Quantification of chemotactic peptides (C5a anaphylatoxin and IL-8) in psoriatic lesional skin

Takematsu, Hideaki

doi:10.1001/archderm.129.1.74

Cited by 26 publications

(22 citation statements)

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“…Both IL-1 and IL-8 have been implicated in this response. Indeed, IL-8 and IL-6, as well as other T-cell-stimulatory cytokines such as GRO-a and MCP-1, can be elevated in psoriatic skin lesions (43)(44)(45)(46)(47)(48)(49)(50)(51)64). On the other hand, as stated above, lymphokines produced by activated T cells in psoriatic skin lesions have a strong influence on epidermal proliferation.…”

Section: Epidermal Hyperplasia Is Maintained By a T-cellmediated Inflmentioning

confidence: 89%

“…In the study using flowcytometry of freshly isolated lesional T cells, Szabo et al (42) concluded that both CD4 π and CD8 π T cells are IFN-g producers. Other cytokines that mediate skin inflammation such as IL-1b, IL-6, IL-8, growth-related oncogene a (GRO-a), and TGF-a have also been reported to be increased in psoriatic plaques (43)(44)(45)(46)(47)(48)(49)(50)(51)(52). These cytokines are thought to be produced by activated keratinocytes as well as by infiltrating macrophages and T cells.…”

Section: Psoriasis Is a T-cell-mediated Immune Dermatosismentioning

confidence: 99%

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Role of neutrophils in induction of acute inflammation in T‐cell‐mediated immune dermatosis, psoriasis: A neutrophil‐associated inflammation‐boosting loop

Terada

Ozawa

Tagami

2000

Experimental Dermatology

133

111

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A growing body of evidence has indicated that T-cell-mediated immunity plays an important role in triggering and maintenance of psoriatic lesions. In this review we present our own experimental results as well as those from the literature related to the pathomechanism of the development of inflammatory changes in psoriatic lesions. First of all it is important to acknowledge the fact that psoriatic lesions are not uniform as assumed by many authors but that they are actually rather heterogeneous both clinically and histologically even within the same plaques. Lymphokines produced by activated T cells in psoriatic lesions have a strong influence on the proliferation of the epidermis, whose stimulated kertinocytes released several cytokines, which in turn enhance the activation state of T cells. Thus, they form a vicious cycle, a T-cell-mediated inflammationsustaining loop. Although the interaction between T-cell-mediated immunity and epidermal keratinocytes may well explain the maintenance of background ''chronic'' inflammatory changes diffusely observed throughout psoriatic lesions, it is not enough to explain the island-like, ''acute'' inflammatory changes observed within and at the border of the plaque lesions. Characteristic neutrophil accumulation under the stratum corneum can be observed in the highly inflamed and therapeutically recalcitrant areas of psoriatic lesions. They are chemotactically attracted and activated there by synergistic action of chemokines, IL-8 and Gro-a released by the stimulated keratinocytes, and particularly C5a/C5a des arg produced via the alternative complement pathway activation possibly on the surface of corneocytes. In this review, we emphasize that the accumulation of neurophils is not simply a passive event. We think that those stimulated neutrophils are able to influence not only the growth that may well explain the localized ''acute'' inflammatory changes scate-mail: terui/mail.cc.tohoku.ac.jp tered over the ''chronic'' psoriatic plaques as well as in the acutely inflamed lesions of pustular psoriasis.

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Section: Epidermal Hyperplasia Is Maintained By a T-cellmediated Inflmentioning

confidence: 89%

Section: Psoriasis Is a T-cell-mediated Immune Dermatosismentioning

confidence: 99%

Role of neutrophils in induction of acute inflammation in T‐cell‐mediated immune dermatosis, psoriasis: A neutrophil‐associated inflammation‐boosting loop

Terada

Ozawa

Tagami

2000

Experimental Dermatology

133

111

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“…Based on the fact that the psoriatic lesions are not uniform but rather heterogeneous in regard to the position of highly inflamed portions, which are characterized by phase-wise transepidermal neutrophil chemotaxis, we speculate that IL-6 might be generated only in lesional skin under special circumstances like chemotactic C5a anaphylatoxin (Takematsu and Tagami 1993). In fact, Ohta et al (1991) demonstrated the strongest mRNA expression of both IL-6 and IL-6 receptors in the narrow transitional zone between perilesional uninvolved epidermis and fully developed psoriatic epidermis.…”

Section: Discussionmentioning

confidence: 98%

Lack of Correlation between Interleukin 6 and Interleukin 1 Levels in Psoriatic Lesional Skin.

Takematsu

Tagami

1994

Tohoku J. Exp. Med.

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“…For immunohistochemistry analysis the samples were treated with formalin and paraffin embedded. The tissue samples were used for isolation of RNA, quantification protein expression levels of CRH, CRHBP, IL-8 and IL-33 as described previously [15,16]. The study was carried out after the ethical approval was provided by the ethical committee of Wuhan No.1 Hospital.…”

Section: Collection Of Samplesmentioning

confidence: 99%

Up-regulation of corticotropin releasing hormone is associated with the downregulation of corticotropin releasing hormone binding protein and up-regulation of IL- 33 and IL-8 expression in psoriasis

Su¹,

Xia²,

Huang³

et al. 2018

Trop. J. Pharm Res

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Quantification of chemotactic peptides (C5a anaphylatoxin and IL-8) in psoriatic lesional skin

Cited by 26 publications

References 0 publications

Role of neutrophils in induction of acute inflammation in T‐cell‐mediated immune dermatosis, psoriasis: A neutrophil‐associated inflammation‐boosting loop

Role of neutrophils in induction of acute inflammation in T‐cell‐mediated immune dermatosis, psoriasis: A neutrophil‐associated inflammation‐boosting loop

Lack of Correlation between Interleukin 6 and Interleukin 1 Levels in Psoriatic Lesional Skin.

Up-regulation of corticotropin releasing hormone is associated with the downregulation of corticotropin releasing hormone binding protein and up-regulation of IL- 33 and IL-8 expression in psoriasis

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