title: Interleukins 6 and 11 protect mice from mortality in a staphylococcal enterotoxin-induced toxic shock model.
abstract: BALB/By mice given doses of D-galactosamine plus Staphylococcus aureus enterotoxin B die within 48 h of administration. The cause of death is a syndrome much like toxic shock syndrome in humans. We used this model to investigate the role of two cytokines, interleukin 6 and interleukin 11, which share the signal transducing subunit, gp130, of their respective receptors. We observed that pretreatment of mice with antibody to interleukin 6 increased mortality from 55% to nearly 90% (P < 0.001), while pretreatment with either cytokine reduced death. The protection was dose dependent; however, interleukin 6 was about 10-fold more potent that interleukin 11. These data indicate that endogenous interleukin 6 plays a protective role in attenuating acute inflammatory responses; furthermore, interleukin 6 and interleukin 11 can abrogate T-cell activation due to triggering by superantigen. A possible clinical role for these cytokines in the treatment of toxic shock merits further investigation.
authors.affiliation: Department of Immunology, Schering-Plough Research Institute, Kenilworth, New Jersey 07033, USA.
authors.forename: B E
authors.initials: BE
authors.lastname: Barton
authors.forename: J
authors.initials: J
authors.lastname: Shortall
authors.forename: J V
authors.initials: JV
authors.lastname: Jackson
mesh_terms: D000818:Animals; D004768:Enterotoxins / Q000633:toxicity*; D017370:Interleukin-11 / Q000627:therapeutic use*; D015850:Interleukin-6 / Q000627:therapeutic use*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D012772:Shock, Septic / Q000401:mortality* / Q000628:therapy*; D013211:Staphylococcus aureus / Q000472:pathogenicity*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D004768:Enterotoxins; D017370:Interleukin-11; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; C031818:enterotoxin B, staphylococcal