Tryptanthrin Inhibits Interferon-.GAMMA. Production by Peyer's Patch Lymphocytes Derived from Mice That Had Been Orally Administered Staphylococcal Enterotoxin.

Takei, Yasuhiko; Kunikata, Toshio; Aga, Miho; Inoue, Shin‐ichiro; Ushio, Shimpei; Iwaki, Kanso; Ikeda, Masao; Kurimoto, Masashi

doi:10.1248/bpb.26.365

Cited by 43 publications

(40 citation statements)

References 23 publications

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“…It is a potent inhibitor of prostaglandin and leukotriene synthases in various cell lines and a selective inhibitor of cyclooxygenase 2 (COX-2) (73) and of inducible nitric oxide synthase (iNOS) (NOS II) expression (162). It inhibits the production of IFN-␥ and IL-2 after the stimulation of Peyer's patch lymphocytes with staphylococcal enterotoxin B (SEB) (309). Tryptanthrin was also found to inhibit P-glycoprotein (Pgp) through MDR1 gene suppression (346).…”

Section: Malassezia-produced Ahr Ligands and Significance Of Ahr Actimentioning

confidence: 99%

The Malassezia Genus in Skin and Systemic Diseases

et al. 2012

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SUMMARY In the last 15 years, the genus Malassezia has been a topic of intense basic research on taxonomy, physiology, biochemistry, ecology, immunology, and metabolomics. Currently, the genus encompasses 14 species. The 1996 revision of the genus resulted in seven accepted taxa: M. furfur , M. pachydermatis , M. sympodialis , M. globosa , M. obtusa , M. restricta , and M. slooffiae. In the last decade, seven new taxa isolated from healthy and lesional human and animal skin have been accepted: M. dermatis , M. japonica , M. yamatoensis , M. nana , M. caprae , M. equina , and M. cuniculi. However, forthcoming multidisciplinary research is expected to show the etiopathological relationships between these new species and skin diseases. Hitherto, basic and clinical research has established etiological links between Malassezia yeasts, pityriasis versicolor, and sepsis of neonates and immunocompromised individuals. Their role in aggravating seborrheic dermatitis, dandruff, folliculitis, and onychomycosis, though often supported by histopathological evidence and favorable antifungal therapeutic outcomes, remains under investigation. A close association between skin and Malassezia IgE binding allergens in atopic eczema has been shown, while laboratory data support a role in psoriasis exacerbations. Finally, metabolomic research resulted in the proposal of a hypothesis on the contribution of Malassezia -synthesized aryl hydrocarbon receptor (AhR) ligands to basal cell carcinoma through UV radiation-induced carcinogenesis.

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Section: Malassezia-produced Ahr Ligands and Significance Of Ahr Actimentioning

confidence: 99%

The Malassezia Genus in Skin and Systemic Diseases

et al. 2012

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“…Tryptanthrin has a range of biological activities, such as anti-microbial (Kataoka et al, 2001), anti-tumor Koya-Miyata et al, 2001), and anti-inflammatory activities (Ishihara et al, 2000). In our previous reports, we found that Tryptanthrin suppressed dextran sodium sulfate-induced colitis in mice (Micallef et al, 2002) and inhibited IFN-␥ production by Peyer's Patch lymphocytes derived from mice that had been orally administered Staphylococcal enterotoxin (Takei et al, 2003). However, to our knowledge, possible immunoregulatory effects of Tryptanthrin on Th cell activation have not been studied.…”

Section: Introductionmentioning

confidence: 79%

Tryptanthrin inhibits Th2 development, and IgE-mediated degranulation and IL-4 production by rat basophilic leukemia RBL-2H3 cells

Iwaki

Ohashi

Arai

et al. 2011

Journal of Ethnopharmacology

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“…This similarity is worthy of further study because retinoic acid and the aryl hydrocarbon receptor agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin have been shown to elicit a number of common biochemical and toxic responses, including teratogenic effects in mice and inhibition of cell proliferation of various cell lines, 55) and some tryptanthrin derivatives biosynthesized in incubations of Candida lipolytica with tryptophan and anthranilic acid or its derivatives have been reported to activate the aryl hydrocarbon receptor. 56) Other studies have demonstrated that tryptanthrin inhibits the production of interferon g and interleukin 2 by mouse spleen cells and Peyer's patch lymphocytes in culture at concentrations comparable to those for inhibition of HGF induction, 57) but the cellular signaling pathway involved in tryptanthrin-mediated inhibition of production of these cytokines remains unknown. It is possible that determination of the exact target for tryptanthrin in attenuating HGF induction may enable the molecular mechanism underlying tryptanthrin-mediated inhibition of production of interferon g and interleukin 2 to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Hepatocyte Growth Factor Induction in Human Dermal Fibroblasts by Tryptanthrin

Motoki

Takami

Yagi

et al. 2005

Biological & Pharmaceutical Bulletin

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In addition to regulation of normal cell functions, hepatocyte growth factor (HGF) has also been shown to be involved in malignant cell transformation and in growth, invasion and metastasis in cancer cells. Inhibitors of HGF production have a potential for interfering with malignant cell transformation and progression of tumors. We found that tryptanthrin, one of the major compounds extracted from the medicinal plant Polygonum tinctorium, which is known for its antitumor activity, strongly inhibited HGF production stimulated by various HGF inducers in human dermal fibroblasts. HGF production induced by phorbol 12-myristate 13-acetate (PMA) was potently inhibited by tryptanthrin without any appreciable cytotoxic effect. Tryptanthrin also inhibited HGF production induced by epidermal growth factor (EGF) and platelet-derived growth factor. Moreover, proliferation of the fibroblasts induced by the two growth factors was potently suppressed by tryptanthrin to the level of proliferation of unstimulated fibroblasts. However, tryptanthrin did not inhibit HGF production induced by the protein kinase A-activating agents cholera toxin and 8-bromo-cAMP. These effects of tryptanthrin were different from the effects of transforming growth factor b b1 and dexamethasone, both of which inhibit HGF production induced by all the above inducers. Upregulations of HGF gene expression by PMA and EGF were also inhibited by tryptanthrin. Activation of the mitogen-activated protein kinase (MAPK) signaling pathway is crucial for PMAinduced HGF production, but tryptanthrin did not attenuate phosphorylation of MAPK induced by PMA. These results indicate that tryptanthrin potently inhibited induction of HGF production probably through events downstream of MAPK activation.

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Tryptanthrin Inhibits Interferon-.GAMMA. Production by Peyer's Patch Lymphocytes Derived from Mice That Had Been Orally Administered Staphylococcal Enterotoxin.

Cited by 43 publications

References 23 publications

The Malassezia Genus in Skin and Systemic Diseases

The Malassezia Genus in Skin and Systemic Diseases

Tryptanthrin inhibits Th2 development, and IgE-mediated degranulation and IL-4 production by rat basophilic leukemia RBL-2H3 cells

Inhibition of Hepatocyte Growth Factor Induction in Human Dermal Fibroblasts by Tryptanthrin

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