HMGB1-induced ILC2s activate dendritic cells by producing IL-9 in asthmatic mouse model

Wan, Jie; Huang, Lan; Ji, Xiaoyun; Yao, Shun; Abdelaziz, Mohamed Hamed; Cai, Wei; Wang, Huixuan; Cheng, Jianjun; Dineshkumar, Kesavan; Vasudevan, Aparna; Su, Zhaoliang; Wang, Shengjun; Xu, Huaxi

doi:10.1016/j.cellimm.2020.104085

Cited by 19 publications

(14 citation statements)

References 58 publications

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“… 3 Currently, increasingly aggravated environmental pollution also contributes greatly to the high incidence of asthma. 2 , 4 At present, glucocorticoids are the first-line choice for asthma treatment, but this treatment can cause side effects in patients, especially for those with chronic asthma. 5 , 6 Therefore, it is of great significance to better understand the pathogenesis of chronic asthma and explore an effective targeted therapy for treating chronic asthma.…”

Section: Introductionmentioning

confidence: 99%

Curcumol Ameliorates Lung Inflammation and Airway Remodeling via Inhibiting the Abnormal Activation of the Wnt/β-Catenin Pathway in Chronic Asthmatic Mice

Jia¹,

Guo²,

Lü³

et al. 2021

DDDT

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Background Curcumol exhibits anti-inflammatory effect, but its effect on chronic asthma lacked research. Therefore, this study explored the role of curcumol in asthma. Methods A chronic asthmatic mice model was established by ovalbumin induction. After treatment with curcumol, airway resistance in mice was detected by forced oscillation technique. The histopathological features of airway tissues, pulmonary inflammation, and inflammation cell recruitment in the bronchoalveolar lavage fluid (BALF) of mice were detected by hematoxylin-eosin staining. Collagen deposition in the airways of mice was examined by Masson staining. The secretion of ovalbumin-IgE, IL-4, IL-5, IL-13 in mouse serum and VEGFA secretion in BALF were analyzed by ELISA. Finally, the expressions of β-catenin, Wnt5a, VEGFA, TGF-β1, Fibronectin, and MMP-9 in mice lung tissues were determined by Western blot or immunohistochemical. Results Curcumol attenuated airway hyperresponsiveness, airway remodeling, and pulmonary inflammation in chronic asthmatic mice. Curcumol relieved collagen deposition in airway tissues, inflammation cell recruitment in BALF, and reduced the up-regulation of serum ovalbumin-IgE, IL-4, IL-5, and IL-13 and BALF VEGFA in chronic asthmatic mice. In addition, curcumol attenuated the up-regulated expressions of β-catenin, Wnt5a, VEGFA, TGF-β1, Fibronectin, and MMP-9 in the lung tissues of chronic asthmatic mice, but curcumol treatment did not show such effects on healthy mice. Conclusion Our findings revealed that curcumol could ameliorate lung inflammation and airway remodeling by inhibiting the abnormal activation of the Wnt/β-catenin pathway in chronic asthmatic mice, indicating that curcumol could be used as a novel anti-asthma drug for basic and clinical research.

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Section: Introductionmentioning

confidence: 99%

Curcumol Ameliorates Lung Inflammation and Airway Remodeling via Inhibiting the Abnormal Activation of the Wnt/β-Catenin Pathway in Chronic Asthmatic Mice

Jia¹,

Guo²,

Lü³

et al. 2021

DDDT

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“…Dendritic cells (DCs) serve as professional antigen-presenting cells that capture antigen in one location, then migrate to lymph nodes, where they present it to native T cells, initiating the adaptive immune response [ 127 ]. In addition to presenting foreign antigens, DCs stimulate the proliferation of T lymphocytes and regulatory T cells, which depends on the ratio of mature to immature DCs [ 128 ]. Normally, the immature DCs express low amounts of MHCII, CD86, CD80, CD11c, but high amounts of CD45RB.…”

Section: Effects Of Hmgb1 On Immune Cell Types and The Regulatory Mechanisms Involvedmentioning

confidence: 99%

“…HMGB1 finely tunes the maturation, differentiation and immune functions of DCs, so it influences the shift of helper T (Th) 1 cells and Th17 polarization necessary for T cell-mediated immunity [ 127 , 128 , 129 , 130 ]. HMGB1 is critical for CXCL12 activity, which attracts myeloid-derived cells, thereby promoting recruitment and motility of leukocytes [ 119 ].…”

Section: Effects Of Hmgb1 On Immune Cell Types and The Regulatory Mechanisms Involvedmentioning

confidence: 99%

“…The HMGB1/PI3K/Akt/mTOR axis promotes adhesion, maturation, chemotactic and antigen-presenting ability of lung DCs, implicating it in lung inflammation [ 135 ]. Similarly, HMGB1 promotes IL-9 release to activate group 2 innate lymphoid cells and DCs, aggravating asthma [ 128 ]. In asthma, HMGB1 also contributes to hyper-responsiveness and airway inflammation via the pathway involving adenosine triphosphate (ATP)/purinergic receptor P2X ligand-gated ion channel 7 [ 135 ].…”

Section: Effects Of Hmgb1 On Immune Cell Types and The Regulatory Mechanisms Involvedmentioning

confidence: 99%

“…Asthma is a clinical syndrome characterized by three distinct components: airway inflammation, exaggerated bronchoconstrictor responses and recurrent episodes of airway obstruction [ 34 , 199 ]. HMGB1 was shown to strongly stimulate the differentiation of Th cells and innate lymphocytes (e.g., DCs, group 2 innate lymphoid cells (ILC2s)) and contribute to asthma [ 128 , 135 , 136 , 148 , 200 ]. Levels of HMGB1 in the airway are elevated in animal models and patients with asthma.…”

Section: Role Of Hmgb1 In Various Inflammatory Disordersmentioning

confidence: 99%

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The Effect and Regulatory Mechanism of High Mobility Group Box-1 Protein on Immune Cells in Inflammatory Diseases

Huang

Yao

2021

Cells

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High mobility group box-1 protein (HMGB1), a member of the high mobility group protein superfamily, is an abundant and ubiquitously expressed nuclear protein. Intracellular HMGB1 is released by immune and necrotic cells and secreted HMGB1 activates a range of immune cells, contributing to the excessive release of inflammatory cytokines and promoting processes such as cell migration and adhesion. Moreover, HMGB1 is a typical damage-associated molecular pattern molecule that participates in various inflammatory and immune responses. In these ways, it plays a critical role in the pathophysiology of inflammatory diseases. Herein, we review the effects of HMGB1 on various immune cell types and describe the molecular mechanisms by which it contributes to the development of inflammatory disorders. Finally, we address the therapeutic potential of targeting HMGB1.

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An ER‐Targeting Iridium(III) Complex That Induces Immunogenic Cell Death in Non‐Small‐Cell Lung Cancer

et al. 2021

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Immunogenic cell death (ICD) is a vital component of therapeutically induced anti‐tumor immunity. An iridium(III) complex (Ir1), containing an N,N‐bis(2‐chloroethyl)‐azane derivate, as an endoplasmic reticulum‐localized ICD inducer for non‐small cell lung cancer (NSCLC) is reported. The characteristic discharge of damage‐associated molecular patterns (DAMPs), that is, cell surface exposure of calreticulin (CRT), extracellular exclusion of high mobility group box 1 (HMGB1), and ATP, were generated by Ir1 in A549 lung cancer cells, accompanied by an increase in endoplasmic reticulum stress and reactive oxygen species (ROS). The vaccination of immunocompetent mice with Ir1‐treated dying cells elicited an antitumor CD8+ T cell response and Foxp3+ T cell depletion, which eventually resulted in long‐acting anti‐tumor immunity by the activation of ICD in lung cancer cells. Ir1 is the first Ir‐based complex that is capable of developing an immunomodulatory response by immunogenic cell death.

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HMGB1-induced ILC2s activate dendritic cells by producing IL-9 in asthmatic mouse model

Cited by 19 publications

References 58 publications

Curcumol Ameliorates Lung Inflammation and Airway Remodeling via Inhibiting the Abnormal Activation of the Wnt/β-Catenin Pathway in Chronic Asthmatic Mice

Curcumol Ameliorates Lung Inflammation and Airway Remodeling via Inhibiting the Abnormal Activation of the Wnt/β-Catenin Pathway in Chronic Asthmatic Mice

The Effect and Regulatory Mechanism of High Mobility Group Box-1 Protein on Immune Cells in Inflammatory Diseases

An ER‐Targeting Iridium(III) Complex That Induces Immunogenic Cell Death in Non‐Small‐Cell Lung Cancer

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