Anti-TNF monoclonal antibody [Pacific Blue®]

Rheumatoid arthritis (RA) is a systemic inflammatory autoimmune disease that leads to joint destruction and disability. Despite a significant progress in administration of biological agents for RA patients, there is still a need for improved therapy. Intravenous immunoglobulins (IVIG), a pooled polyspecific immunoglobulin (Ig)G extracted from 5000 to 20 000 healthy subjects, showed beneficial therapeutic effect in patients with immune deficiency, sepsis and autoimmune diseases. The current study aimed to investigate the beneficial effect of treatment with IVIG in established collagen-induced arthritis in DBA/1j mice. Murine arthritis was induced in DBA/1j mice. Treatment with IVIG began when the disease was established. The clinical score was followed twice a week until day 48. The mice were bled for plasma and the paws were hematoxylin and eosin (H&E)-stained. Cytokine profile in the plasma was analyzed by Luminex technology and titers of circulating anti-collagen antibodies in the plasma was tested by enzyme-linked immunosorbent assay. Our results show that treatment with IVIG in murine significantly reduced the clinical arthritis score (P < 0 center dot 001). Moreover, mode of action showed that IVIG significantly reduced circulating levels of inflammatory cytokines [interferon (IFN)-gamma, interleukin (IL)-1 beta, IL-17, IL-6, tumor necrosis factor (TNF)-alpha, P < 0 center dot 001], inhibiting anti-collagen antibodies (P < 0 center dot 001) in the plasma of collagen-induced arthritis mice. Importantly, histopathological examination revealed that IVIG treatment prevented the migration of inflammatory immune cells into the cartilage and synovium, reduced the extent of joint damage and preserved joint architecture. Our results proved for the first time the valuable anti-inflammatory treatment of IVIG in experimental RA. We propose IVIG therapy for a subgroup of patients with rheumatologically related diseases.

This study was performed to assess the ability of Clostridium perfringens types A and D to induce immunological and inflammatory alterations, and mortalities in Nile tilapia (Oreochromis niloticus). Healthy Nile tilapia (n = 90) with an average body weight of 35 +/- 0.5 g were randomly divided into three triplicate groups with ten fish in each aquarium. Fish were injected intraperitoneally (IP) with 0.1 mL of 2.4 x 10(8) CFU/mL of C. perfringens type A in the first group (G(1)) and type D in the second group (G(2)). Fish in the third group (G(3)) were IP injected with sterile saline and served as control. Clinical signs and postmortem lesions of infected fish started appearing on day 1 post-infection (PI), and the cumulative mortality rates were recorded as 50%, 73%, and 0% in G(1), G(2), and G(3) groups, respectively. Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) activities in the G(1) and G(2) showed a significant gradual decrease, and reached a peak on day 14, compared to the control group, whereas malondialdehyde (MDA) activity was significantly increased at all-time intervals in G(1) and G(2). TNF-alpha showed a significant increase only on day 14 in G(1) and G(2) compared to the control group. Myeloperoxidase activity (MPO) of both G(1) and G(2) was increased significantly on day 7 and day 14 compared to the control group and other time periods of exposure. Nitric oxide (NO) activity decreased gradually at 24 h and on day 7 and day 14 for G(1) and G(2), respectively. The inflammatory biomarker IL-1 beta showed a significant gradual increase, which reached a peak on day 7 for both G(1) and G(2) in comparison to control. IL-6 reached a peak on day 14 for G(1) and on day 7 for G(2). Significant down-regulation of IL-10 occurred on days 7 and 14 post challenge. There was a gradual increase in serum proteins in G(1) and G(2) which attained a peak on day 14, except gamma-globulin, which showed a significant decrease in the same trend. The albumin level decreased gradually in G(1) and G(2) and among the different periods, and reached a peak at 24 h, followed by on day 7 and finally, on day 14. Lysozyme activity and IgM initially showed a significant increase at 24 h in the G(1) and G(2) groups compared to the control group and other time periods of exposure; later, decreased gradually on day 7 and day 14. There was a significant decline in complement 3 in G(1) and G(2) on day 14, followed by day 7 and a significant increase at 24 h. This study has shown that C. perfringens types A and D could be important causative agents of disease and mortality in cultured Nile tilapia species.