function in CA rats likely via inhibition of signal pathways of neuroinflammation and oxidative stress, suggesting that miR-155 may be a target in preventing and/or alleviating development of the impaired neurological functions during CA-evoked global cerebral ischemia.

Role of Quercetin in Mitigation of Lindane Induced Toxicity in Terms of Oxidative Responses and Metabolic Status in Mice Brain

2020 ◽  
Vol 16 ◽  
Author(s):  
Anupama Sharma ◽  
Renu Bist ◽  
Hemant Pareek
Keyword(s):  
Citrate Synthase ◽  
Thiobarbituric Acid ◽  
Tca Cycle ◽  
Treated Group ◽  
Protein Carbonyl ◽  
Protein Carbonyl Content ◽  
Mice Brain ◽  
The Brain ◽  
Oxidative Responses

Background:: Current study evaluated the protective potential of quercetin against lindane induced toxicity in mice brain. For investigation, mice were allocated into four groups; First group was control. Second group was administered with oral dose of lindane (25 mg/kg bw) for 4 consecutive days. Third group was exposed to quercetin (40 mg/kg bw) and in fourth group, quercetin was administered 1 hour prior to the exposure of lindane. Objective:: Two major objectives were decided for study. First was to create lesions in the brain by lindane and; second was to evaluate the neuroprotective potential of quercetin. Methods:: To study oxidative responses, level of thiobarbituric acid reactive substances (TBARS), protein carbonyl content (PCC), reduced glutathione (GSH), superoxide dismutase (SOD), Catalase (CAT), and glutathione peroxidase (GPx) were measured in brain homogenates. Three key step regulating enzymes of tricarboxylic acid (TCA) cycle viz citrate synthase (CS), pyruvate dehydrogenase (PDH) and fumarase were also assayed. Results:: Lindane treatment significantly enhanced the levels of TBARS (P<0.001),PCC (P<0.001), GPx (P<0.001), SOD (P<0.05), PDH (P<0.05) and fumarase (P<0.001) in brains of mice compared to control. Meanwhile, it alleviated GSH, CAT and CS (P<0.05) activity. Conclusion:: Pretreatment with quercetin in lindane treated group not only restored, previously altered biochemical parameters after lindane treatment and also significantly improved them too which suggests that quercetin is not only invulnerable rather neuroprotective against lindane intoxication.

scholarly journals Acute interstitial nephritis and drug-induced systemic lupus erythematosus due to chlorthalidone and amiodarone: A case report

2020 ◽  
Vol 8 ◽  
pp. 2050313X2091002 ◽  
Author(s):  
Umut Selamet ◽  
Ramy M Hanna ◽  
Anthony Sisk ◽  
Lama Abdelnour ◽  
Lena Ghobry ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Interstitial Nephritis ◽  
Lupus Erythematosus ◽  
Kidney Biopsy ◽  
Kidney Injury ◽  
Acute Interstitial Nephritis ◽  
Systemic Lupus ◽  
Drug Induced ◽  
Systemic Manifestations

Drug-induced lupus erythematosus has features distinct from primary systemic lupus erythematosus. It can occur with a wide variety of agents that result in the generation of anti-histone or other types of antibodies. Systemic manifestations of drug-induced systemic lupus erythematosus may include renal dysfunction due to circulating immune complexes or due to other immune reactions to the culprit medication(s). Acute interstitial nephritis occurs due to DNA–drug or protein–drug complexes that trigger an allergic immune response. We report a patient who developed acute kidney injury, rash, and drug-induced systemic lupus diagnosed by serologies after starting chlorthalidone and amiodarone. A renal biopsy showed acute interstitial nephritis and not lupus-induced glomerulonephritis. It is important to note that systemic lupus erythematosus and acute interstitial nephritis can occur together, and this report highlights the role of the kidney biopsy in ascertaining the pathological diagnosis and outlining therapy in drug-induced lupus erythematosus.

scholarly journals The Immune Tolerance Role of the HMGB1-RAGE Axis

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 564
Author(s):  
Haruki Watanabe ◽  
Myoungsun Son
Keyword(s):  
Immune Responses ◽  
Immune Tolerance ◽  
Lupus Erythematosus ◽  
Advanced Glycation Endproducts ◽  
High Mobility ◽  
Chromatin Binding ◽  
Advanced Glycation ◽  
Glycation Endproducts ◽  
Extracellular Milieu

The disruption of the immune tolerance induces autoimmunity such as systemic lupus erythematosus and vasculitis. A chromatin-binding non-histone protein, high mobility group box 1 (HMGB1), is released from the nucleus to the extracellular milieu in particular environments such as autoimmunity, sepsis and hypoxia. Extracellular HMGB1 engages pattern recognition receptors, including Toll-like receptors (TLRs) and the receptor for advanced glycation endproducts (RAGE). While the HMGB1-RAGE axis drives inflammation in various diseases, recent studies also focus on the anti-inflammatory effects of HMGB1 and RAGE. This review discusses current perspectives on HMGB1 and RAGE’s roles in controlling inflammation and immune tolerance. We also suggest how RAGE heterodimers responding microenvironments functions in immune responses.

scholarly journals OP0240 EPIDEMIOLOGY, PREDICTORS OF MORTALITY AND ROLE OF PROPHYLAXIS FOR PNEUMOCYSTITIS JIROVECI PNEUMONIA AMONG RHEUMATIC PATIENTS: A TERRITORY-WIDE STUDY

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 147-147
Author(s):  
C. W. S. Chan ◽  
H. Y. Chung ◽  
W. Y. Yeung ◽  
C. S. Lau ◽  
P. H. LI
Keyword(s):  
Lupus Erythematosus ◽  
Absolute Risk ◽  
Absolute Risk Reduction ◽  
Number Needed To Treat ◽  
Healthcare Database ◽  
Pneumocystis Jiroveci ◽  
Predictors Of Mortality ◽  
Prednisolone Dose ◽  
Rheumatic Patients

Background:Pneumocystis jiroveci pneumonia (PJP) is an opportunistic infection affecting immunocompromised individuals. Due to its high mortality, PJP prophylaxis is commonly recommended for many immunocompromising conditions. However, evidence regarding the burden and role of prophylaxis in PJP among rheumatic patients remains limited. There is lack of consensus for when and for whom to initiate prophylaxis. Delineating the epidemiology, predictors of mortality and efficacy of prophylaxis in PJP among rheumatic patients is urgently needed.Objectives:To delineate the epidemiology of PJP, identify predictors of mortality and evaluate the usefulness of prophylaxis in rheumatology patients.Methods:We performed a big-data cohort study based on the territory-wide healthcare database of the Hong Kong Hospital Authority. All patients with a diagnosis of anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV), immune-mediated myositis (IMM), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), or spondyloarthritis (SpA) between 2015-2019 were included. PJP were identified based on physician diagnosis and/or positive microbiological results from deep respiratory tract specimens. Prophylaxis was defined as prescription of a prophylactic dose of co-trimoxazole for at least 2 weeks and/or inhaled pentamidine. Prevalence of PJP, prophylaxis and mortality among rheumatic patients were calculated. Demographics, blood parameters and immunosuppressants use was also collected for multivariate analysis. Number needed to treat (NNT) analysis was performed based on absolute risk reduction of PJP in patients with and without prior PJP prophylaxis.Results:A total of 21,587 unique rheumatic patients were analysed (54% RA, 25% SLE, 13% SpA, 5% IMM, 2% AAV and 1% SSc). Between 2015-2019, 1141 (5.3%) patients were prescribed PJP prophylaxis and 48 (0.2%) developed PJP. None of those patients who developed PJP had received prophylaxis prior to infection. The risk of PJP was highest among SSc (1.8%), AAV (1.4%) and IMM (0.7%) patients, with NNT of SSc 36, AAV 48 and IMM 114. Within these disease entities, the majority of PJP occurred at prednisolone dose of 15mg/day (P15) or above (100% in SSc and IIM, 66.7% in AAV). Overall, PJP was associated with a mortality-rate of 39.6%. Glucocorticoid dose (daily prednisolone dose equivalent 29.1±23.5mg vs 11.4±7.2mg, P<0.01) and lymphopenia (0.44x109/L vs 0.90x109/L, P= 0.04) at PJP diagnosis were associated with PJP mortality in rheumatic patients.Conclusion:PJP is an uncommon but important infection in rheumatic patients associated with significant mortality. PJP prophylaxis is effective and should be considered in patients with SSc, AAV and IMM, especially in those receiving a steroid dose above P15.Disclosure of Interests:None declared

Symptomatic osteonecrosis of the hip and knee in patients with systemic lupus erythematosus: Prevalence, pattern, and comparison of natural course

Lupus ◽  
2021 ◽  
pp. 096120332110310
Author(s):  
Mehmet Ersin ◽  
Mehmet Demirel ◽  
Mehmet Ekinci ◽  
Lezgin Mert ◽  
Çiğdem Çetin ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Rheumatic Diseases ◽  
Lupus Erythematosus ◽  
Bone Structure ◽  
Survival Rates ◽  
Knee Joints ◽  
Joint Involvement ◽  
Systemic Lupus ◽  
Kaplan Meier ◽  
The Mean

Objective Osteonecrosis (ON), also known as avascular necrosis, is characterized by the collapse of the architectural bone structure secondary to the death of the bone marrow and trabecular bone. Osteonecrosis may accompany many conditions, especially rheumatic diseases. Among rheumatic diseases, osteonecrosis is most commonly associated with systemic lupus erythematosus (SLE). We assessed prevalence and distribution pattern of symptomatic ON in patients with SLE and compare the natural courses of hip and knee ON. Methods 912 SLE patients admitted between 1981 and 2012 were reviewed. SLE patients with symptomatic ON were retrospectively identified both from the existing SLE/APS database. The prevalence of symptomatic ON was calculated; with ON, the joint involvement pattern was determined by examining the distribution of the joints involved, and then the data about the hip and knee joints were entered in the Kaplan-Meier analysis. Kaplan-Meier methods were used to calculate 5- and 10-year rates of ON-related hip (the hip group) and knee survival (the knee group). Results Symptomatic ON developed in various joints in 97 of 912 patients with SLE, and the overall prevalence of ON was detected as 10.6%. The mean age at the time of SLE and ON diagnoses were 27.9 ± 9.9 (14–53) and 34.2 ± 11.3 (16–62) years, respectively. The mean duration from diagnosis of SLE to the first development of ON was 70.7± 60.2 (range = 0–216) months. The most common site for symptomatic ON was the hips (68%, n=66), followed by the knees (38%, n = 37). According to Kaplan-Meier analysis, hip and knee joint survival rates associated with 5-year ON were 51% and 88%, and 10-year survival rates were 43% and 84%, respectively. Conclusion We observed that the prevalence of symptomatic ON in patients with SLE was 10.6%. With the estimated 10-year survival rates of 40% versus 84% for the hip and knee joints, respectively, hip involvement may demonstrate a more aggressive course to end-stage osteoarthritis than the knee involvement.

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