scholarly journals Immunomodulation with IL-17 and TNF-α in spondyloarthritis: focus on the eye and the central nervous system

2021 ◽  
Vol 13 ◽  
pp. 1759720X2110258
Author(s):  
Elsa How Shing Koy ◽  
Pierre Labauge ◽  
Athan Baillet ◽  
Clément Prati ◽  
Hubert Marotte ◽  
...  
Keyword(s):  
Interleukin 17 ◽  
Necrosis Factor Alpha ◽  
Neurologic Diseases ◽  
Tnf Α ◽  
Neuropsychiatric Diseases ◽  
The Central Nervous System ◽  
Factor Alpha ◽  
Inflammatory Drugs ◽  
Necrosis Factor

Tumor necrosis factor alpha (TNF-α) and interleukin-17 (IL-17) are two pro-inflammatory cytokines involved in the pathophysiology of spondyloarthritis (SpA). Therapies targeting TNF-α or IL-17 are used as a second line among SpA patients failing non-steroidal anti-inflammatory drugs. The choice of such treatment has to take into account the patient’s comorbidities. Neurologic diseases are common and their association with SpA deserves to be studied. Therefore, the role of TNF-α and IL-17 cytokines is worth investigating in these neuropsychiatric diseases. This review aimed to explore the role of TNF-α and IL-17 in the pathogenesis of uveitis, multiple sclerosis, neuromyelitis optica, Alzheimer’s disease, Parkinson’s disease and depression. This update is critical to guide the therapeutic management of these co-morbidities in SpA patients.

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 Role of Tumor Necrosis Factor Alpha in Disease Using a Mouse Model of Shiga Toxin-Mediated Renal Damage

2010 ◽  
Vol 78 (9) ◽  
pp. 3689-3699 ◽  
Author(s):  
Erin K. Lentz ◽  
Rama P. Cherla ◽  
Valery Jaspers ◽  
Bradley R. Weeks ◽  
Vernon L. Tesh
Keyword(s):  
Renal Function ◽  
Tumor Necrosis Factor ◽  
Shiga Toxin ◽  
Tumor Necrosis ◽  
Renal Damage ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACTMice have been extensively employed as an animal model of renal damage caused by Shiga toxins. In this study, we examined the role of the proinflammatory cytokine tumor necrosis factor alpha (TNF-α) in the development of toxin-mediated renal disease in mice. Mice pretreated with TNF-α and challenged with Shiga toxin type 1 (Stx1) showed increased survival compared to that of mice treated with Stx1 alone. Conversely, mice treated with Stx1 before TNF-α administration succumbed more quickly than mice given Stx1 alone. Increased lethality in mice treated with Stx1 followed by TNF-α was associated with evidence of glomerular damage and the loss of renal function. No differences in renal histopathology were noted between animals treated with Stx1 alone and the TNF-α pretreatment group, although we noted a sparing of renal function when TNF-α was administered before toxin. Compared to that of treatment with Stx1 alone, treatment with TNF-α after toxin altered the renal cytokine profile so that the expression of proinflammatory cytokines TNF-α and interleukin-1β (IL-1β) increased, and the expression of the anti-inflammatory cytokine IL-10 decreased. Increased lethality in mice treated with Stx1 followed by TNF-α was associated with higher numbers of dUTP-biotin nick end labeling-positive renal tubule cells, suggesting that increased lethality involved enhanced apoptosis. These data suggest that the early administration of TNF-α is a candidate interventional strategy blocking disease progression, while TNF-α production after intoxication exacerbates disease.

scholarly journals ROLE OF HERBAL MEDICINES IN VITILIGO TREATMENT - CURRENT STATUS AND FUTURE PERSPECTIVES

2018 ◽  
Vol 11 (9) ◽  
pp. 19 ◽  
Author(s):  
Radhakrishnan Narayanaswamy ◽  
Intan Safinar Ismail
Keyword(s):  
Herbal Medicines ◽  
Current Status ◽  
Interleukin 17 ◽  
Future Perspectives ◽  
Psoralea Corylifolia ◽  
Necrosis Factor Alpha ◽  
Ammi Visnaga ◽  
Factor Alpha ◽  
Necrosis Factor

Vitiligo is a depigmentation disorder with complex causes. Nonetheless, recent progress has been made to unravel the pathophysiology of vitiligo. In this review, we provide an overview of the currently known herbal medicine for vitiligo treatment and also highlighted the herbs that have been used in clinical trials. In view of traditional uses, herbs such as Ammi visnaga L., Angelica sinensis, Eclipta alba L, Ginkgo biloba, Picrorhiza kurroa Royle Ex Benth, and Psoralea corylifolia L, have been highlighted. Enormous efforts in vitiligo drug discovery are currently needed. Interleukin-17 inhibition, tumor necrosis factor-alpha inhibition, heat shock protein-70i (HSP70i) inhibition, keratinocyte turnover modulators, and regulatory T cells (Tregs) modulators have been discussed as promising new targets for vitiligo drug development. Thus, we strongly believe that this review may be useful for rationalize new herbal drug for vitiligo treatment.

scholarly journals Role of Adiponectin and Tumor Necrosis Factor-Alpha in the Pathogenesis and Evolution of Type 1 Diabetes Mellitus in Children and Adolescents

Diagnostics ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 945
Author(s):  
Csilla Enikő Szabo ◽  
Oana Iulia Man ◽  
Alexandru Istrate ◽  
Eva Kiss ◽  
Andreea Catana ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Tumor Necrosis ◽  
Diabetic Patients ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Risk Patients ◽  
Factor Alpha ◽  
Necrosis Factor

Type 1 diabetes mellitus (T1DM) is a complex condition caused by the destruction of pancreatic beta cells by autoimmune mechanisms. As a result, insulin deficiency and subsequent hyperglycemia occur. The aim of the present study is to investigate the role of adiponectin and tumor necrosis factor alpha (TNF-α) in the development of T1DM. The study is designed as an observational case-control study, involving 52 diabetic patients and 66 controls. Z scores for Body Mass Index (BMI), weight, height, and adiponectin and TNF-α serum levels were assessed in both groups. The T1DM group had significantly higher TNF-α levels and a significantly higher proportion of high-risk patients for inflammation based on TNF-α values as compared to the control group, while both groups had statistically similar adiponectin levels and a similar proportion of high/medium-risk patients based on adiponectin values. TNF-α plays a significant role in the pathogenesis and evolution of T1DM and it may represent an additional marker of disease progression, as well as a potential target of immunotherapeutic strategies. In the present study, no statistically significant differences were recorded in adiponectin levels neither in diabetic patients and controls, nor in high/medium severity risk diabetic patients.

scholarly journals Toll-Like Receptor 9 Is Required for Full Host Resistance toMycobacteriumaviumInfection but Plays No Role in Induction of Th1 Responses

2011 ◽  
Vol 79 (4) ◽  
pp. 1638-1646 ◽  
Author(s):  
Natália B. Carvalho ◽  
Fernanda S. Oliveira ◽  
Fernanda V. Durães ◽  
Leonardo A. de Almeida ◽  
Manuela Flórido ◽  
...  
Keyword(s):  
Interleukin 12 ◽  
Toll Like Receptor ◽  
Necrosis Factor Alpha ◽  
Histocompatibility Complex ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ifn Γ ◽  
Myd88 Signaling ◽  
Necrosis Factor

ABSTRACTTo investigate the role of Toll-like receptor 9 (TLR9) in innate immunity toMycobacteriumavium, TLR9, TLR2, and MyD88 knockout (KO) mice were infected with this bacterium. Bacterial burdens were higher in the spleens, livers, and lungs of infected TLR9 KO mice than in those of C57BL/6 mice, indicating that TLR9 is required for efficient control ofM.aviuminfection. However, TLR9 KO or TLR2 KO spleen cells displayed normalM.avium-induced tumor necrosis factor alpha (TNF-α) and gamma interferon (IFN-γ) responses. This finding was confirmed by determining the number of splenic CD4+T cells producing IFN-γ by flow cytometry. Furthermore, TLR2 and MyD88, but not TLR9, played a major role in interleukin-12 and TNF-α production byM.avium-infected macrophages and dendritic cells (DCs). We also found that major histocompatibility complex class II molecule expression on DCs is regulated by TLR2 and MyD88 signaling but not by TLR9. Finally, lack of TLR9, TLR2, or MyD88 reduced the numbers of macrophages, epithelioid cells, and lymphocytes inM.avium-induced granulomas but only MyD88 deficiency affected the number of liver granulomas. In summary, our data demonstrated that the involvement of TLR9 in the control ofM.aviuminfection is not related to the induction of Th1 responses.

Serum Levels of IL-17, IL-6, TNF-α and Disease Activity in Patients with Rheumatoid Arthritis

2016 ◽  
Vol 42 (04) ◽  
pp. 323-328 ◽  
Author(s):  
M. Beyazal ◽  
G. Devrimsel ◽  
M. Cüre ◽  
A. Türkyılmaz ◽  
E. Çapkın ◽  
...  
Keyword(s):  
Disease Activity ◽  
Severe Disease ◽  
Serum Levels ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
High Level ◽  
Necrosis Factor

Abstract Objective: The aim of this study was to evaluate serum levels of interleukin (IL)-17, IL-6, and tumor necrosis factor alpha (TNF-α) in RA patients and to assess the correlation of these cytokines with clinical and laboratory parameters. Materials and Methods: 48 patients with RA and 35 healthy volunteers were enrolled in the study. Disease activity was determined by disease activity score (DAS28) in patients with RA. Patients with RA were categorized as mild (DAS28≤3.2), moderate (3.2<DAS28≤5.1), and severe (5.1<DAS28) according to DAS28. The serum levels of IL-17, IL-6 and TNF-α cytokines were measured by enzyme-linked immuno sorbent assay. Results: The mean serum IL-17 and TNF-α levels did not differ between RA patients and controls (P>0.05). Serum IL-6 levels were significantly elevated in RA patients compared with controls (P<0.001). The increasing trend in mean serum IL-6 levels across group with mild, moderate, and severe disease activity was significant (P<0.001, respectively). In RA patients, serum IL-6 concentrations were significantly correlated with ESR, CRP, DAS28, and VAS (r=0.371, P=0.009; r=0.519, P<0.001; r=0.536, P<0.001; r=0.539, P<0.001, respectively). Also, Serum IL-17 concentrations demonstrated significant correlations with ESR, CRP, but not DAS28 (r=0.349, P=0.015; r=0.299, P=0.039; r=0.274, P=0.060, respectively). Serum TNF-α showed no significant correlation with disease activity indices. Conclusions: This study showed that patients with RA had significantly increased cytokine level for IL-6, but not IL-17 and TNF-α and high level of serum IL-6 cytokine was associated with disease activity. However, further follow-up studies involving large samples are required to clarify precise role of these cytokines in disease development and progress.

MMPs, IL-1, and TNF are Regulated by IL-17 in Periodontitis

2007 ◽  
Vol 86 (4) ◽  
pp. 347-351 ◽  
Author(s):  
A. Beklen ◽  
M. Ainola ◽  
M. Hukkanen ◽  
C. Gürgan ◽  
T. Sorsa ◽  
...  
Keyword(s):  
Tumor Necrosis ◽  
Interleukin 17 ◽  
Periodontal Tissue ◽  
Gingival Fibroblasts ◽  
Tissue Destruction ◽  
Necrosis Factor Alpha ◽  
Regulatory Cytokine ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Periodontitis is characterized by periodontal tissue destruction. Since interleukin-17 (IL-17) has been reported to up-regulate IL-1β and tumor necrosis factor-alpha (TNF-α), it was hypothesized that it is increased in periodontitis and up-regulates these cytokines and tissue-destructive matrix metalloproteinases (MMP) in local migrant and resident cells. Immunocytochemistry disclosed elevated IL-1β, TNF-α, and IL-17 levels in periodontitis. These cytokines induced proMMP-1 and especially MMP-3 in gingival fibroblasts, whereas MMP-8 and MMP-9 were not induced. IL-17 was less potent as a direct MMP inducer than IL-1β and TNF-α, but it induced IL-1β and TNF-α production from macrophages, and IL-6 and IL-8 from gingival fibroblasts. In accordance with these findings, immunocytochemistry disclosed that MMP-1 and MMP-3 were increased in periodontitis. Gingival fibroblasts may play an important role in tissue destruction in periodontitis via cytokine-inducible MMP-1 and MMP-3 production, in which IL-17 plays a role as a key regulatory cytokine.

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