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      Rheumatoid arthritis mediator CD18 expression by Staphylococcus aureus superantigen C in rats

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          Abstract

          Background and Objectives:

          Microbial superantigens have been reported in the blood and synovial fluid of rheumatoid arthritis patients, raising the question of whether the presence of these superantigens could provoke the induction of inflammatory biomarkers expression or not. The purpose of this study was to examine the Staphylococcus aureus superantigen C on CD18 expression.

          Materials and Methods:

          The superantigen C was purified by ultrafiltration. Immunoblotting was performed using a specific antibody. Also, 50 micrograms of superantigens (toxin) were injected intraperitoneally and intra-articularly into separate rat groups. Blood was collected and RNA extracted. Then, the cDNA was synthesized. The expression of CD18 marker was evaluated using RT-real-time PCR, and the results were descriptively analyzed.

          Results:

          The results of this study revealed that 50 μg of toxin, injected intra-articularly and intraperitoneally, showed the surplus expression of the marker CD18 in the blood of rats after 20 days. By this method, the expression of the marker CD18 was significantly different between rats that received the superantigen intra-articularly and intraperitoneally (2.10; 2.3 and 3.3 folds) and the controls (P≤ 0.05).

          Conclusion:

          The results indicated that the presence of Staphylococcal of superantigen C in the body of rats has enhanced the expression of the CD18 inflammatory marker more than 3 times. This valuable finding is an introduction to further research and could provide new methods to prevent and control inflammatory diseases, including rheumatoid arthritis.

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          Most cited references25

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          The microbiome and rheumatoid arthritis.

          Humans are not (and have never been) alone. From the moment we are born, millions of micro-organisms populate our bodies and coexist with us rather peacefully for the rest of our lives. This microbiome represents the totality of micro-organisms (and their genomes) that we necessarily acquire from the environment. Micro-organisms living in or on us have evolved to extract the energy they require to survive, and in exchange they support the physiological, metabolic and immune capacities that have contributed to our evolutionary success. Although currently categorized as an autoimmune disorder and regarded as a complex genetic disease, the ultimate cause of rheumatoid arthritis (RA) remains elusive. It seems that interplay between predisposing genetic factors and environmental triggers is required for disease manifestation. New insights from DNA sequence-based analyses of gut microbial communities and a renewed interest in mucosal immunology suggest that the microbiome represents an important environmental factor that can influence autoimmune disease manifestation. This Review summarizes the historical clues that suggest a possible role for the microbiota in the pathogenesis of RA, and will focus on new technologies that might provide scientific evidence to support this hypothesis.
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            Wound-healing defect of CD18(-/-) mice due to a decrease in TGF-beta1 and myofibroblast differentiation.

            We studied the mechanisms underlying the severely impaired wound healing associated with human leukocyte-adhesion deficiency syndrome-1 (LAD1) using a murine disease model. In CD18(-/-) mice, healing of full-thickness wounds was severely delayed during granulation-tissue contraction, a phase where myofibroblasts play a major role. Interestingly, expression levels of myofibroblast markers alpha-smooth muscle actin and ED-A fibronectin were substantially reduced in wounds of CD18(-/-) mice, suggesting an impaired myofibroblast differentiation. TGF-beta signalling was clearly involved since TGF-beta1 and TGF-beta receptor type-II protein levels were decreased, while TGF-beta(1) injections into wound margins fully re-established wound closure. Since, in CD18(-/-) mice, defective migration leads to a severe reduction of neutrophils in wounds, infiltrating macrophages might not phagocytose apoptotic CD18(-/-) neutrophils. Macrophages would thus be lacking their main stimulus to secrete TGF-beta1. Indeed, in neutrophil-macrophage cocultures, lack of CD18 on either cell type leads to dramatically reduced TGF-beta1 release by macrophages due to defective adhesion to, and subsequent impaired phagocytic clearance of, neutrophils. Our data demonstrates that the paracrine secretion of growth factors is essential for cellular differentiation in wound healing.
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              Gene targeting yields a CD18-mutant mouse for study of inflammation.

              CD18 is the common beta subunit for the heterodimeric leukocyte integrins that mediate many inflammatory cell adhesion responses including binding to intercellular adhesion molecules 1 and 2. CD18 deficiency in humans causes a severe granulocyte disorder with susceptibility to bacterial infections and high morbidity and mortality. Gene targeting was used to prepare an insertion mutation in the murine CD18 gene. The insertion mutation resulted in a hypomorphic rather than a null allele due to low expression from a cryptic promoter in the plasmid construct. Homozygous mutant mice are viable and fertile, demonstrate a mild granulocytosis, and have 2 or 16% of normal CD18 expression on granulocytes in the resting or activated state, respectively. Mutant mice show an impaired inflammatory response to a chemical peritonitis and delayed rejection of cardiac transplants. These CD18-mutant mice provide a model of the moderate form of the human disease and should be extremely valuable for in vivo analysis of the role of leukocyte integrin-dependent adhesion in inflammatory disease models.
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                Author and article information

                Journal
                Iran J Microbiol
                Iran J Microbiol
                IJM
                IJM
                Iranian Journal of Microbiology
                Tehran University of Medical Sciences
                2008-3289
                2008-4447
                August 2019
                : 11
                : 4
                : 337-344
                Affiliations
                [1 ]Applied Microbiology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
                [2 ]Department of Biology, Central Tehran Branch, Islamic Azad University, Tehran, Iran
                [3 ]Department of Medical Microbiology, School of Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran
                [4 ]Department of Rheumatology, School of Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran
                [5 ]Chemical Injuries Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
                Author notes
                [* ]Corresponding author: Ramezan Ali Ataee, Ph.D, Applied Microbiology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran; Department of Medical Microbiology, School of Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran. Tel: +98 021 87555427, Fax: +98 021 8862 0843, Email: ataee216@ 123456gmail.com
                Article
                IJM-11-337
                6829107
                bd322937-ea33-4ac6-b97c-d51511f5955e
                Copyright© 2019 Iranian Neuroscience Society

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : October 2018
                : June 2019
                Categories
                Original Article

                Microbiology & Virology
                staphylococcal superantigen,rheumatoid arthritis,cd18 lymphocytes,biomarker

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