✍ Scribed by A. O. Inman; N. A. Monteiro-Riviere; J. E. Riviere
No coin nor oath required. For personal study only.
Jet propellant (JP)‐8, the primary jet fuel used by the U.S. military, consists of hydrocarbon‐rich kerosene base commercial jet fuel (Jet‐A) plus additives DC1‐4A, Stadis 450 and diethylene glycol monomethyl ether. Human epidermal keratinocytes (HEK) were exposed to JP‐8, aliphatic hydrocarbon (HC) fuel S‐8 and aliphatic HC pentadecane (penta), tetradecane (tetra), tridecane (tri) and undecane (un) for 5 min. Additional studies were conducted with signal transduction pathway blockers parthenolide (P; 3.0 µm), isohelenin (I; 3.0 µm), SB 203580 (SB; 13.3 µm), substance P (SP; 3.0 µm) and recombinant human IL‐10 (rHIL‐10; 10 ng ml^−1^). In the absence of inhibitors, JP‐8 and to a lesser extent un and S‐8, had the greatest toxic effect on cell viability and inflammation suggesting, as least in vitro, that synthetic S‐8 fuel is less irritating than the currently used JP‐8. Each inhibitor significantly (P < 0.05) decreased HEK viability. DMSO, the vehicle for P, I and SB, had a minimal effect on viability. Overall, IL‐8 production was suppressed at least 30% after treatment with each inhibitor. Normalizing data relative to control indicate which inhibitors suppress HC‐mediated IL‐8 to control levels. P was the most effective inhibitor of IL‐8 release; IL‐8 was significantly decreased after exposure to un, tri, tetra and penta but significantly increased after JP‐8 exposure compared with controls. Inhibitors were not effective in suppressing IL‐8 release in JP‐8 exposures to control levels. This study shows that inhibiting NF‐__κ__B, which appears to play a role in cytokine production in HC‐exposed HEK in vitro, may reduce the inflammatory effect of HC in vivo. Copyright © 2007 John Wiley & Sons, Ltd.
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