Linked Life Data

12504339

Source:http://linkedlifedata.com/resource/pubmed/id/12504339

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-3
pubmed:dateCreated
2002-12-30
pubmed:abstractText
Gulf War personnel were given pyridostigmine bromide (PB) as a prophylactic treatment against organophosphate nerve agent exposure, and were exposed to the insecticide permethrin and the insect repellent N,N-diethyl-m-toluamide (DEET). The purpose of this study was to assess the effects of PB to modulate release of inflammatory biomarkers after topical chemical exposure to chemical mixtures containing permethrin and DEET applied in ethanol or water vehicles. Treatments were topically applied to isolated perfused porcine skin flaps (IPPSFs). Concentrations of interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha) and prostaglandin E(2) (PGE(2)) were assayed in perfusate to probe for potential inflammatory effects after complex mixture application. IPPSFs (n=4/treatment) were topically dosed with mixtures of permethrin, DEET, and permethrin/DEET, in ethanol. Each treatment was repeated with perfusate spiked with 50 ng/ml of PB. Perfusate was also spiked with 30 ng/ml diisopropylfluorophosphate to simulate low level organophosphate nerve agent exposure. Timed IPPSF venous effluent samples (0.5,1,2,4, and 8 h) were assayed by ELISA for IL-8 and TNF-alpha and by EIA for PGE(2). Overall, PB infusion caused a decrease or IL-8 and PGE(2) release. Effects on TNF-alpha were vehicle dependent. To probe the potential mechanism of this PB effect, human epidermal keratinocyte HEK cell cultures were exposed to permethrin DEET permethrin/DEET, with and without PB in DMSO. IL-8 was assayed at 1, 2, 4, 8, 12 and 24 h. PB suppressed IL-8 in permethrin and ethanol treatment from 4 to 24 h confirming the IPPSF results. In conclusion, these studies suggest that systemic exposure to PB suppressed IL-8 release at multiple time points in two skin model systems. This interaction merits further study.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0300-483X
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
183
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
15-28
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12504339-Administration, Cutaneous, pubmed-meshheading:12504339-Animals, pubmed-meshheading:12504339-Cells, Cultured, pubmed-meshheading:12504339-Cholinesterase Inhibitors, pubmed-meshheading:12504339-Cytokines, pubmed-meshheading:12504339-DEET, pubmed-meshheading:12504339-Dinoprostone, pubmed-meshheading:12504339-Drug Interactions, pubmed-meshheading:12504339-Female, pubmed-meshheading:12504339-Humans, pubmed-meshheading:12504339-Insect Repellents, pubmed-meshheading:12504339-Insecticides, pubmed-meshheading:12504339-Interleukin-8, pubmed-meshheading:12504339-Keratinocytes, pubmed-meshheading:12504339-Permethrin, pubmed-meshheading:12504339-Persian Gulf Syndrome, pubmed-meshheading:12504339-Pyridostigmine Bromide, pubmed-meshheading:12504339-Skin, pubmed-meshheading:12504339-Skin Absorption, pubmed-meshheading:12504339-Swine, pubmed-meshheading:12504339-Tumor Necrosis Factor-alpha
pubmed:year
2003
pubmed:articleTitle
Pyridostigmine bromide modulates topical irritant-induced cytokine release from human epidermal keratinocytes and isolated perfused porcine skin.
pubmed:affiliation
Center for Chemical Toxicology Research and Pharmacokinetics, North Carolina State University, 4700 Hillsborough Street, Raleigh, NC 27606, USA. nancy_monteiro@ncsu.edu
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, Non-P.H.S.