Osthole treatment ameliorates Th2-mediated allergic asthma and exerts immunomodulatory effects on dendritic cell maturation and function

Chiang, Chen Yuan; Lee, Chen Chen; Fan, Chia Kwung; Huang, Huei Mei; Chiang, Bor Luen; Lee, Yueh Lun

doi:10.1038/cmi.2017.71

Cited by 44 publications

(35 citation statements)

References 49 publications

(58 reference statements)

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“…Meanwhile, 2 μg/mL of osthole was added into wells to detect the effects on CD4 + T‐cell responses. After culture, [3H]‐thymidine incorporation was used to detect CD4 + T‐cell proliferation . The collected supernatant was used to IL‐4 and IL‐13 detection using ELISA.…”

Section: Methodsmentioning

confidence: 99%

Osthole attenuates mouse atopic dermatitis by inhibiting thymic stromal lymphopoietin production from keratinocytes

Hong²

2019

Experimental Dermatology

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Atopic dermatitis is one of the most common skin diseases. Dysregulation of immune system and chronic inflammation were believed to be associated with atopic dermatitis. Osthole was reported to play important roles in antitumor and anti‐inflammation. However, whether osthole has effects on atopic dermatitis remains unclear. In this present study, we explored the biological role of osthole in atopic dermatitis and the molecular mechanism. Atopic dermatitis was induced by 2,4‐dinitrochlorobenzene. Pathological damage of ear was detected by H&E staining. IgE level in serum or thymic stromal lymphopoietin (TSLP) level in supernatant was detected by ELISA. Interleukin (IL)‐4 expression and IL‐13 expression in CD4+ T cells were detected using flow cytometry. The expression levels of mRNA or protein levels were detected by RT‐PCR or Western blot. Osthole attenuated atopic dermatitis development in mouse model. Osthole inhibits Th2 cell response, but have on influence on Th1 or Th17 cell response in the skin. In mouse model, osthole treatment significantly inhibited atopic dermatitis via directly inhibiting TLSP expression levels in keratinocytes. Osthole treatment alleviates atopic dermatitis through directly down‐regulating TSLP production from keratinocytes. Osthole may serve as a potential choice for atopic dermatitis treatment in clinic.

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Section: Methodsmentioning

confidence: 99%

Osthole attenuates mouse atopic dermatitis by inhibiting thymic stromal lymphopoietin production from keratinocytes

Hong²

2019

Experimental Dermatology

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“…To obtain cells in pulmonary alveoli, we performed bronchoalveolar lavage as described before ( 20 , 21 ) with slight modifications. The whole lung was perfused through the trachea with 1 mL of phosphate-buffered saline (PBS) containing 5 mM of EDTA for 4 times.…”

Section: Methodsmentioning

confidence: 99%

Activation of TLR Signaling in Sensitization-Recruited Inflammatory Monocytes Attenuates OVA-Induced Allergic Asthma

et al. 2018

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The activation of Toll-like receptor (TLR) signaling is widely reported to be involved in preventing the development of allergic asthma. However, the mechanism of the protective function of TLR signaling remains limited. Here, we studied the mouse model of ovalbumin (OVA)-induced allergic asthma and found that deficiency of TLR signaling or activating TLR signaling with agonist would aggravate or attenuate OVA-induced allergic asthma, respectively, and TLR signaling-mediated protective effect mainly affected the sensitization phase. After OVA/alum sensitization, neutrophils and inflammatory monocytes were recruited into peritoneal cavity and up-regulated TLRs expression. However, adoptive transfer of inflammatory monocytes but not peritoneal macrophages or neutrophils induced allergic symptoms in recipient mice after OVA challenge even without OVA/alum sensitization, and treating the inflammatory monocytes with TLR agonist in vitro before transfer could abolish this effect, indicating that recruited inflammatory monocytes played a determinant role in OVA-induced allergic asthma, and activation of TLR signaling in them could attenuate allergic symptoms. Finally, we found that activation of TLR signaling could increase the expression of T-helper (Th) 1-associated cytokines in inflammatory monocytes. Our results suggest that activation of TLR signaling in sensitization-recruited inflammatory monocytes attenuates OVA-induced allergic asthma by promoting the expression of Th1-associated cytokines.

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“…Recently, inhaled cortiand asthma control. The use of complementary and alternapatients [44] - [45][46][47] -- [48][49][50] - [15,19,51] -Acknowledgements o 81373424, 81573438, o Author contribution -…”

Section: Discussionmentioning

confidence: 99%

Emodin alleviates alternatively activated macrophage and asthmatic airway inflammation in a murine asthma model

Song

et al. 2018

Acta Pharmacol Sin

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Alternatively activated macrophages (AAMs) are not only associated with asthma but also lead to asthmatic airway inflammation and remodeling. Inhibition of AAMs is an alternative therapeutic strategy for treating asthma. In this study we investigated whether emodin (1,3,8-trihydroxy-6-methylanthraquinone), isolated from the rhizome of Rheum palmatum, alleviated asthmatic airway inflammation and reduced AAM polarization in a murine asthma model. Mice were sensitized with a triple allergen mix containing dust mite, ragweed and aspergillus (DRA). In mice with DRA-induced asthma, asthmatic inflammation was significantly enhanced. Intraperitoneal injection of emodin (20 mg·kg·d, ip) 1 h prior to DRA challenge on days 12-14 significantly decreased pulmonary eosinophil and lymphocyte infiltration, mucus secretion and serum IgE production, as well as IL-4 and IL-5 production in bronchoalveolar lavage fluid. In response to emodin treatment, activated markers of AAM Ym-1, Fizz-1 and arginase-1 in the lung tissues were remarkably decreased. In mouse bone marrow-derived macrophages (BMDMs) in vitro, emodin (2-50 μmol/L) dose-dependently inhibited IL-4-induced AAM polarization and STAT6 phosphorylation. Collectively, our results suggest that emodin effectively ameliorates asthmatic airway inflammation and AAM polarization, and it may therefore become a potential agent for the treatment of asthma.

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Osthole treatment ameliorates Th2-mediated allergic asthma and exerts immunomodulatory effects on dendritic cell maturation and function

Cited by 44 publications

References 49 publications

Osthole attenuates mouse atopic dermatitis by inhibiting thymic stromal lymphopoietin production from keratinocytes

Osthole attenuates mouse atopic dermatitis by inhibiting thymic stromal lymphopoietin production from keratinocytes

Activation of TLR Signaling in Sensitization-Recruited Inflammatory Monocytes Attenuates OVA-Induced Allergic Asthma

Emodin alleviates alternatively activated macrophage and asthmatic airway inflammation in a murine asthma model

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