scholarly journals Cytokines and immunoglobulin g response in donkeys with spontaneous Setaria equine infection

2019 ◽  
Vol 22 (2) ◽  
pp. 180-189 ◽  
Author(s):  
A.H. El Namaky ◽  
S. H. Hendawy ◽  
F. A. Abo-Aziza ◽  
H. M. Ashry
Keyword(s):  
Immunoglobulin G ◽  
Protein Profile ◽  
Sodium Dodecyl ◽  
Protein Band ◽  
Interleukin 4 ◽  
Necrosis Factor Alpha ◽  
Predictive Values ◽  
Reactive Protein ◽  
Apparent Prevalence ◽  
Tnf Α

Setaria equina (S. equina) is a filarial worm that exists in peritoneal cavity of equines. This study aimed to evaluate cytokine mediators tumour necrosis factor alpha (TNF-α), interleukin-4 (IL-4) and immunoglobulin G (IgG) responses in spontaneously S. equina infected and non-infected donkeys with emphasis on choosing the best antigen that could be used in diagnosis of such filarial infection. A total of 87 donkeys were examined. Two S. equina antigens: crude somatic S. equina antigen (CSS) and excretory secretory S. equina antigen (ESS) were prepared. They were evaluated in diagnosis of the infection using indirect ELISA and electrophoretically characterised through sodium dodecyl sulphate poly acrylamide gel electrophoresis (SDS-PAGE) and western blotting technique. The results indicated that both TNF-α and IL-4 in the serum of infected donkeys were significantly higher compared with the non-infected group at P<0.05 and P<0.01, respectively. However, the IL-4 level of infected donkeys was significantly higher than that of TNF-a (P<0.01). Apparent prevalence, specificity and positive predictive values (96.55%, 100%, and 100% each) of CSS showed higher diagnostic accuracy than that of ESS. In addition, electrophoretic protein profile and IgG reactivity of CSS antigen via western blot presented a prominent reactive protein band at 28 kDa. It was concluded that the CSS antigen was the best antigen that could be used in serodiagnosis of S. equina infection. The cytokine responses were explored in order to differentiate infected from non-infected donkeys.

THE EFFECT OF ATORVASTATINUM IN THE TREATMENT OF PATIENTS WITH RHEUMATOID ARTHRITIS

2020 ◽  
Vol 73 (11) ◽  
pp. 2427-2430
Author(s):  
Sergii V. Shevchuk ◽  
Yuliia S. Seheda ◽  
Inna P. Kuvikova ◽  
Olena V. Shevchuk ◽  
Olena Y. Galiutina
Keyword(s):  
Inflammatory Process ◽  
Necrosis Factor Alpha ◽  
Traditional Treatment ◽  
Reactive Protein ◽  
Tnf Α ◽  
Endothelium Function ◽  
Factor Alpha ◽  
Inflammatory Drugs ◽  
Serum Paraoxonase ◽  
Necrosis Factor

The aim: Was to evaluate the effect of 6-month pathogenetic treatment in combination with atorvastatinum on the endothelium function, lipid and adipokine levels, paroxonase activity and activity of inflammatory process in RA patients. Materials and methods: The study included 55 patients with RA, dividing into two groups depending on the intended therapy. The first group included 33 patients with “traditional” treatment by methotrexate, glucocorticoids, and non-steroid anti-inflammatory drugs. The second group included 22 patients with “traditional” treatment and additionally prescribed of atorvastatinum 20 mg/day. The lipid profile, leptin, adipokine, paroxonase activity. C-reactive protein (CRP) and tumor necrosis factor-alpha (TNF-α) levels, FMDBA and IMT of carotid artery were determined in all participants of the study. Control parameters were recorded before the start, after 1 and 6 months of treatment. Results: The FMDBA has increased by 32% in the second group, compared by only 10.9% in the first group. The dynamics of IMT in the first group was also twice lower than in group with the additional use of atorvastatinum. The leptin levels in the second group significantly decreased by 27% and adiponectin levels increased by 12.8%, than in the first group – by 12.8% and by 7% respectively. The appointment of statins over 6 months resulted in DAS28, TNF-α, ESR and CRP reduction by 15%, 31%, 25% and 21.5% respectively. In the first group the dynamics of indicate rates ranged from 7.8% to 22.5%, and was significantly lower than in the second group. Conclusions: As a result of the study, it was found that the appointment of atorvastatinum 20 mg/day during 6 months not only reduces dyslipidemia, but also significantly reduces the inflammatory process and adipokine dysregulation, normalizes serum paraoxonase activity and improves the endothelium function.

scholarly journals EVALUATION OF INFLAMMATION AND ENDOTHELIAL DYSFUNCTION BIOMARKERS IN CHRONIC KIDNEY DISEASE (CKD) PATIENTS IN SOKOTO, NIGERIA

2021 ◽  
Vol 1 (1) ◽  
pp. 1-9
Author(s):  
C. A. Otitolaiye ◽  
D. M. Sahabi ◽  
A. M. Makusidi ◽  
Y. Saidu ◽  
L. S. Bilbis
Keyword(s):  
Chronic Kidney Disease ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Kidney Disease ◽  
Progressive Increase ◽  
Necrosis Factor Alpha ◽  
Reactive Protein ◽  
Cardiovascular Morbidity And Mortality ◽  
Tnf Α ◽  
Variable Equation

Inflammation and endothelial dysfunction have been known to be involved in the pathogenesis of cardiovascular diseases. As such, examining the levels of inflammation and endothelial dysfunction is very critical to the prevention of cardiovascular diseases among chronic kidney disease (CKD) patients. This study aimed to investigate the progression of inflammation and endothelial dysfunction among CKD patients in Sokoto. A total of 67 CKD patients were divided into 5 groups based on the stages of their kidney disease calculated using the MDRD 4-variable equation for estimated glomerular filtration rate (eGFR). The presence of inflammation was determined by C-Reactive Protein (CRP) and Tumor Necrosis Factor alpha, while endothelial dysfunction was determined by the levels of Asymmetric dimethylarginine (ADMA) using ELISA kits. The mean eGFR of the patients was 49.97 ± 4.69 ml/min/1.73m2. There was significant increase (p<0.05) in CRP, TNF-α and ADMA of the CKD patients across the stages as compared to the non-CKD subjects. It was observed that as the CRP, TNF-α and ADMA increase, the eGFR significantly (p<0.05) decreases. Both CRP and TNF-α indicated a significantly positive correlation (p<0.05) with ADMA. The results indicated progressive increase in inflammation and endothelial dysfunction as CKD deteriorates. In addition, increased levels of inflammation could directly affect endothelial dysfunction, thereby aggravating cardiovascular morbidity and mortality among CKD patients in Sokoto. Otitolaiye, C. A. | Department of Biochemistry, Sokoto State University, Sokoto, Nigeria

scholarly journals Delanzomib, a Novel Proteasome Inhibitor, Combined With Adalimumab Drastically Ameliorates Collagen-Induced Arthritis in Rats by Improving and Prolonging the Anti-TNF-α Effect of Adalimumab

2021 ◽  
Vol 12 ◽  
Author(s):  
Lei Wang ◽  
Lixiong Liu ◽  
Xiaoping Hong ◽  
Dongzhou Liu ◽  
Zeneng Cheng
Keyword(s):  
Proteasome Inhibitor ◽  
Proteasome Inhibitors ◽  
Collagen Induced Arthritis ◽  
Initial Finding ◽  
Necrosis Factor Alpha ◽  
Reactive Protein ◽  
Tnf Α ◽  
Factor Alpha ◽  
Α Level

Delanzomib is a novel proteasome inhibitor initially developed for treating multiple myeloma. It was found to inhibit the expression of tumor necrosis factor alpha (TNF-α). This study aimed to investigate the ameliorating effect of delanzomib on collagen-induced arthritis (CIA) and to explore the pharmacodynamics and pharmacokinetics (PK) interactions between delanzomib and adalimumab. Rats with CIA were randomly assigned to receive the treatment with delanzomib, adalimumab, delanzomib combined with adalimumab, or placebo. Visual inspection and biochemical examinations including TNF-α, interleukin 6, and C-reactive protein were performed to assess arthritis severity during the treatment. The adalimumab concentration in rats was determined to evaluate the PK interaction between delanzomib and adalimumab. Also, the levels of neonatal Fc receptor (FcRn) and FcRn mRNA were measured to explore the role of FcRn in the PK interaction between delanzomib and adalimumab. As a result, delanzomib combined with adalimumab exhibited stronger anti-arthritis activity than a single drug because both drugs synergistically reduced TNF-α level in vivo. Delanzomib also decreased adalimumab elimination in rats by increasing the level of FcRn. The slower elimination of adalimumab in rats further prolonged the anti-TNF-α effect of adalimumab. Moreover, FcRn level was increased by delanzomib via suppressing FcRn degradation rather than promoting FcRn production. In conclusion, delanzomib combined with adalimumab may be a potential therapeutic approach for treating rheumatoid arthritis. The initial finding that the PK interaction occurred between delanzomib and adalimumab may have clinical relevance for patients who simultaneously take proteasome inhibitors and anti-TNF-α therapeutic proteins.

scholarly journals Flow Cytometric Determination of Cellular Sources and Frequencies of Key Cytokine-Producing Lymphocytes Directed against Recombinant LACK and Soluble Leishmania Antigen in Human Cutaneous Leishmaniasis

2001 ◽  
Vol 69 (5) ◽  
pp. 3232-3239 ◽  
Author(s):  
R. L. A. Bottrel ◽  
W. O. Dutra ◽  
F. A. Martins ◽  
B. Gontijo ◽  
E. Carvalho ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Cutaneous Leishmaniasis ◽  
Ex Vivo ◽  
Protozoan Parasite ◽  
Recombinant Antigen ◽  
Interleukin 4 ◽  
Leishmania Braziliensis ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Ifn Γ

ABSTRACT Leishmaniasis, caused by infection with the protozoan parasiteLeishmania, affects millions of individuals worldwide, causing serious morbidity and mortality. This study directly determined the frequency of cells producing key immunoregulatory cytokines in response to the recombinant antigen Leishmania homolog of receptors for activated kinase C (LACK) and soluble leishmania antigen (SLA), and it determined relative contributions of these antigens to the overall cytokine profile in individuals infected for the first time with Leishmania braziliensis. All individuals presented with the cutaneous clinical form of leishmaniasis and were analyzed for proliferative responses to LACK antigen and SLA, frequency of lymphocyte subpopulations (analyzed ex vivo), and antigen-induced (LACK and SLA) cytokine production at the single-cell level (determined by flow cytometry). The following were determined. (i) The Th1-type response previously seen in patients with cutaneous leishmaniasis is due to gamma interferon (IFN-γ) production by several different sources, listed in order of contribution: CD4+ T lymphocytes, CD4−, CD8− lymphocytes, and CD8+ T lymphocytes. (ii) SLA induced a higher frequency of lymphocytes producing IFN-γ and tumor necrosis factor alpha (TNF-α) than did LACK. (iii) LACK induced an activation of monocyte populations as reflected by an increased percentage of CD14-positive cells. (iv) Neither SLA nor LACK induced detectable frequencies of cells producing interleukin-4 (IL-4) or IL-5. These data demonstrated a multifaceted immune response to SLA in human leishmaniasis involving Th1 CD4+ T lymphocytes (IFN-γ+ and IL-10−/IL-4−), Tc1 CD8+ T cells (IFN-γ+, and IL-10−/IL-4−), and a high frequency of TNF-α-producing lymphocytes. Moreover, it was determined that the recombinant antigen LACK acts as a weak inducer of Th1-type lymphocyte responses compared to SLA.

scholarly journals Candida albicans Yeast and Germ Tube Forms Interfere Differently with Human Monocyte Differentiation into Dendritic Cells: a Novel Dimorphism-Dependent Mechanism To Escape the Host's Immune Response

2004 ◽  
Vol 72 (2) ◽  
pp. 833-843 ◽  
Author(s):  
Antonella Torosantucci ◽  
Giulia Romagnoli ◽  
Paola Chiani ◽  
Annarita Stringaro ◽  
Pasqualina Crateri ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Candida Albicans ◽  
Germ Tube ◽  
Immune Surveillance ◽  
Human Monocyte ◽  
Interleukin 4 ◽  
Human Monocytes ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Mrna Transcripts

ABSTRACT The ability of Candida albicans to convert from the yeast (Y) form to mycelial forms through germ tube (GT) formation is considered a key feature of the transition of the organism from commensalism to virulence. We show here that human monocytes cultured with granulocyte-macrophage colony-stimulating factor and interleukin-4 (IL-4) after phagocytosis of Y forms did not differentiate into dendritic cells (DCs); they retained CD14, did not acquire CD1a, and were unable to express the maturation markers CD83 and CCR7. Moreover, they did not produce IL-12p70 but secreted IL-10. In addition, they spontaneously expressed high levels of tumor necrosis factor alpha (TNF-α), IL-6, and IL-8 mRNA transcripts and were able to induce proliferation of alloreactive memory but not naïve T lymphocytes. Conversely, monocytes that had phagocytosed GT forms differentiated into mature CD83+ and CCR7+ DCs; however, there was no up-regulation of CD40, CD80, and major histocompatibility complex class II, irrespective of lipopolysaccharide (LPS) treatment. In addition, these cells were unable to produce IL-12 even after LPS stimulation, but they were not functionally exhausted, as shown by their capacity to express TNF-α and IL-8 mRNA transcripts. These cells were able to prime naïve T cells but not to induce their functional polarization into effector cells. These data indicate that phagocytosis of Y and GT forms has profound and distinct effects on the differentiation pathway of monocytes. Thus, the differentiation of human monocytes into DCs appears to be tunable and exploitable by C. albicans to elude immune surveillance.

scholarly journals Influence of TNF-α inhibition on oxidative stress of rheumatoid arthritis patients

Reumatismo ◽  
2016 ◽  
Vol 67 (3) ◽  
pp. 97 ◽  
Author(s):  
F. Cacciapaglia ◽  
M.G. Anelli ◽  
D. Rizzo ◽  
E. Morelli ◽  
C. Scioscia ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Health Assessment ◽  
Good Control ◽  
Oxidative Stress Marker ◽  
Reactive Oxygen Metabolites ◽  
Necrosis Factor Alpha ◽  
Reactive Protein ◽  
Tnf Α ◽  
Oxidative Stress Status

The aim of this study was to assess circulating levels of reactive oxygen metabolites (ROMs) as a marker of oxidative stress in rheumatoid arthritis (RA) patients during an anti-tumor necrosis factor alpha (TNF-α) treatment. We enrolled 40 patients with RA (36 females; age 53±13 yrs) treated with different subcutaneously administered TNF-α inhibitors. The oxidative status was determined on the basis of plasma samples taken before, at 24 and 52 weeks of the anti-TNF-α treatment. Hydroperoxide levels were measured using the d-ROMs test, a useful clinically proven oxidative stress marker. During the anti-TNF-α therapy, we observed a significant reduction in serum ROMs levels in RA patients from 33.2±10 mg H2O2/L at baseline to 29.5±7 and 29.3±9 mg H2O2/L, at 24 and 52 weeks, respectively (p&lt;0.05). We also identified a significant correlation between the oxidative stress status and the disease activity score on 28 joints/C-reactive protein and health assessment questionnaire disability index. The results of our study demonstrate that a good control of the disease with anti-TNF-α agents can reduce oxidative stress in RA patients. However, further studies of larger patient cohorts are needed to confirm these preliminary data.

scholarly journals Modulation of the Gut Microbiota by Sihocheonggan-Tang Shapes the Immune Responses of Atopic Dermatitis

2021 ◽  
Vol 12 ◽  
Author(s):  
Jaemoo Chun ◽  
So Min Lee ◽  
You Mee Ahn ◽  
Min-Gyung Baek ◽  
Hana Yi ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Gut Microbiota ◽  
Gut Microbiome ◽  
Immunoglobulin E ◽  
Therapeutic Potential ◽  
Interleukin 4 ◽  
Hacat Cells ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Ifn Γ

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by complex immune dysregulation and closely related to the gut microbiome. The present study investigated the microbiome-mediated effect of Sihocheonggan-Tang (SHCGT) on AD-like symptoms induced by 2,4-dinitrochlorobenzene (DNCB) in BALB/c mice. DNCB was applied regularly to the ear and dorsal skin of BALB/c mice, and SHCGT was administered orally daily for 2 weeks. The composition of the gut microbiota was analyzed using 16S rRNA sequencing, and the effect of gut microbiome-derived metabolites, specifically short-chain fatty acids (SCFAs), was evaluated in tumor necrosis factor-alpha (TNF-α)- and interferon-gamma (IFN-γ)-treated HaCaT cells. SHCGT alleviated DNCB-induced symptoms of AD and the immune response to AD by decreasing the plasma immunoglobulin E level and splenic interleukin-4, interleukin-10, TNF-α, and IFN-γ levels. The gut microbiome composition and the damaged gut epithelial barrier in mice with AD were also significantly altered by SHCGT, and the reduced SCFA levels therein were elevated. We found that SFCAs directly inhibited the mRNA expression of IL-6 and ICAM-1 in TNF-α- and INF-γ-treated HaCaT cells. The finding that SHCGT regulates the gut microbiome and improves DNCB-induced AD in mice suggests that this herbal medicine has therapeutic potential in patients with AD.

scholarly journals Serum Interleukin Profile in Patients with Graves Orbithopathy

2013 ◽  
Vol 59 (1) ◽  
pp. 31-35
Author(s):  
Zsuzsánna Réti ◽  
Iz Kun ◽  
Corina Cristina Radu Pop
Keyword(s):  
Disease Activity ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Interleukin 10 ◽  
Interleukin 4 ◽  
Disease Stage ◽  
Clinical Activity ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Ifn Γ

Abstract Background: Graves’ orbitopathy (GO) is considered an autoimmune condition in close relationship with Graves’ disease (GD) affecting the thyroid. Several similarities exist between the two conditions, sharing the common antigen and the characteristics of the inflammation mediated by a number of cytokines. The result of the immune reactions will lead to the expansion of adipose tissue, production of glycosaminoglycans and soft tissue inflammation. Material and methods: In our study we examined the serum level of interleukin-1 (IL-1), interleukin 2 (IL-2), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), and interferon-gamma (IFN-γ) in correlation with the activity of disease and smoking habits in 25 patients with GD and GO. Results: We found that smokers had higher serum IL-6 and lower serum MCP-1, IL-8 and TNF-α level compared to non-smokers. Also, we found a weak positive correlation between serum IL-10, IFN-γ and disease activity (clinical activity score, CAS) and negative correlation between serum IL-1 and activity. Conclusion: Our findings support the fact that some cytokines (IL-10, IFN-γ, IL-1) play a role in active disease, while others are influenced by environmental factors, such as smoking (IL-6, IL-8, TNF-α). The discrepancy of cytokine profiles may reflect different patient characteristics, such as disease stage and disease activity and determination of serum cytokines would be useful in selecting patients who need more aggressive treatment protocols.

scholarly journals Cardiorenal Syndrome in Hypertensive Rats: Microalbuminuria, Inflammation and Ventricular Hypertrophy

2012 ◽  
pp. 13-24 ◽  
Author(s):  
M. MOUBARAK ◽  
H. JABBOUR ◽  
V. SMAYRA ◽  
E. CHOUERY ◽  
Y. SALIBA ◽  
...  
Keyword(s):  
Ventricular Hypertrophy ◽  
Cardiorenal Syndrome ◽  
Left Ventricular ◽  
Low Grade ◽  
Necrosis Factor Alpha ◽  
Reactive Protein ◽  
Tnf Α ◽  
Male Wistar Rats ◽  
Factor Alpha ◽  
Low Grade Inflammation

The aim of our study was to evaluate a possible association between microalbuminuria (MA), several low-grade inflammation factors and left ventricular hypertrophy (LVH) by using a pharmacological approach. This may provide new insights into the pathophysiologic mechanisms of the cardiorenal syndrome (CRS) linking early renal impairment with elevated cardiovascular risk. Two kidney-one clip (2K-1C) renovascular hypertension was induced in 24 male Wistar rats (220-250 g). After the development of hypertension, rats were divided into four groups: 2K-1C (untreated), calcium channel blocker (amlodipine-treated), angiotensin receptor blocker (losartan-treated) and peripheral vasodilator (hydralazine-treated), which were treated for 10 weeks. Rats in the 2K-1C group had all developed hypertension, a significant increase in plasma levels of tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), brain natriuretic peptide (BNP) and C-reactive protein (CRP). Moreover MA and creatininaemia underwent a significant increase. Under treatment decreases were observed in systolic blood pressure (SBP), TNF-α, CRP, IL-6, BNP concentrations and creatininaemia. These results were related to the absence of MA which was significantly associated with reductions in cardiac mass and hypertrophy markers (BNP and β-MHC gene expression) as well as renal interstitial inflammation. In conclusion, our results suggest that the reduction of MA is correlated with the decrease of the inflammatory components and seems to play an important role in protecting against cardiac hypertrophy and renal injury.

scholarly journals Curcumin Alleviates Potassium Bromate-Induced Hepatic Damage by Repressing CRP Induction through TNF-α and IL-1β and by Suppressing Oxidative Stress

2019 ◽  
Vol 11 (4) ◽  
pp. 337-344 ◽  
Author(s):  
Omowumi O. ADEWALE ◽  
Seun F. AKOMOLAFE ◽  
Nnaemeka T. ASOGWA
Keyword(s):  
Enzyme Linked Immunosorbent Assay ◽  
Necrosis Factor Alpha ◽  
Reactive Protein ◽  
Tnf Α ◽  
Serum Transaminases ◽  
Factor Alpha ◽  
Inflammatory Proteins ◽  
Biochemical Mechanisms ◽  
Molecular And Biochemical Mechanisms ◽  
Necrosis Factor

This study evaluated the prospective molecular and biochemical mechanisms behind the hepatoprotective effects of curcumin in Wistar rats exposed to KBrO3. Techniques for assessment of hepatic oxidative injury and histological biomarkers were used. The concentrations of proteins connected with inflammation (e.g. tumor necrosis factor-alpha (TNF-α), interleukins 1β (IL-1β) and C-reactive protein (CRP)) were estimated by enzyme-linked immunosorbent assay (ELISA) techniques. Results showed that, curcumin administered orally at a dose of 20 mg/kg for 28 days significantly suppressed the activities of serum transaminases and alkaline induced by KBrO3 administration (20 mg/kg, twice weekly) and protected the integrity of the liver tissue. Also, curcumin at the tested dose abridged the KBrO3-induced increase in hepatic malondialdehyde (MDA) levels and reversed KBrO3 mediated reduction in activities of hepatic antioxidant molecules including reduced glutathione (GSH), total thiol (TSH), glutathione peroxidase (GPx), catalase and superoxide dismutase (SOD). In addition, curcumin significantly assuaged inflammatory response in KBrO3-lesioned liver as revealed by the decrease in inflammatory biomarkers. This study suggests that curcumin exhibits a protective effect via induction of hepatic detoxification proteins and inhibition of inflammatory proteins in addition to its antioxidative ability in KBrO3- induced hepatic injury in rats.

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