Endotoxin, tumor necrosis factor-α and interleukin 1 induce interleukin 6 production in vivo

1989; Academic Press; Volume: 53; Issue: 3 Linguagem: Inglês

10.1016/0090-1229(89)90010-x

ISSN

1090-2341

Autores

M R Shalaby, Anders Waage, L Aarden, Terje Espevik,

Tópico(s)

Chemokine receptors and signaling

Resumo

The ability of Escherichia coli-derived lipopolysaccharide (LPS), recombinant (r) interleukin 1-β (rIL-1β), and r murine tumor necrosis factor-α (rMuTNF-α) to induce interleukin 6 (IL-6) production in vivo was investigated. Peak serum IL-6 concentration was attained after 2 hr of LPS injection into mice. The coinjection of antiserum against rMuTNF-α with LPS resulted in a reduction of the induced serum IL-6 level, indicating the involvement of endogenous TNF-α in LPS induction of IL-6. Recombinant IL-1β and rMuTNF-α injected directly caused the production of substantial amounts of IL-6 within 30 min. The injection of a combination of rIL-1β and rTNF-α induced a significantly greater level of IL-6 than either agent alone. The greater level of serum IL-6 was associated with hypothermia and an increased lethality among mice injected with both cytokines. These data demonstrate the abilities of IL-1β and TNF-α to induce IL-6 production in vivo and indicate that LPS induction of IL-6 may be mediated, at least partially, through TNF-α action. The data describe a new in vivo biologic activity shared between IL-1β and TNF-α and suggest that IL-6 may be an important effector in the manifestation of TNF-α and IL-1β actions in vivo.

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