Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to characterize the changes in the quantitative expression of beta 2-integrins and L-selectin detected by means of fluorochrome-conjugated monoclonal antibodies and flow cytometry on leukocytes in the systemic circulation after a major musculoskeletal trauma, i.e. hip replacement surgery, and to relate these changes to parameters of the acute-phase response [plasma acute-phase reactants (C-reactive protein, CRP, and interleukin-6, IL-6) and parameters of coagulation activation (thrombin-antithrombin III complexes, TAT)]. Eight patients with either primary or secondary osteoarthritis of the hip received uncemented total hip prostheses. LFA-1 (CD11a/CD18) was upregulated on granulocytes during the operation. MAC-1 (CD11b/CD18) expression on monocytes increased to peak levels 20 h after surgery, whereas the L-selectin (CD62L) expression on monocytes and granulocytes reached peak values at the end of surgery. The changes in expression of LFA-1 on monocytes, MAC-1 on granulocytes and p150,95 (CD11c/CD18) on monocytes and granulocytes during and after the operation did not reach statistical significance. TAT and IL-6 increased during surgery and reached peak values at the end of the operation and 20 h after surgery, respectively. In contrast, CPR concentrations increased after surgery with peak levels 44 h postoperatively. Significant upregulation of LFA-1 on granulocytes and L-selectin on monocytes and granulocytes preceded the increase in IL-6 which again preceded the increase in CRP. However, the up- or downregulation of leukocyte beta 2-integrins and L-selectin during and after surgery was not significantly correlated with the increase in IL-6. The increases in TAT correlated well with the upregulation of L-selectin on monocytes, but not with the beta 2-integrins known to participate in the coagulation process in vitro. The rise in CRP was inversely correlated with the maximal increase in expression of MAC-1 on monocytes. In conclusion, the changes in leukocyte adhesion molecules during and after surgery indicate changes in critical leukocyte functions. The lack of correlation between quantitative up- and downregulation of leukocyte beta 2-integrins and parameters of the acute phase response suggests that these processes are regulated through independent pathways or that functional up- and downregulation of adhesion molecules, shedding, leukocyte-endothelial adhesion and mobilization of new unactivated cells may result in a net estimate of leukocyte activation not suspected to be positively correlated to acute-phase reactants.
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PMID:Expression of beta-2-integrins and L-selectin by leukocytes and changes in acute-phase reactants in total hip replacement surgery. 873 29

All total joint replacements generate wear debris; yet, some implant prostheses fail while others survive despite the presence of ultrahigh molecular weight polyethylene particulate. It was hypothesized that patients with failed hip implants who have osteolysis will secrete higher inflammatory cytokines than patients receiving total joint replacements. Our study evaluated the peripheral blood monocyte response to varying polyethylene particle volume ratios through cytokine quantification in two patient populations: patients having revision surgery for failed total hip replacements (failed implant group) and patients having primary total hip surgery for osteoarthritis of the hip (primary implant group). We observed elevation of all three proinflammatory cytokines tested (interleukin-6, interleukin-1, and tumor necrosis factor-alpha) in response to polyethylene particulate challenge when compared with the controls in both patient groups. The population with failed implants also had a higher absolute cytokine response to polyethylene exposure compared with the control patients having primary implants. These findings suggest that patients with failed implants have a greater inflammatory cytokine response to polyethylene than seen in patients with primary implants.
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PMID:Increased cytokine secretion in patients with failed implants compared with patients with primary implants. 1586 48

Inflammation is currently believed not only to influence clinical manifestations ofosteoarthrosis (OA) but also to be a key pathogenetic link in the chain reaction underlying progress of the disease. Patients with OA and signs of local inflammation undergo a change of algofunctional index and markers of inflammation, such as C-reactive protein (C-RP) and interleukin-6 (IL-6). Inflammation markers in patients with isolated disease of large joints are more affected than in women with OA and concomitant pathologies. Increased levels of C-RP and IL-6 in women with gonarthrosis/coxarthrosis confirm the key role of inflammation in the progress of this OA variant. Imbalance of IL-6 and its soluble receptors is an indicator of substantial impairment of the adaptive capacity in these patients. Elevated C-RP and IL-6 levels in patients with OA suggest chronic inflammation in patients with degenerative-dystrophic joint affection. Derangement of compensatory and adaptive processes in OA is associated with chronic immuno-inflammatory changes accompanied by hypersecretion of cytokines and proteolitic enzymes. Aggressive action of inflammation mediators in isolated affection of large joints accounts for the predominance of catabolic processes over anabolic ones which leads to further progress of OA due to low efficiency of the recovery of cartilage tissue and activation of its destruction. OA with concomitant pathologies leads to the disturbance of coordinated inflammatory response and cytokine cascade associated with inadequate IL-6 production. It is concluded that local and systemic immunopathologic processes in patients with OA form a vicious circle and contribute to the progress of degenerative-dystrophic processes in the joints.
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PMID:[Clinical and laboratory features of different forms of osteoarthrosis]. 1934 2

BACKGROUND The yearly increase in the number of procedures involving implantation of hip joint endoprostheses forces prosthetics manufacturers to search for biologically neutral implants. The goal of this study was to assess the concentration of Interleukin-6 (IL-6) and its correlation with C-reactive protein (CRP), depending on the type of hip joint endoprosthesis (cemented or cementless endoprosthesis) in order to determine implant biotolerance during the early postoperative period. MATERIAL AND METHODS The sample comprised 200 patients [mean age=64 (31-81) years] with coxarthrosis. All patients underwent hip joint arthroplasty using a cemented or cementless endoprosthesis. Blood samples were collected 3 times: before the procedure, on the first day after the procedure, and after 6 weeks. IL-6 and CRP levels were assayed using immunoenzymatic methods. The results were subjected to statistical analysis using the Shapiro-Wilk test. RESULTS On the 1st day after the procedure, CRP and IL-6 concentration increased rapidly after implantation of both cemented and cementless endoprostheses. At 6 weeks postoperatively, the CRP value remained at a similar level in patients after cemented arthroplasty and was almost 2-fold lower in patients who underwent cementless arthroplasty. The IL-6 value returned to the baseline level in patients after cementless arthroplasty and showed an ongoing increasing tendency in patients after cemented arthroplasty. CONCLUSIONS 1. The measurement of C-reactive protein and Interleukin-6 is a high-sensitivity test, assessing implant biotolerance. 2. The implantation of a cemented endoprosthesis induces a higher increase in the level of proinflammatory cytokines as compared with a cementless endoprosthesis. 3. For a complete assessment of both early and later body responses to implantation and the related surgical procedure, further studies using available approaches and tools are recommended.
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PMID:Comparison of Biocompatibility of Cemented vs. Cementless Hip Joint Endoprostheses Based on Postoperative Evaluation of Proinflammatory Cytokine Levels. 2793 73