Sulfur mustard upregulates the expression of interleukin-8 in cultured human keratinocytes

Lardot, C.; Dubois, Vincent; Lison, Dominique

doi:10.1016/s0378-4274(99)00134-4

Cited by 32 publications

(16 citation statements)

References 8 publications

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“…3 In addition to the inductive effect on expression, SM also increases the extracellular release of cytokines. 16 The released proinflammatory cytokines possess considerable vasoactive and chemoattractant potential, thereby promoting inflammatory cell recruitment and activation. 17 A number of findings on the induction of inflammatory biomarkers following SM exposure have been summarized in Table 4.…”

Section: Discussionmentioning

confidence: 99%

A randomized controlled trial on the anti-inflammatory effects of curcumin in patients with chronic sulphur mustard-induced cutaneous complications

et al. 2012

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Background: Chronic cutaneous complications such as pruritus are among the very frequent complaints of sulphur mustard (SM)-exposed patients. The present trial investigated the impact of curcumin on serum inflammatory biomarkers and their association with pruritus severity and quality of life (QoL). Methods: This was a randomized, double-blind trial among 96 male Iranian veterans (age 37-59 y) who were suffering from chronic SM-induced pruritic skin lesions. Patients were randomly assigned to curcumin (1 g/d, n ¼ 46) or placebo (n ¼ 50) for four weeks. Serum concentrations of interleukins 6 (IL-6) and 8 (IL-8) together with high-sensitivity C-reactive protein (hs-CRP) and calcitonin gene-related peptide (CGRP) were measured at baseline and at the end of the trial. Assessment of pruritus severity was performed using the pruritus score and QoL using the Dermatology Life Quality Index (DLQI). Results: Serum IL-8 and hs-CRP were significantly reduced in both groups but the magnitude of reduction was greater in the curcumin group (P , 0.001). Serum CGRP was only decreased in the curcumin group (P , 0.001). No significant change was observed in serum IL-6. There were significant correlations between CGRP and IL-6 changes (P ¼ 0.011) and between DLQI and IL-8 changes (P ¼ 0.026) in the curcumin group. In the curcumin group, changes in serum IL-8 concentrations were found as the significant predictor of DLQI scores (P ¼ 0.026) but none of the independent variables could predict pruritus scores. Conclusions: Curcumin supplementation effectively mitigates inflammation in patients suffering from chronic SM-induced cutaneous complications. This anti-inflammatory effect might account for the observed pruritus alleviation and QoL improvement by this phytochemical.

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Section: Discussionmentioning

confidence: 99%

A randomized controlled trial on the anti-inflammatory effects of curcumin in patients with chronic sulphur mustard-induced cutaneous complications

et al. 2012

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“…SM [23,24]. Each of these cytokine/chemokine has been identified as key in initiating an inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

Cytokine, chemokine, and matrix metalloproteinase response after sulfur mustard injury to weanling pig skin

Sabourin

Danne

Buxton

et al. 2002

J Biochem & Molecular Tox

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Cutaneous exposure to sulfur mustard [bis(2-chloroethyl) sulfide; SM] produces a delayed inflammatory skin response and severe tissue injury. Pig skin has organ similarities to human skin that is characterized by the content and types of epidermal lipids, the density of hair follicles and presence of sweat glands, which together afford penetration of topically applied compounds, complex inflammatory responses, and subsequent wound healing. The goal of this study was to identify in vivo proinflammatory biomarkers of the SM porcine skin injury within 72 h after SM challenge, using the weanling pig model. Changes in gene expression of inflammatory mediators were examined at 3, 6, 24, 48, and 72 h, using subtraction library analyses and by quantitation of selected transcripts by reverse transcription-polymerase chain reaction (RT-PCR). Sequence analysis of subtraction libraries identified up-regulation of IL-8 at 24, 48, and 72 h. No other specific proinflammatory gene transcripts were isolated from the libraries. Specific transcript RT-PCR analysis showed increased production of interleukin-1beta (IL-1beta), interleukin-6 (IL-6), interleukin-8 (IL-8), and matrix metalloproteinase-9 (MMP-9, gelatinase B) mRNA levels in response to SM exposure. Tumor necrosis factor-alpha (TNF-alpha) expression was only slightly increased and no change in the levels of expression was observed for monocyte chemoattractant protein-1 and MMP-2. This study identifies the main proinflammatory mediators involved in SM-induced skin injury in a weanling pig model. The results suggest transcriptional activity in the inflammatory response proteins IL-8, IL-6, IL-1beta, and MMP-9 and modest changes in TNF-alpha that together produce inflammation and contribute to the pathogenesis of SM dermatotoxicity. Therefore, drugs preventing SM-induced inflammation should be prime candidates for medical intervention to lessen collateral inflammation associated with tissue destruction.

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“…A hallmark of NHEK exposure to sulfur mustard is a significant increase in the expression of the pro-inflammatory cytokines, mainly interleukin 1␤(IL-1␤), interleukin 6 (IL-6), interleukin 8 (IL-8), and tumor necrosis factor alpha (TNF-␣) [6][7][8][9]. The increased production of IL-8 in cultured NHEK cells, in particular, was found to be due to transcriptional activation resulting in elevated levels of postexposure mRNA [7]. IL-8 appeared in the media of stimulated cells as early as 6 h and persisted up to 24 h postexposure [7].…”

Section: Introductionmentioning

confidence: 99%

Modulation of sulfur mustard induced cell death in human epidermal keratinocytes using IL‐10 and TNF‐α

Qabar¹,

Nelson²,

Guzman³

et al. 2005

J Biochem & Molecular Tox

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We compared the effects of overexpressing a tightly regulated anti-inflammatory cytokine, interleukin 10 (IL-10), and the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) on sulfur mustard induced cytotoxicity in human epidermal keratinocytes. Both cytokines were overexpressed when compared with the cells transfected with the empty vector as determined by quantitative ELISA. Cells overexpressing interleukin 10 suppressed the pro-inflammatory cytokines interleukin 8 and interleukin 6 following exposure to 50-300 microM sulfur mustard. These cells exhibited delayed onset of sulfur mustard induced cell death. On the other hand, cells overexpressing tumor necrosis factor alpha induced a sustained elevation in both interleukin 6 and 8 expression following exposure to 50-300 microM sulfur mustard. These cells were sensitized to the effects of sulfur mustard that resulted in an increased sulfur mustard induced cell death. Normal human epidermal keratinocytes treated with sulfur mustard exhibited elevated levels of tumor necrosis factor alpha expression and increased activity of nuclear factor kappa B. Gene array data indicated that cells overexpressing interleukin 10 induced several genes that are involved in growth promotion and cell-fate determination. We, therefore, identify IL-10 and TNF-alpha signal transduction pathways and their components as possible candidates for early therapeutic intervention against sulfur mustard induced cell injury.

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Sulfur mustard upregulates the expression of interleukin-8 in cultured human keratinocytes

Cited by 32 publications

References 8 publications

A randomized controlled trial on the anti-inflammatory effects of curcumin in patients with chronic sulphur mustard-induced cutaneous complications

A randomized controlled trial on the anti-inflammatory effects of curcumin in patients with chronic sulphur mustard-induced cutaneous complications

Cytokine, chemokine, and matrix metalloproteinase response after sulfur mustard injury to weanling pig skin

Modulation of sulfur mustard induced cell death in human epidermal keratinocytes using IL‐10 and TNF‐α

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