JP-8 jet fuel exposure induces inflammatory cytokines in rat skin

Gallucci, Randle M.; O'Dell, Sijy K; Rabe, Daniel C.; Fechter, Laurence D.

doi:10.1016/j.intimp.2004.05.012

Cited by 19 publications

(35 citation statements)

References 47 publications

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“…Notably, IL-6 deficiency greatly increased TNFα mRNA and protein expression following either BKC or JP-8 exposure as compared to outcomes seen in C57 WT control mice (see Figures 1a and 1c). Previous studies utilizing rats have reported increases in both IL-1α and IL-1β in response to jet fuel exposure (Kabbur et al, 2001;Gallucci et al, 2004;Chatterjee et al, 2006;Gallucci and Mickle, 2006). In the present study, IL-1β mRNA expression was induced by either irritant, with the highest expression associated with IL-6 deficiency (see Figure 1b).…”

Section: Discussionsupporting

confidence: 63%

“…These cytokines can be up-regulated by numerous inflammatory stimuli, including primary inflammatory cytokines such as TNFα or IL-6. Previous studies utilizing rats (Gallucci et al, 2004;Gallucci and Mickle, 2006) showed significantly greater CCL2, CCL3, and CXCL1 mRNA expression following JP-8 exposure. In the present study, BKC exposure induced profound induction of these chemokines as well as CXCL10 at the protein level (see Figures 2 and 3, gray bars), with IL-6KO mice having significantly higher protein expression of CCL2.…”

Section: Discussionmentioning

confidence: 76%

“…In previous studies, this laboratory has shown that specific cytokine profiles in skin were observed following JP-8 exposure and that the inflammatory cytokine IL-6 was modulated disparately at the mRNA and protein levels in rats (Gallucci et al, 2004;Gallucci, and Mickle, 2006). However, it was not known what role IL-6 played in the pathology of JP-8 irritant dermatitis, or if these observed effects were specifically associated with jet fuel exposure.…”

Section: Discussionmentioning

confidence: 99%

“…Real-time quantitative RT-PCR was performed on an ABI PRISM 7000 SDS (Life Technologies, Carlsbad, CA). Results are reported as percent (%) acetone-treated C57 control, as it was previously noted that these animals had minimal, if any, skin inflammation (Gallucci et al, 2004). …”

Section: Real-time Quantitative Rt-pcrmentioning

confidence: 99%

“…Since IL-6 is closely linked to wound healing (Gallucci et al, 2000) and inflammation-where it is known to modulate the expression of various chemokines that influence inflammatory cell trafficking (Hurst et al, 2001;Fielding et al, 2008)-modulation of its gene could profoundly affect the pathology of dermatitis. Indeed, the expressions of specific chemokines that influence the recruitment of monocytes and dendritic cells (i.e., CCL2 and CCL3), PMN (i.e., CXCL1), as well as T-cells (i.e., CXCL10) were altered in skin following JP-8 exposure (Gallucci et al, 2004;Gallucci and Mickle, 2006). Thus, the purpose of this study was to further investigate the observation that IL-6 protein was decreased in dermatitis lesions caused by JP-8 jet fuel (Gallucci and Mickle, 2006), an irritant associated with moderate-to-severe skin pathology.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

IL-6 deficiency exacerbates skin inflammation in a murine model of irritant dermatitis

Lee

Mickle-Kawar

Gallucci

2012

Journal of Immunotoxicology

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Section: Discussionsupporting

confidence: 63%

Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Section: Real-time Quantitative Rt-pcrmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

IL-6 deficiency exacerbates skin inflammation in a murine model of irritant dermatitis

Lee

Mickle-Kawar

Gallucci

2012

Journal of Immunotoxicology

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Toxicity of jet fuel aliphatic and aromatic hydrocarbon mixtures on human epidermal Keratinocytes: evaluation based on in vitro cytotoxicity and interleukin-8 release

et al. 2006

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Jet fuels are complex mixtures of aliphatic (ALI) and aromatic (ARO) hydrocarbons that vary significantly in individual cytotoxicity and proinflammatory activity in human epidermal keratinocytes (HEK). In order to delineate the toxicological interactions among individual hydrocarbons in a mixture and their contributions to cutaneous toxicity, nine ALI and five ARO hydrocarbons were each divided into five (high/medium/low cytotoxic and strong/weak IL-8 induction) groups and intra/inter-mixed to assess for their mixture effects on HEK mortality and IL-8 release. Addition of single hydrocarbon to JP-8 fuel was also evaluated for their changes in fuel dermatotoxicity. The results indicated that when hydrocarbons were mixed, HEK mortality and IL-8 release were not all predictable by their individual ability affecting these two parameters. The lowest HEK mortality (7%) and the highest IL-8 production were induced with mixtures including high cytotoxic and weak IL-8 inductive ARO hydrocarbons. Antagonistic reactions not consistently correlated with ALI carbon chain length and ARO structure were evident and carried different weight in the overall mixture toxicities. Single addition of benzene, toluene, xylene or ethylbenzene for up to tenfold in JP-8 did not increase HEK mortality while single addition of ALI hydrocarbons exhibited dose-related differential response in IL-8. In an all ALI environment, no single hydrocarbon is the dominating factor in the determination of HEK cytotoxicity while deletion of hexadecane resulted in a 2.5-fold increase in IL-8 production. Overall, decane, undecane and dodecane were the major hydrocarbons associated with high cytotoxicity while tetradecane, pentadecane and hexadecane were those which had the greatest buffering effect attenuating dermatotoxicity. The mixture effects must be considered when evaluating jet fuel toxicity to HEK.

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Stress induced in heart and other tissues by rat dermal exposure to JP-8 fuel

et al. 2005

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Limited information is available regarding the development of systemic organ stress by dermal exposure to JP-8 fuel. In this study, the systemic stress potential of this fuel is evaluated in a rat model subjected to dermal applications of JP-8 for 7 days at 300 microl per day. Tissue histology indicated that JP-8 induces morphological alterations that suggest that tissue stress in the heart is more substantial than stress in the kidney and liver. Immunoblot analysis of tissues revealed increased levels of the inducible heat shock protein 70 (HSP70) in the heart, kidney, and liver after this dermal JP-8 exposure. This exposure also leads to increased levels of heme oxygenase-1 (HO-1/HSP3) in the liver. Additionally during this exposure, a negative regulator of inflammation, IkappaBalpha (inhibitor of NF-kappaB), was increased in the liver, slightly increased in the kidney, and not increased in the heart. Two regions of the rat brain were also examined and HSP70 and IkappaBalpha were increased in the cerebellum but not significantly increased in the cortex. This study indicates dermal JP-8 exposure causes systemic alterations that are associated with cytoprotective activities (e.g., in the liver) as well as potentially toxic mechanisms (heart and kidney).

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JP-8 jet fuel exposure induces inflammatory cytokines in rat skin

Cited by 19 publications

References 47 publications

IL-6 deficiency exacerbates skin inflammation in a murine model of irritant dermatitis

IL-6 deficiency exacerbates skin inflammation in a murine model of irritant dermatitis

Toxicity of jet fuel aliphatic and aromatic hydrocarbon mixtures on human epidermal Keratinocytes: evaluation based on in vitro cytotoxicity and interleukin-8 release

Stress induced in heart and other tissues by rat dermal exposure to JP-8 fuel

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