Epigallocatechin-3-gallate improves Dermatophagoides pteronissinus extract-induced atopic dermatitis-like skin lesions in NC/Nga mice by suppressing macrophage migration inhibitory factor

Noh, Sun Up; Cho, Eun Ah; Kim, Hyung Ok; Park, Young Min

doi:10.1016/j.intimp.2008.04.002

Cited by 43 publications

(31 citation statements)

References 46 publications

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“…There are some reports that serum IgE levels are elevated in proportion to the development of AD-like skin lesions in NC/Nga mice [4,20,21,22]. As shown in the present study, serum total IgE levels in the control group were elevated after day 33 and day 61, and levels in strain L-55 groups were significantly low compared with the control group.…”

Section: Discussionsupporting

confidence: 73%

Effect of Lactobacillus acidophilus strain L-55 on the development of atopic dermatitis-like skin lesions in NC/Nga mice

Sunada¹,

Nakamura²,

Kamei

2008

International Immunopharmacology

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Section: Discussionsupporting

confidence: 73%

Effect of Lactobacillus acidophilus strain L-55 on the development of atopic dermatitis-like skin lesions in NC/Nga mice

Sunada¹,

Nakamura²,

Kamei

2008

International Immunopharmacology

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“…For example, Kim and the colleagues reported that EGCG treatment protects toluene diisocyanate-induced airway inflammation in a murine model of asthma by supressing matrix metalloproteinase (MMP-9) expression in toluene diisocyanate-inhalation lung tissues as well as TNF-α and Th2 cytokine (IL-5) production in bronchoalveolar lavage fluid [22]. Moreover, Noh and the colleagues demonstrated that EGCG treatment improved Dermatophagoides pteronissinus extract-induced atopic dermatitis-like skin lesions in NC/Nga mice by suppressing macrophage migration inhibitory factor [23]. These studies did not examine CCL11 production in inflammatory lesions though CCL11 is related to the etiology of asthma and atopic dermatitis.…”

Section: Discussionmentioning

confidence: 99%

(-)-Epigallocatechin-3-Gallate Inhibits CC Chemokine Ligand 11 Production in Human Gingival Fibroblasts

Hosokawa

Shindo

et al. 2013

Cell Physiol Biochem

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Background: CC chemokine ligand 11 (CCL11) is related to Th2 cells migration via CC chemokine receptor 3 (CCR3). Th2 cells are involved in the etiology of periodontal disease. However, how the infiltration of Th2 cells is controlled in periodontally diseased tissues is unknown. (-)-Epigallocatechin gallate (EGCG), the major catechin in green tea, has multiple beneficial effects, but the effects of EGCG on CCL11 production are uncertain. In this study, we investigated whether cytokines could induce CCL11 production in human gingival fibroblasts (HGFs). Moreover, we examined the effects of EGCG on CCL11 production in HGFs. Methods and Results: ELISA analysis disclosed that interleukin (IL)-4 synergistically enhanced CCL11 production in IL-1β or tumor necrosis factor (TNF)-α-stimulated HGFs. EGCG prevented IL-1β/ IL-4 or TNF-α/IL-4-mediated CCL11 production in a concentration dependent manner. CCL11 production in HGFs was positively regulated by p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), and c-Jun N terminal kinase (JNK). Western blot analysis revealed that EGCG treatment prevented IL-1β/IL-4 or TNF-α/IL-4-induced ERK and JNK activation in HGFs. Conclusions: These data provide that CCL11 production in HGFs could be associated with Th2 cells infiltration in periodontal lesions. Moreover, EGCG is useful for periodontitis treatment to inhibit CCL11 production.

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“…Noh et al showed that EGCG improves Dermatophagoides pteronissinus extract-induced atopic dermatitis-like skin lesions in a mouse model by suppressing MIF [437]. In addition, EGCG can inhibit TNF-α [438], iNOS [439, 440], AKT [441], the CXC group of cytokines [442], and by by reducing the transcriptional activity of NF-κB, COX-2 expression and PGE-2 synthesis [443–448].…”

Section: Low Toxicity Approachesmentioning

confidence: 99%

A multi-targeted approach to suppress tumor-promoting inflammation

Samadi

Bilsland

Georgakilas

et al. 2015

Seminars in Cancer Biology

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Cancers harbor significant genetic heterogeneity and patterns of relapse following many therapies are due to evolved resistance to treatment. While efforts have been made to combine targeted therapies, significant levels of toxicity have stymied efforts to effectively treat cancer with multi-drug combinations using currently approved therapeutics. We discuss the relationship between tumor-promoting inflammation and cancer as part of a larger effort to develop a broad-spectrum therapeutic approach aimed at a wide range of targets to address this heterogeneity. Specifically, macrophage migration inhibitory factor, cyclooxygenase-2, transcription factor nuclear factor-kappaB, tumor necrosis factor alpha, inducible nitric oxide synthase, protein kinase B, and CXC chemokines are reviewed as important antiinflammatory targets while curcumin, resveratrol, epigallocatechin gallate, genistein, lycopene, and anthocyanins are reviewed as low-cost, low toxicity means by which these targets might all be reached simultaneously. Future translational work will need to assess the resulting synergies of rationally designed antiinflammatory mixtures (employing low-toxicity constituents), and then combine this with similar approaches targeting the most important pathways across the range of cancer hallmark phenotypes.

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Epigallocatechin-3-gallate improves Dermatophagoides pteronissinus extract-induced atopic dermatitis-like skin lesions in NC/Nga mice by suppressing macrophage migration inhibitory factor

Cited by 43 publications

References 46 publications

Effect of Lactobacillus acidophilus strain L-55 on the development of atopic dermatitis-like skin lesions in NC/Nga mice

Effect of Lactobacillus acidophilus strain L-55 on the development of atopic dermatitis-like skin lesions in NC/Nga mice

(-)-Epigallocatechin-3-Gallate Inhibits CC Chemokine Ligand 11 Production in Human Gingival Fibroblasts

A multi-targeted approach to suppress tumor-promoting inflammation

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