The effect of inhaled inactived Mycobacterium phlei as a treatment for asthma

Ming, Moyu; Li, Chaoqian; Luo, Zhixi; Lv, Shengqiu; Sun, Qi-Xiang

doi:10.3892/mmr.2016.6087

Cited by 7 publications

(11 citation statements)

References 36 publications

(40 reference statements)

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“…Emerging evidence has suggested that γδT cells, a T cell subset, have a critical role in the pathogenesis of asthma, such as airway inflammation and remodeling through the release of cytokines ( 4 , 5 ). Our previous studies have confirmed that γδT cells not only have a Th1/Th2 immune pattern ( 6 ), but also display a predominantly Th17 phenotype ( 7 ). It has previously been reported that γδT17 cells, as important proinflammatory cells that produced the IL-17 cytokine, were associated with the pathogenesis of various inflammation diseases, such as bronchial asthma, cancer, skin inflammation, and others ( 8 – 10 ).…”

Section: Introductionmentioning

confidence: 65%

Imbalance of γδT17/γδTreg cells in the pathogenesis of allergic asthma induced by ovalbumin

Xia

Zhang

Deng

et al. 2018

Braz J Med Biol Res

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We aimed to explore the imbalance between the T helper 17 γδT cells (γδT17) and the regulatory γδT cells (γδTreg) in asthmatic mice. Male Balb/c mice were randomly divided into the normal control group and the asthmatic model group. The asthmatic model group mice were intraperitoneally injected with the mixture of ovalbumin (OVA)/Al(OH)3 and then activated by exposure of the animals to OVA atomization. Airway hyperresponsiveness (AHR) was determined by a non-invasive lung function machine. Hematoxylin and eosin and Alcian blue-periodic acid Schiff staining were done for histopathological analysis. Interleukin (IL)-17 and IL-35 levels in bronchoalveolar lavage fluid were detected by ELISA. The percentage of IL-17+ γδT cells and Foxp3+ γδT cells in spleen cells suspension were detected and the transcription levels of RORγt and Foxp3 in the lung tissue were determined. Compared with the normal control, the severity of airway inflammation and AHR were higher in the asthmatic mice. Furthermore, mice in the asthmatic group displayed significant increases of IL-17+ γδT cells, expression of IL-17A, and RORγt, whereas control mice displayed marked decreases of Foxp3+ γδT cells, expression of IL-35, and transcription factor Foxp3. In addition, the mRNA expression of RORγt was positively correlated with the percentage of IL-17+γδT cells, and the mRNA level of Foxp3 was positively correlated with the percentage of Foxp3+ γδT cells. The imbalance of γδT17/γδTreg in the asthmatic mice may contribute to the pathogenesis of OVA-induced asthma.

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Section: Introductionmentioning

confidence: 65%

Imbalance of γδT17/γδTreg cells in the pathogenesis of allergic asthma induced by ovalbumin

Xia

Zhang

Deng

et al. 2018

Braz J Med Biol Res

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“…In response to allergen triggers, the epithelium secretes various cytokines that are strongly imphcatedinTh2-polarized inflammation [15]. The release ofIL-33/TSLPbythe epithelium is an important proximal eventin the induction and maintenance of Th2 inflammation [16, 17], and they are known as initiative key factors of allergic inflammation. TSLP expression level increases in AD patients, which can be used as a biomarker of AD severity and particularly the epidermal barrier status [18].…”

Section: Introductionmentioning

confidence: 99%

Calycosin Suppresses Epithelial Derived Initiative Key Factors and Maintains Epithelial Barrier in Allergic Inflammation via TLR4 Mediated NF-κB Pathway

Wang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Calycosin is a bioactive component of Astragali Radix, a Chinese herb for treating allergy. We have previously demonstrated that calycosin effectively inhibited allergic inflammation efficiently. The aim of this study was to explore the mechanism of calycosin on epithelial cells in allergic inflammation. Methods: An initial stage of atopic dermatitis (AD) model in which mice were just sensitized with FITC, was established in vivo and immortalized human keratinocytes (HaCaT cells) were utilized in vitro. Initiative key cytokines, TSLP and IL-33, were measured by ELISA, qPCR, immunofluorescence and Western blot. The junctions in epithelial cells were observed by electron microscopy and tight junctions (TJs) (Occludin and ZO-1) were assessed by Western blot and immunofluorescence. TLR4, MyD88, TAK1, TIRAP and NF-κB were measured by qPCR or Western blot. Results: The results showed that TSLP and IL-33 were inhibited significantly by calycosin in the initial stage of AD model. Simultaneously, calycosin attenuated the separated gap among the epithelial cells and increased the expression of TJs. TSLP/IL-33 and TJs were similarly affected in LPS-stimulated HaCaT cells in vitro. Meanwhile, calycosin not only inhibited the expressions of TLR4, MyD88, TAK1 and TIRAP, but also reduced NF-κB activation in vitro and in vivo. An NF-κB inhibitor enhanced the expressions of TJs and reduced that of TSLP/IL-33 in LPS-stimulated HaCaT cells. Conclusion: These results indicated that calycosin reduced the secretion of TSLP/IL-33 and attenuated the disruption of epithelial TJs by inhibiting TLR4 mediated NF-κB signaling pathway. These findings help to understand the beneficial effects of calycosin on AD, and to develop effective preventive or therapeutic strategies to combat this disease and other epithelial barrier deletion-mediated allergic diseases.

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“… Model Short summary References 1 Fungal asthma: Aspergillus fumigates ; C57BL/6 mice γδ T cells among others as source of IL-22; Reeder et al ( 2018 ) 2 Ozone exposure; db/db obese mice and C57BL/6 mice Ozone-related release of IL-33 promotes Th2-type of response in γδ T cells Matthews et al (2017) 3 OVA-induced asthma; BALB/c mice. Treatment with Mycobacterium phlei M. phlei regulates IL-17 production by γδ T cells by lowering the expression of IL-23R Ming et al ( 2017 ) 4 House dust mite-induced asthma; various mice strains incl. C57BL/6, Atg5-deficient mice Disruption of autophagy promotes IL-17A production by γδ T cells Suzuki et al ( 2016 ) 5 OVA-induced asthma; BALB/c mice, RSV infection pre- or post-induction pre-induction RSV infection partially suppresses asthma due to FasL-dependent apoptosis of pulmonary γδ T cells Zeng et al ( 2014 ) 6 House dust mite or cockroach-induced asthma; C57BL-6 mice + transgenic mice Both stimuli induced inflammatory response.…”

Section: Introductionmentioning

confidence: 99%

γδ T Lymphocytes in Asthma: a Complicated Picture

Zarobkiewicz

Wawryk‐Gawda

Kowalska

et al. 2021

Arch. Immunol. Ther. Exp.

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A minor subset (approximately 5%) of peripheral T cells has their TCR build up from γ and δ chains instead of α and β—those are the γδ T lymphocytes. They can be functionally divided into subsets, e.g., Th1-, Th2-, Th9-, Th17-, Tfh-, and Treg-like γδ T cells. They share some specifics of both innate and adaptive immunity, and are capable of rapid response to a range of stimuli, including some viral and bacterial infections. Atopic diseases, including asthma, are one of major health-related problems of modern western societies. Asthma is one of the most common airway diseases, affecting people of all ages and having potential life-threatening consequences. In this paper, we review the current knowledge about the involvement of γδ T cells in the pathogenesis of asthma and its exacerbations. We summarize both the studies performed on human subjects as well as on the murine model of asthma. γδ T cells seem to be involved in the pathogenesis of asthma, different subsets probably perform opposite functions, e.g., symptom-exacerbating Vγ1 and symptom-suppressing Vγ4 in mice model of asthma.

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The effect of inhaled inactived Mycobacterium phlei as a treatment for asthma

Cited by 7 publications

References 36 publications

Imbalance of γδT17/γδTreg cells in the pathogenesis of allergic asthma induced by ovalbumin

Imbalance of γδT17/γδTreg cells in the pathogenesis of allergic asthma induced by ovalbumin

Calycosin Suppresses Epithelial Derived Initiative Key Factors and Maintains Epithelial Barrier in Allergic Inflammation via TLR4 Mediated NF-κB Pathway

γδ T Lymphocytes in Asthma: a Complicated Picture

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