The Effect of Human Recombinant Tumor Necrosis Factor Receptor-2 on Reducing Inflammatory of Collagen -Induced Arthritis in Balb/c Mice

Abstract

Background The tumor necrosis factor alpha (TNFα) is a cytokine that produced principally by monocyte/macrophages and T lymphocytes, respectively. TNFα is recognized as the primary mediator of immunity in inflammation reaction. One important application of Tumor Necrosis Factor Receptor 2 (TNFR2) is for the treatment of autoimmune diseases like rheumatoid arthritis (RA). Objectives The aim of this study is to examine the therapeutic trace of the recombinant humanTNFR2 on collagen-induced arthritis (CIA) in mice. Materials and Methods CIA was created in 20 mice by immunization with bovine type II collagen (CII). After the mice were boosted on day 21, they were injected with the recombinant protein in test group (1 mg.kg-1) and assessed edema in paws and knee joints after two weeks. The quantities of inflammatory cytokines such as TNF-α, interleukin-1 beta (IL-β1), interleukin-6 (IL-6), and interleukin-10(IL-10) in serum were evaluated through enzyme-linked immunosorbent assay (ELISA) kit. In addition, the histopathology of joints sections was analyzed. Results The cytokines TNF-α, IL-1β, and IL-6 values in serum markedly decreased in groups treated with TNFR2 (P < 0.01–0.001). The results showed that treatment with TNFR2 significantly reduced edema in paws and joints (P < 0.01–0.001). Conclusions Pathological investigations proved that administration of recombinant TNF receptor has blocked or protected joints from progressive damage. This study suggests that the anti-arthritic effectiveness of TNFR2 will repress the symptoms of rheumatoid arthritis. Moreover, it seems that TNFR2 is a strong candidate for the treatment of the RA disease.

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“…At the same time, in the groups that were injected with P-ASA, the number of GRA is increased only at the peak of inflammation, and after 24 hours it is fully normalized, which may be due, on the one hand, to prolongation, and, on the other hand, to immunomodulating properties, that is, with the peculiarities of the action of pectin [9][10][11] . The decrease in the intensity of oxidative processes at the peak of inflammation (5 h after carrageenan injection) under the action of ASA, assessed by the level of malondialdehyde in serum, can be explained by a decrease in the activity of neutrophils as a result of the immunosuppressive effect of ASA 26,27 or by the manifestation of its antioxidant properties which is in agreement with a report 28 . In the groups that were treated with the molecular complex P-ASA, the level of malondialdehyde was not decreased, and when P-ASA was administered at the dose of 200 mg/kg, at the peak of inflammation, malondialdehyde was increased sharply, which may be due to the activation of oxidative processes occurring primarily in neutrophils in response to the injection of an antigen.…”

“…Analyzing the results obtained for catalase activity in the groups that were injected with P-ASA, it can be concluded that the complexation of pectin with ASA reduced the effect of ASA on the antioxidant catalase enzyme: on a decrease in its activity at the peak of inflammation and on an increase in its activity after 24 h later on administration, which is especially noticeable at a low dose of P-ASA of 100 mg/kg. In reports 24,28,29 , changes in the level of cytokines TNFα, IL-6, IL-1β, IL-8 are mentioned in conjunction with the study of the intensity of inflammatory reactions.…”

“…It is noted that the level of these cytokines decreases when anti-inflammatory agents affected arthritis induced by Freund's adjuvant 24 or collagen-induced arthritis 28 . In work 29 it is noted an increase in IL-6 and IL-8 in osteoarthritis.…”

Role and mechanism of miR‑144‑5p in LPS‑induced macrophages

“…In particular, TNF-α serves a pivotal role in inflammation associated with RA (23). TNF-α is mainly produced by macrophages, neutrophils, natural killer cells and endothelial cells, whilst activated lymphocytes can also produce small levels of TNF-α (24). The presence of TNF-α can also induce the production of other proinflammatory factors, including IL-1, IL-8, IL-6 and matrix metalloproteinases (25).…”

Estimation levels of prostate-specific antigen, interleukin-8, oxidative stress and some inflammatory markers in sera of benign prostatic hyperplasia patients who have smoking habits as a risk factor

“…which considers MDA as an index of inflammation and oxidative stress in BPH patients (48). Inflammatory factor has been investigated in previous studies (49)(50)(51)(52)(53)(54).…”