Different pathways in irritant contact eczema?

Abstract

The epidermal response to 2 different irritants, nonanoic acid (NAA) and sodium lauryl sulfate (SLS), was investigated with 2 different methods. NAA 80% and SLS 4% were applied under occlusion for up to 24 h. Elemental changes were determined in cryosections by x-ray microanalysis. Compared to unexposed skin a significantly higher sodium/potassium ratio was found after 6 h in NAA-exposed skin and a lower ratio in SLS-exposed. At 24 h both substances had induced similar changes, compatible with a cell injury. The findings demonstrate a time-dependent NAA and SLS response. With reverse transcription polymerase chain reaction, the mRNA expression of interleukin-1 alpha (IL-1 alpha), -1 beta (IL-1 beta), -6 (IL-6), and -8 (IL-8), tumor necrosis factor alpha (TNF alpha) and granulocyte macrophage colony stimulating factor (GM-CSF) in shave biopsies from irritated and unexposed skin was studied at 0. 4. 8 and 24 h. NAA, but not SLS, induced an increase in mRNA expression for IL-6 mRNA-expression for GM-CSF was increased after SLS exposure, but not after NAA. These findings indicate a time and substance dependent difference in the up-regulation of mRNA for different cytokines in epidermis during the first 24 h of the irritant reaction. This might be the effect of differences in the irritants action on the cell membranes, which is also reflected by the differences found in the elemental content at 6 h.

Cytokines and Chemokines in Irritant Contact Dermatitis

“…The disruption of the skin barrier leads to release of preformed IL-1 α [18], which represents an initial step in the inflammatory cascade of ICD. Numerous in vitro studies have also shown that various irritants induce IL-1 α expression in keratinocytes [5, 6, 19–22]. Activation of IL-1 α is subsequently thought to stimulate further production of proinflammatory cytokines and chemokines such as IL-1 β , TNF- α , IL-6, and CXCL8 (IL-8) by surrounding epidermal and dermal cells [23, 24].…”

“…Other cytokines and factors that have been implicated in the pathogenesis of ICD and which are also produced by keratinocytes include vascular endothelial growth factor (VEGF) [21, 39, 40] and IL-6 [19, 27, 39]. VEGF which is mainly secreted by keratinocytes is a potent mediator of angiogenesis that stimulates the migration and proliferation of endothelial cells, facilitates vascular permeability, and induces the expression of adhesion molecules ICAM-1 and VCAM-1 on endothelial cells [39].…”

Contact allergy, irritancy and ‘danger’

“…Various studies on cytokine production in response to irritants have shown production of TNFa, IL-8, IL-1b, IL-1a and IL-8 (23). The cytokines that give Langerhans cells an immunostimulatory morphology, namely GMCSF, IL-1 and TNFa, are also produced by irritants (24)(25)(26).…”

Genetic Basis of Irritant Susceptibility in Health Care Workers

“…Since acute inflammatory response in epidermis depends on the chemical structure of the applied irritant. 19 three structurally different irritants, sodium lauryl sulfate (SLS), NaOH (sodium hydroxide) and benzalkonium chloride (BKC), were used as model irritants. To date, most published studies have investigated a small number of genes and/or SNPs and focused on clinical ICD.…”