Effect of a topical steroid on gene expressions for chemokines in mice with contact hypersensitivity

Mitsui, Gaku; Hirano, Takeo; Niwano, Yoshimi; Mitsui, Kazutaka; Ohara, Osamu; Yanagihara, Satoshi; Kato, Masaaki

doi:10.1016/j.intimp.2003.10.005

Cited by 15 publications

(9 citation statements)

References 50 publications

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“…For instance, phenoltreated contact dermatitis in mice produced an acute inflammation accompanied by dermal edema, and an animal model of delayed hypersensitivity induced an infiltration of inflammatory cells in the lesion. 19,20) Multiple TPA treatment used in this study, on the other hand, provoked the characteristic changes such as edema and epidermal keratinocyte proliferation. These results were well matched with other's finding.…”

Section: Discussionmentioning

confidence: 84%

Effects of Anti-inflammatory Biflavonoid, Ginkgetin, on Chronic Skin Inflammation

Lim

Son

Chang

et al. 2006

Biological & Pharmaceutical Bulletin

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Although the etiology of chronic skin inflammatory disorders including psoriasis and atopic dermatitis (AD) is not clearly understood, many studies have shown that various proinflammatory enzymes/cytokines play an important role in these inflammatory diseases. For example, phospholipase A 2 (PLA 2 ) was highly expressed in some psoriatic tissues. 1)In addition to lipoxygenase products, 2) cyclooxygenase (COX) and prostaglandins (PG) were involved in dermal inflammation and skin wound healing.3,4) Moreover, it was found that high concentrations of cytokines, such as tumor necrosis factor (TNF)-a, and adhesion molecules, including intercellular adhesion molecule (ICAM)-1, were deeply involved in the regional site of chronic skin inflammation. 5,6) Recent studies have also indicated that inducible nitric oxide synthase (iNOS) may be associated with psoriasis, and its reaction product, NO, is involved in various skin disorders. 7,8) Therefore, it is reasonably thought that an interference of activity and/or expression of these proinflammatory molecules may result in attenuation of chronic skin inflammatory syndromes, and the agents acting on these points may give beneficial effects.Biflavonoids are flavonoid-flavonoid dimers and some of them possess anti-inflammatory activity. For instance, several biflavonoids including amentoflavone, ginkgetin and isoginkgetin inhibited histamine release.9) Amentoflavone and tetrahydroamentoflavone were found to inhibit COX-1 and/or COX-2.10,11) Some biflavonoids were revealed to suppress the expression of proinflammatory molecules such as COX-2 and iNOS.12,13) These previous investigations have shown the potential of certain biflavonoids for anti-inflammatory agents. In particular, ginkgetin (Fig. 1) mainly found in Ginkgo biloba leaves (Ginkgoaceae) was previously demonstrated as an inhibitor of group IIA sPLA 2 inhibitor 14) and cPLA 2 .15) In addition, ginkgetin was reported to suppress COX-2 expression from lipopolysaccharide (LPS)-treated macrophages without affecting COX-2 activity, and in vivo study has also revealed that ginkgetin inhibited COX-2 expression and PGE 2 production from mouse skin induced by 3-d treatment of 12-O-tetradecanoylphorbol-13-acetate (TPA).16) All these findings strongly suggest that ginkgetin may show an inhibition against inflammatory disorders, especially skin inflammation by topical application. Thus, for further characterization of the pharmacological property, the effects of ginkgetin were examined on an animal model of chronic skin inflammation and proinflammatory gene expression in the present investigation. MATERIALS AND METHODSChemicals TPA and prednisolone were obtained from Sigma-Aldrich Co. (St. Louis, MO, U.S.A.). Ginkgetin was isolated from the methanol extract of Ginkgo biloba leaves according to the previously described procedure.17) The purity was Ͼ95% based on HPLC analysis. Animals Male ICR mice (4 weeks, specific pathogenfree) were obtained from Orient Co. (Korea). Animals were fed with laboratory chow (Purina Korea) and water ...

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Section: Discussionmentioning

confidence: 84%

Effects of Anti-inflammatory Biflavonoid, Ginkgetin, on Chronic Skin Inflammation

Lim

Son

Chang

et al. 2006

Biological & Pharmaceutical Bulletin

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“…In TNCB-induced CHS, capillary vasodilation occurs within 3 hours after the challenge, and neutrophils accumulate in the skin around 6 hours later. Lymphocytes then start to infiltrate into the skin within 12 hours after the challenge, and massive infiltration of lymphocytes and to a lesser extent of neutrophils constitutes the inflammatory cells 24 hours after the challenge (Mitsui et al, 2003(Mitsui et al, , 2004. Differential and sequential expressions of multiple chemoattractant factors, mainly chemokines, regulate such sequential cell infiltration patterns.…”

Section: Kinetics Of Histological Change and Chemokine Expressionmentioning

confidence: 99%

Update of Immune Events in the Murine Contact Hypersensitivity Model: Toward the Understanding of Allergic Contact Dermatitis

Honda

Egawa

Grabbe

et al. 2013

Journal of Investigative Dermatology

329

367

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Allergic contact dermatitis (ACD) is one of the most common skin diseases, consisting of sensitization and elicitation phases. With the advancement of technology and the discovery of new types of immune cells, our knowledge of the immunological mechanisms of contact hypersensitivity (CHS) as a murine model of ACD has expanded significantly in the past decade. For example, by introducing regulatory T cells, CD4(+) T-helper 17 cells, and Langerin-positive dermal dendritic cells, the initiation and termination mechanism of CHS has been revealed. In addition, the role of mast cells in CHS, long a matter of debate, has become apparent by developing conditional mast cell-deficient mice. Moreover, the role of the innate immunity system, such as that of Toll-like receptor signaling, has made a breakthrough in this field. In this review, we will integrate the recent advancement of immunological mechanisms of both the sensitization and elicitation phases of CHS into the classic view, and we will discuss updated mechanisms on its development and future directions.

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“…CCL3, CCL4 and CCL5 (CCR5 ligands) and CXCL9 and CXCL10 (CXCR3 ligands) are expressed in the skin following induction of CHS 35 36 . CCR5 expression by Tregs is required for the migration of Tregs to Leishmania major -infected skin and subsequent downregulation of the effector immune response 37 .…”

Section: Discussionmentioning

confidence: 99%

A rare subset of skin-tropic regulatory T cells expressing Il10/Gzmb inhibits the cutaneous immune response

Ikebuchi

Teraguchi

Vandenbon

et al. 2016

Sci Rep

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Foxp3+ regulatory T cells (Tregs) migrating from the skin to the draining lymph node (dLN) have a strong immunosuppressive effect on the cutaneous immune response. However, the subpopulations responsible for their inhibitory function remain unclear. We investigated single-cell gene expression heterogeneity in Tregs from the dLN of inflamed skin in a contact hypersensitivity model. The immunosuppressive genes Ctla4 and Tgfb1 were expressed in the majority of Tregs. Although Il10-expressing Tregs were rare, unexpectedly, the majority of Il10-expressing Tregs co-expressed Gzmb and displayed Th1-skewing. Single-cell profiling revealed that CD43+ CCR5+ Tregs represented the main subset within the Il10/Gzmb-expressing cell population in the dLN. Moreover, CD43+ CCR5+ CXCR3− Tregs expressed skin-tropic chemokine receptors, were preferentially retained in inflamed skin and downregulated the cutaneous immune response. The identification of a rare Treg subset co-expressing multiple immunosuppressive molecules and having tissue-remaining capacity offers a novel strategy for the control of skin inflammatory responses.

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Effect of a topical steroid on gene expressions for chemokines in mice with contact hypersensitivity

Cited by 15 publications

References 50 publications

Effects of Anti-inflammatory Biflavonoid, Ginkgetin, on Chronic Skin Inflammation

Effects of Anti-inflammatory Biflavonoid, Ginkgetin, on Chronic Skin Inflammation

Update of Immune Events in the Murine Contact Hypersensitivity Model: Toward the Understanding of Allergic Contact Dermatitis

A rare subset of skin-tropic regulatory T cells expressing Il10/Gzmb inhibits the cutaneous immune response

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