{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T11:47:03Z","timestamp":1773834423174,"version":"3.50.1"},"reference-count":45,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[1999,7,1]],"date-time":"1999-07-01T00:00:00Z","timestamp":930787200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Clin Diagn Lab Immunol"],"published-print":{"date-parts":[[1999,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Tumor necrosis factor alpha (TNF-\u03b1) is a critical cytokine that mediates the toxic effects of bacterial superantigens like staphylococcal enterotoxin B (SEB) and toxic shock syndrome toxin 1 (TSST-1). Pentoxifylline, an anti-inflammatory agent that inhibits endotoxemia and lipopolysaccharide (LPS)-induced release of TNF-\u03b1, was tested for its ability to inhibit SEB- and TSST-1-induced activation of human peripheral blood mononuclear cells (PBMCs) in vitro and toxin-mediated shock in mice. Stimulation of PBMCs by SEB or TSST-1 was effectively blocked by pentoxifylline (10 mM), as evidenced by the inhibition of TNF-\u03b1, interleukin 1\u03b2 (IL-1\u03b2), gamma interferon (IFN-\u03b3), and T-cell proliferation. The levels of TNF-\u03b1, IL-1\u03b1, and IFN-\u03b3 in serum after an SEB or TSST-1 injection were significantly lower in mice given pentoxifylline (5.5 mg\/animal) versus control mice. Additionally, pentoxifylline diminished the lethal effects and temperature fluctuations elicited by SEB and TSST-1. Thus, in addition to treating endotoxemias, the cumulative in vitro and in vivo data suggest that pentoxifylline may also be useful in abrogating the ill effects of staphylococcal enterotoxins and TSST-1.<\/jats:p>","DOI":"10.1128\/cdli.6.4.594-598.1999","type":"journal-article","created":{"date-parts":[[2019,12,31]],"date-time":"2019-12-31T19:23:05Z","timestamp":1577820185000},"page":"594-598","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":47,"title":["Pentoxifylline Inhibits Superantigen-Induced Toxic Shock and Cytokine Release"],"prefix":"10.1128","volume":"6","author":[{"given":"Teresa","family":"Krakauer","sequence":"first","affiliation":[{"name":"<!--label omitted: 1-->Department of Immunology and Molecular Biology, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, Maryland 21702-5011"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bradley G.","family":"Stiles","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Department of Immunology and Molecular Biology, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, Maryland 21702-5011"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.55.12.2865-2869.1987"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(84)91241-8"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830270405"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1093\/clinids\/11.Supplement_1.S248"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1093\/infdis\/166.4.847"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1981.03320070025019"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.22.8941"},{"key":"e_1_3_2_9_2","first-page":"331","article-title":"The effects of pentoxifylline on the deformability of erythrocytes and on the muscular oxygen pressure in patients with chronic arterial disease.","volume":"10","author":"Ehrly A. 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