@article{allen_riviere_monteiro-riviere_2001, title={Analysis of interleukin-8 release from normal human epidermal keratinocytes exposed to aliphatic hydrocarbons: delivery of hydrocarbons to cell cultures via complexation with alpha-cyclodextrin}, volume={15}, ISSN={["0887-2333"]}, url={http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=ORCID&SrcApp=OrcidOrg&DestLinkType=FullRecord&DestApp=WOS_CPL&KeyUT=WOS:000172508300009&KeyUID=WOS:000172508300009}, DOI={10.1016/S0887-2333(01)00075-3}, abstractNote={While inhalation exposures represent the predominant route for jet fuel toxicity, increased concern has been placed on topical exposures due to reports of severe contact dermatitis among military personnel. All three of the predominant aviation fuels currently used by the commercial and military sectors have been demonstrated experimentally to induce the production of interleukin-8 (IL-8), a proinflammatory cytokine, in normal human epidermal keratinocytes (NHEK). The objective of this study was to examine the effects of individual hydrocarbon components found in these fuels on IL-8 production by NHEK. In order to circumvent the extreme hydrophobicity of these compounds, inclusion complexes were formed between alpha-cyclodextrin/aliphatic hydrocarbons by adding 2 mM hydrocarbons to 4 mM alpha-cyclodextrin. NHEK were exposed to four aliphatic hydrocarbons (undecane, dodecane, tridecane, hexadecane) for 24 h at concentrations of 7.8-500 microM. These hydrocarbons caused a peak in IL-8 release at a concentration of 31.2 microM, with the exception of dodecane which peaked at 62.5 microM. Subtoxic concentrations of the aliphatic hydrocarbons were those < 62.5 microM. These studies demonstrate that the etiology of proinflammatory cytokine expression due to jet fuel exposure may be due in large part to the aliphatic hydrocarbon components. Furthermore, these studies provide additional evidence that hydrocarbons can be successfully delivered to cells in culture by encapsulating them in cyclodextrin inclusion complexes.}, number={6}, journal={TOXICOLOGY IN VITRO}, author={Allen, DG and Riviere, JE and Monteiro-Riviere, NA}, year={2001}, month={Dec}, pages={663–669} }
 @article{allen_riviere_monteiro-riviere_2001, title={Cytokine induction as a measure of cutaneous toxicity in primary and immortalized porcine keratinocytes exposed to jet fuels, and their relationship to normal human epidermal keratinocytes}, volume={119}, ISSN={["1879-3169"]}, url={http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=ORCID&SrcApp=OrcidOrg&DestLinkType=FullRecord&DestApp=WOS_CPL&KeyUT=WOS:000167667000005&KeyUID=WOS:000167667000005}, DOI={10.1016/S0378-4274(00)00316-7}, abstractNote={The purpose of this study was to identify biomarkers of toxicity in primary porcine keratinocytes (PKC) and an immortalized porcine keratinocyte cell line (MSK3877) exposed to jet fuels Jet A, JP-8, and JP-8+100. Cells were exposed to 0.1% jet fuels and assayed for interleukin-8 (IL-8) and tumor necrosis factor alpha (TNF-alpha) mRNA using the TaqMan real time quantitative reverse transcriptase PCR assay. IL-8 and TNF-alpha protein release was measured using an ELISA. PKC exposed to jet fuels caused a slight upregulation of TNF-alpha mRNA at early time points, but no significant differences in TNF-alpha protein production were detected. IL-8 mRNA was increased at 4 h following exposure, and IL-8 protein was increased at 8 h. In MSK 3877 cells, jet fuels were shown to increase the production and expression of TNF-alpha mRNA and protein at 30 min and 1 h following exposure, respectively. IL-8 mRNA was only slightly induced compared to control. IL-8 protein release was suppressed by jet fuel exposure. These results were compared with those of a previous study in our laboratory to evaluate the utility of using porcine cells in lieu of normal human epidermal keratinocytes (NHEK). Similarities exist between PKC and NHEK with respect to both TNF-alpha and IL-8 production. The expression profile of TNF-alpha in MSK3877 cells mimics that of NHEK. In contrast, the profile of IL-8 expression opposes that of PKC and NHEK. These results suggest that porcine keratinocytes are susceptible to jet fuel toxicity. However, the responses of immortalized cells may vary from those of PKC and NHEK necessitating cautious interpretation of such data.}, number={3}, journal={TOXICOLOGY LETTERS}, author={Allen, DG and Riviere, JE and Monteiro-Riviere, NA}, year={2001}, month={Mar}, pages={209–217} }
 @article{allen_riviere_monteiro-riviere_2000, title={Identification of early biomarkers of inflammation produced by keratinocytes exposed to jet fuels Jet A, JP-8, and JP-8(100)}, volume={14}, ISSN={["1099-0461"]}, url={http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=ORCID&SrcApp=OrcidOrg&DestLinkType=FullRecord&DestApp=WOS_CPL&KeyUT=WOS:000088822300001&KeyUID=WOS:000088822300001}, DOI={10.1002/1099-0461(2000)14:5<231::AID-JBT1>3.0.CO;2-K}, abstractNote={The purpose of this study was to identify biomarkers of inflammation in normal human epidermal keratinocytes (NHEK) exposed to three jet fuel mixtures, Jet A, JP8, and JP8(100). NHEK were treated over 24 hours with 0.1% jet fuels, and mRNA production and protein release of two proinflammatory cytokines, IL‐8 and TNF‐α, were determined. Using an enzyme‐linked immunosorbent assay (ELISA), NHEK were found to release both TNF‐α and IL‐8 in response to exposure to all three jet fuels. IL‐8 release was noted within 8 hours and continued to rise through 24 hours compared to controls. Maximal levels of TNF‐α release were seen at 4 hours and decreased in a time‐dependent manner, although these levels remained above control levels at all time points assayed. mRNA for IL‐8 was elevated 4 hours following exposure to the fuels, which was detected via a quantitative competitive reverse transcriptase‐polymerase chain reaction (RT‐PCR). mRNA for TNF‐α was detected at all time points assayed but was not quantified. These results demonstrate that jet fuels induce the production and release of proinflammatory cytokines in NHEK and thus create the potential for chronic inflammation, which may contribute to the development or progression of disease states in the skin. © 2000 John Wiley & Sons, Inc. J Biochem Toxicol 14:231–237, 2000}, number={5}, journal={JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY}, author={Allen, DG and Riviere, JE and Monteiro-Riviere, NA}, year={2000}, pages={231–237} }
 @article{allen_monteiro-riviere_1999, title={Alteration of cytokeratin expression following transdermal lidocaine hydrochloride iontophoresis}, volume={16}, ISSN={["0724-8741"]}, url={http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=ORCID&SrcApp=OrcidOrg&DestLinkType=FullRecord&DestApp=WOS_CPL&KeyUT=WOS:000082536800025&KeyUID=WOS:000082536800025}, DOI={10.1023/A:1018979831854}, number={9}, journal={PHARMACEUTICAL RESEARCH}, author={Allen, DG and Monteiro-Riviere, NA}, year={1999}, month={Sep}, pages={1487–1490} }