Cytokine-Stimulated Human Dermal Microvascular Endothelial Cells Produce Interleukin6 - Inhibition by Hydrocortisone, Dexamethasone, and Calcitriol

Hettmannsperger, U.; Detmar, Michael; Owsianowski, M; Tenorio, Susanne; Kammler, Hans-Jürgen; Orfanos, Constantin B

doi:10.1111/1523-1747.ep12667288

Cited by 38 publications

(21 citation statements)

References 42 publications

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“…Peripheral blood monocytes from psoriasis patients have also been shown to produce increased quantities of IL-6 [21]. Further TNF-α has been shown to induce IL-6 [22]. …”

Section: Discussionmentioning

confidence: 99%

Generalised Pustular Psoriasis Induced by Cyclosporin A Withdrawal Responding to the Tumour Necrosis Factor Alpha Inhibitor Etanercept

et al. 2002

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We report a 50-year-old male patient with a 15-year history of psoriasis including mutilating psoriatic arthritis, in whom the withdrawal of cyclosporin A induced a generalised pustular exacerbation and a aggravation of the joint condition. Two weekly injections of 25 mg of the tumour necrosis factor α inhibitor etanercept led to a rapid improvement of his psoriatic arthritis, as well as regression of the pustular eruption, while residual erythema was still present. The clinical response was reflected by an increase in circulating interleukin (IL) 10 and a decrease in IL-6 and IL-8 serum levels during treatment. We conclude that etanercept may be a safe and effective therapy not only in severe psoriatic arthritis, but also in cases of pustular rebound after withdrawal of immunosuppressive agents.

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“…Peripheral blood monocytes from psoriasis patients have also been shown to produce increased quantities of IL-6 [21]. Further TNF-α has been shown to induce IL-6 [22]. …”

Section: Discussionmentioning

confidence: 99%

Generalised Pustular Psoriasis Induced by Cyclosporin A Withdrawal Responding to the Tumour Necrosis Factor Alpha Inhibitor Etanercept

et al. 2002

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“…TNF-injection, in mice, can cause fibroblast and epidermal cell proliferation as well as increased numbers of blood vessels [38]. Human dermal microvascular endothelial cell IL-6 production is also up-regulated by TNF-and IL-1 [39]. Nickoloff [40] has hypothesized that TNF-is the orchestrator of the psoriatic pathology.…”

Section: Discussionmentioning

confidence: 99%

In vivo effects of cytokines on psoriatic skin grafted on nude mice: involvement of the tumour necrosis factor (TNF) receptor

Gilhar

David

Kalish³

et al. 1996

Clinical and Experimental Immunology

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SUMMARYFollowing engraftment of human involved psoriatic skin to nude mice there is a partial normalization of pathology associated with a loss of inflammatory leucocytes. However, the epidermis remains hyperproliferative, which may reflect a primary defect. The roles of TNF-®, IL-1 and IL-6 in epidermal hyperproliferation of grafted psoriatic lesions were investigated. Before and after treatment, grafts were analysed to determine epidermal thickness and labelling index (LI). HLA-DR, intercellular adhesion molecule-1 (ICAM-1), and TNF receptor (TNF-R; p75 and p55) expression were determined by immunoperoxidase staining. Psoriatic epidermis was found consistently to be negative for p55 TNF-R and p75 TNF-R before grafting. Following engraftment, TNF-R-positive cells (i.e. p55 by keratinocytes; p75 by epidermal dendritic cells) were identified throughout the epidermis. Higher numbers of p75 TNF-R epidermal dendritic cells were found in grafts following a course of TNF-®, IL-6 or IL-1 treatment. The p55 form of the TNF-R expressed by keratinocytes was significantly elevated after treatment with TNF-® or IL-6. HLA-DR and ICAM-1 were also expressed in these grafts. TNF-®, anti-IL-1, and anti-IL-6 treatment induced a marked decrease in the epidermal thickness and LI of psoriatic graft tissue, correcting the hyperproliferation associated with psoriatic epidermis. Supraphysiological levels of TNF-® may saturate and consequently down-regulate their own receptors, leading to a paradoxical inhibitory effect.

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“…Recently, 1α-OHase expression was detected in endothelial cells from human renal arteries and primary cultures of human umbilical vein endothelial cells (HUVEC) [23]; the enzyme activity in HUVEC increased after treatment with TNF-α and LPS [23]. In HMEC calcitriol treatment inhibited the TNF-α and IL-1β-induced IL-6 production [42]. Here we show for the first time that 1α,25-(OH) 2 D 3 modulates the innate immune responses of human microvessel endothelial cells and inhibits TLR4 agonist LPS-induced MyD88-dependent NF-κB activation and proinflammatory cytokine (IL-6 and IL-8) and CCchemokine RANTES release.…”

Section: Treatment Of Hmec With 1αmentioning

confidence: 99%

1,25-Dihydroxyvitamin D3 inhibits lipopolysaccharide-induced immune activation in human endothelial cells

Equils¹,

Naiki²,

Shapiro

et al. 2005

Clinical and Experimental Immunology

122

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Cytokine-Stimulated Human Dermal Microvascular Endothelial Cells Produce Interleukin6 - Inhibition by Hydrocortisone, Dexamethasone, and Calcitriol

Cited by 38 publications

References 42 publications

Generalised Pustular Psoriasis Induced by Cyclosporin A Withdrawal Responding to the Tumour Necrosis Factor Alpha Inhibitor Etanercept

Generalised Pustular Psoriasis Induced by Cyclosporin A Withdrawal Responding to the Tumour Necrosis Factor Alpha Inhibitor Etanercept

In vivo effects of cytokines on psoriatic skin grafted on nude mice: involvement of the tumour necrosis factor (TNF) receptor

1,25-Dihydroxyvitamin D3 inhibits lipopolysaccharide-induced immune activation in human endothelial cells

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