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Murine recombinant TNF-\u03b1 (\u223c100 \u03bcg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup>) in vehicle solution or vehicle solution alone (sham) was administered to C57BL\/6 mice for 7 days via osmotic minipumps. In EDL muscles from TNF-\u03b1-treated mice, neutrophil and macrophage concentrations were elevated seven- and threefold, respectively, compared with sham mice. Neutrophil and macrophage concentrations were also elevated five- and twofold, respectively, in solei of TNF-\u03b1- relative to sham-treated mice. Treatment with TNF-\u03b1 elevated ubiquitin content by \u223c25% relative to sham values for both the EDL and soleus muscles; however, these elevations were not statistically significant. No differences were observed between TNF-\u03b1- and sham-treated mice in body weight, food consumption, muscle mass, myofiber cross-sectional area, carbonyl groups, total protein content, or relative abundance of myosin heavy chain protein. Furthermore, no overt signs of muscle injury or regeneration were observed in muscles from TNF-\u03b1-treated mice in either the EDL or soleus muscles. These observations suggest that 7 days of TNF-\u03b1 administration promote muscle inflammation as indicated by the accumulation of neutrophils and macrophages without overt signs of atrophy, injury, or regeneration.<\/jats:p>","DOI":"10.1152\/japplphysiol.01453.2005","type":"journal-article","created":{"date-parts":[[2006,7,14]],"date-time":"2006-07-14T04:52:12Z","timestamp":1152852732000},"page":"1394-1399","source":"Crossref","is-referenced-by-count":62,"title":["Tumor necrosis factor-\u03b1 promotes the accumulation of neutrophils and macrophages in skeletal muscle"],"prefix":"10.1152","volume":"101","author":[{"given":"Jennifer M.","family":"Peterson","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kevin D.","family":"Feeback","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joel H.","family":"Baas","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Francis X.","family":"Pizza","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1016\/S0304-3835(01)00717-0"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/0165-2478(94)90076-0"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1021\/bi00420a001"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9343(03)00329-2"},{"key":"R5","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjc.6600167"},{"key":"R6","doi-asserted-by":"publisher","DOI":"10.1016\/S0065-2776(08)60791-9"},{"key":"R7","unstructured":"Cicco NA, Lindemann A, Content J, Vandenbussche P, Lubbert M, Gauss J, Mertelsmann R, and Herrmann F.Inducible production of interleukin-6 by human polymorphonuclear neutrophils: role of granulocyte-macrophage colony-stimulating factor and tumor necrosis factor-alpha.Blood75: 2049\u20132052, 1990."},{"key":"R8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2249.1993.tb08230.x"},{"key":"R9","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110054200"},{"key":"R10","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114059"},{"key":"R11","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1989.256.3.R659"},{"key":"R12","doi-asserted-by":"publisher","DOI":"10.1210\/endo.138.10.5450"},{"key":"R13","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.82.24.8667"},{"key":"R14","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(93)81341-V"},{"key":"R15","doi-asserted-by":"publisher","DOI":"10.1007\/BF00926829"},{"key":"R16","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1991.260.5.E727"},{"key":"R17","doi-asserted-by":"publisher","DOI":"10.1096\/fj.00-0274com"},{"key":"R18","doi-asserted-by":"publisher","DOI":"10.1152\/japplphysiol.01026.2004"},{"key":"R19","doi-asserted-by":"crossref","unstructured":"Issekutz TB.In vivo blood monocyte migration to acute inflammatory reactions, IL-1 alpha, TNF-alpha, IFN-gamma, and C5a utilizes LFA-1, Mac-1, and VLA-4. 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