Quantification of Chemotactic Peptides (C5a Anaphylatoxin and IL-8) in Psoriatic Lesional Skin

Takematsu, Hideaki; Tagami, Hachiro

doi:10.1001/archderm.1993.01680220086020

Cited by 46 publications

(16 citation statements)

References 30 publications

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“…In summary, the C5aR is increased on MoDC by PGE 2 , which results in increased chemotactic and immunomodulatory effects of C5a on MoDC. This could be relevant in particular in diseases such as psoriasis, where dendritic cells, PGE 2 and C5a have been demonstrated to play important pathogenetic roles 37,41,42,45,46 …”

Section: Discussionmentioning

confidence: 99%

Up‐regulation of C5a receptor expression and function on human monocyte derived dendritic cells by prostaglandin E₂

et al. 2003

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Summary The expression of the C5a‐receptor (C5aR) on dendritic cells, its regulation and function have not been well established thus far. We show that the C5aR is expressed on human monocyte‐derived dendritic cells (DC) and can be down‐regulated by maturation stimuli such as tumour necrosis factor‐α (TNF‐α), lipopolysaccharide (LPS) or CD40L and by the T helper 1‐cytokine interferon‐γ (INF‐γ). Prostaglandin E2 (PGE2), a proinflammatory mediator supporting dendritic cell activation and necessary for adequate DC migration, leads to the up‐regulation of C5aR expression when incubated alone and prevents down‐regulation when given in combination with TNF‐α or LPS. Stimulation of C5aR on DC triggered F‐actin polymerization, indicating the chemotactic potential of DC elicited by C5a. C5a induced F‐actin polymerization was increased when C5aR was up‐regulated by PGE2. Stimulation of DC with C5a resulted in interleukin‐10 production which was significantly increased after C5aR up‐regulation with TNF‐α and PGE2. Therefore, up‐regulation of the C5aR on human DC alters their chemotactic and immunologic response to C5a.

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Section: Discussionmentioning

confidence: 99%

Up‐regulation of C5a receptor expression and function on human monocyte derived dendritic cells by prostaglandin E₂

et al. 2003

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“…Based of the results of biochemical analyses and in vitro studies, it is clear that IL-8 contributes significantly to the pathological changes seen in psoriasis (Sticherling et al, 1991a(Sticherling et al, , b, 1999Takematsu and Tagami, 1993). The involvement of IL-8 in other dermatoses, such as bullous pemphigoid (Baroni et al, 2002), erythema migrans (Grygorczuk et al, 2002), atopic dermatitis, and allergic contact dermatitis (Albanesi et al, 2001), has also been demonstrated.…”

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confidence: 99%

All-Trans-Retinoic Acid Induces Interleukin-8 via the Nuclear Factor-κB and p38 Mitogen-Activated Protein Kinase Pathways in Normal Human Keratinocytes

Dai

Yamasaki

Shirakata

et al. 2004

Journal of Investigative Dermatology

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Retinoic acid derivatives have been used successfully for the treatment of various dermatoses, such as psoriasis; however, topical application of these compounds often elicits skin irritation. We hypothesized that this irritation was as a result of the local production of interleukin-8 (IL-8). To test this hypothesis, we investigated whether all-trans-retinoic acid (ATRA) induced IL-8 production in normal human keratinocytes. Stimulation with 10(-7) M ATRA enhanced IL-8 mRNA expression and induced IL-8 production. We also studied the intracellular signaling mechanisms of ATRA-induced IL-8 production in keratinocytes. ATRA increased the expression of RelA (p65), RelB, nuclear factor (NF)-kappaB2 (p52), and NF-kappaB1 (p50), and elevated the DNA-binding activity of p65 and phosphorylation of inhibitor kappaB (IkappaB) alpha. Introduction of a dominant-negative mutant of IkappaBalpha completely abolished ATRA-induced IL-8 production, which indicates that this process is NF-kappaB-dependent. We also studied the role of the p38 mitogen-activated protein kinase (MAPK) pathway in this phenomenon. ATRA phosphorylated the p38 MAPK, and SB202180 inhibited ATRA-induced IL-8 production, which indicates that the p38 MAPK is also involved in ATRA-induced IL-8 production. In summary, ATRA induces IL-8 production in both NF-kappaB- and p38 MAPK-dependent manners in normal human keratinocytes.

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“…They are prodticed by nioi-jocytes, fibroblasts, and keratinocytcs itt vitro [1][2][3]. Large quantities of these peptides or their transcripts are found in psoriatic skin [4][5][6][7][8][9][10]. IL-8 and GROa act mainly on neutrophils, inducing cheniotaxis and adhesion to endothelial cells [11,12].…”

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confidence: 99%

Interleukin-8 and GROα Prime Human Neutrophils for Superoxide Anion Production and Induce up-Regulation of N-Formyl Peptide Receptors

Metzner¹,

Barbisch²,

Parlow³

et al. 1995

Journal of Investigative Dermatology

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Interleukin-8 (IL-8) and GRO alpha are leukocyte-attracting peptides of the chemokine family. To study the priming potential of these chemokines, we measured superoxide anion production and up-regulation of N-formyl peptide receptors in human neutrophils. IL-8 and GRO alpha themselves did not stimulate production of significant amounts of superoxide anions but potentiated N-formyl peptide-induced superoxide anion production in a concentration-dependent manner. Binding measurements by flow cytometry at 37 degrees C with fluorescein-labeled N-formyl peptide revealed enhanced total N-formyl peptide binding after pretreatment of neutrophils with IL-8 and GRO alpha. Binding measurements performed at 4 degrees C indicated that the chemokines stimulated the up-regulation of N-formyl peptide receptors at the cell surface but did not alter their affinity for the ligand. This study indicates that IL-8 and GRO alpha, in addition to their known chemotactic activity, prime neutrophils for superoxide anion production, presumably by up-regulating the number of receptors for strong superoxide-anion-triggering stimuli.

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Quantification of Chemotactic Peptides (C5a Anaphylatoxin and IL-8) in Psoriatic Lesional Skin

Cited by 46 publications

References 30 publications

Up‐regulation of C5a receptor expression and function on human monocyte derived dendritic cells by prostaglandin E₂

Up‐regulation of C5a receptor expression and function on human monocyte derived dendritic cells by prostaglandin E₂

All-Trans-Retinoic Acid Induces Interleukin-8 via the Nuclear Factor-κB and p38 Mitogen-Activated Protein Kinase Pathways in Normal Human Keratinocytes

Interleukin-8 and GROα Prime Human Neutrophils for Superoxide Anion Production and Induce up-Regulation of N-Formyl Peptide Receptors

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Quantification of Chemotactic Peptides (C5a Anaphylatoxin and IL-8) in Psoriatic Lesional Skin

Cited by 46 publications

References 30 publications

Up‐regulation of C5a receptor expression and function on human monocyte derived dendritic cells by prostaglandin E2

Up‐regulation of C5a receptor expression and function on human monocyte derived dendritic cells by prostaglandin E2

All-Trans-Retinoic Acid Induces Interleukin-8 via the Nuclear Factor-κB and p38 Mitogen-Activated Protein Kinase Pathways in Normal Human Keratinocytes

Interleukin-8 and GROα Prime Human Neutrophils for Superoxide Anion Production and Induce up-Regulation of N-Formyl Peptide Receptors

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Up‐regulation of C5a receptor expression and function on human monocyte derived dendritic cells by prostaglandin E₂

Up‐regulation of C5a receptor expression and function on human monocyte derived dendritic cells by prostaglandin E₂