Tissue-Resident Type 2 Innate Lymphoid Cells Arrest Alveolarization in Bronchopulmonary Dysplasia

Mi, Lanlan; Zhu, Shaoxuan; Cai, Jiayu; Xu, Suqing; Xue, Zhengyang; Lü, Hongyan

doi:10.1155/2020/8050186

Cited by 9 publications

(8 citation statements)

References 43 publications

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“…Consistent with previous research, 4 , 9 , 10 this study found that AMs expression increased in BPD mice. Depletion of macrophage partially abolished the EMT process of AECII and alleviated pulmonary differentiation arrest, further supporting that macrophages are regulators of arrested alveolarization in BPD.…”

Section: Discussionsupporting

confidence: 93%

“… 3 Previously, we provided evidence that AMs were elevated in the lungs of BPD mice. 4 We hypothesized that AM polarization plays a vital role in the repair of alveolar structure and lung abnormalities in BPD. Furthermore, recent studies have suggested that AM activation is associated with IL‐33 levels.…”

Section: Introductionmentioning

confidence: 99%

“…3 Previously, we provided evidence that AMs were elevated in the lungs of BPD mice. 4 We hypothesized that AM polarization plays a vital role in the repair of alveolar structure…”

mentioning

confidence: 99%

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IL‐33‐ST2 pathway regulates AECII transdifferentiation by targeting alveolar macrophage in a bronchopulmonary dysplasia mouse model

Zhu

Yao

Lü

et al. 2022

J Cellular Molecular Medi

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Evidence points to the indispensable function of alveolar macrophages (AMs) in normal lung development and tissue homeostasis. However, the importance of AMs in bronchopulmonary dysplasia (BPD) has not been elucidated. Here, we identified a significant role of abnormal AM proliferation and polarization in alveolar dysplasia during BPD, which is closely related to the activation of the IL‐33‐ST2 pathway. Compared with the control BPD group, AMs depletion partially abolished the epithelialmesenchymal transition process of AECII and alleviated pulmonary differentiation arrest. In addition, IL‐33 or ST2 knockdown has protective effects against lung injury after hyperoxia, which is associated with reduced AM polarization and proliferation. The protective effect disappeared following reconstitution of AMs in injured IL‐33 knockdown mice, and the differentiation of lung epithelium was blocked again. In conclusion, the IL‐33‐ST2 pathway regulates AECII transdifferentiation by targeting AMs proliferation and polarization in BPD, which shows a novel strategy for manipulating the IL‐33–ST2‐AMs axis for the diagnosis and intervention of BPD.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

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IL‐33‐ST2 pathway regulates AECII transdifferentiation by targeting alveolar macrophage in a bronchopulmonary dysplasia mouse model

Zhu

Yao

Lü

et al. 2022

J Cellular Molecular Medi

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“…Interestingly, ILC2s are amateur antigen-presenting cells (APC) that can cooperate with dendritic cells (DCs) to maintain type 2 immune response [ 48 ]. ILC2s not only mediate neonatal lung development [ 49 ], but also play a role in lung diseases caused by developmental abnormalities, such as bronchopulmonary dysplasia [ 50 ]. The phenotypes of ILC2s in different models of airway inflammation are different, as manifested by ILC2s-specific expressed genes stimulated by house dust mites.…”

Section: Ilc2s In Lung Homeostasismentioning

confidence: 99%

Crosstalk between ILC2s and Th2 CD4+ T Cells in Lung Disease

Guo

2022

Journal of Immunology Research

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Cytokine secretion, such as interleukin-4 (IL-4), IL-5, IL-9, IL-13, and amphiregulin (Areg), by type 2 innate lymphoid cells (ILC2s) is indispensable for homeostasis, remodeling/repairing tissue structure, inflammation, and tumor immunity. Often viewed as the innate cell surrogate of T helper type 2 (Th2) cells, ILC2s not only secrete the same type 2 cytokines, but are also inextricably related to CD4+T cells in terms of cell origin and regulatory factors, bridging between innate and adaptive immunity. ILC2s interact with CD4+T cells to play a leading role in a variety of diseases through secretory factors. Here, we review the latest progress on ILC2s and CD4+T cells in the lung, the close relationship between the two, and their relevance in the lung disease and immunity. This literature review aids future research in pulmonary type 2 immune diseases and guides innovative treatment approaches for these diseases.

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“…These findings, along with those by Saluzzo et al that determined that IL-33 is not required for alveolarization (32), suggest a possible role for Areg+/Icos+ tissue-repairing ILC2 in the lung developmental process. Furthermore, a recent mouse study indicated that bronchopulmonary dysplasia (BPD), a severe complication of the respiratory system seen in preterm infants, was induced by IL-33/ILC2 signaling caused by an arrest in the process of alveolarization, determining a major destructive role of tissue-resident IL-13+ILC2 in the lung (36). This differentiation could help to identify mechanisms for divergent responses caused by alterations in ILC2 during early-life.…”

Section: Ilc2 In the Developing Lungmentioning

confidence: 99%

Role of ILC2 in Viral-Induced Lung Pathogenesis

et al. 2021

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Innate lymphoid type-2 cells (ILC2) are a population of innate cells of lymphoid origin that are known to drive strong Type 2 immunity. ILC2 play a key role in lung homeostasis, repair/remodeling of lung structures following injury, and initiation of inflammation as well as more complex roles during the immune response, including the transition from innate to adaptive immunity. Remarkably, dysregulation of this single population has been linked with chronic lung pathologies, including asthma, chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrotic diseases (IPF). Furthermore, ILC2 have been shown to increase following early-life respiratory viral infections, such as respiratory syncytial virus (RSV) and rhinovirus (RV), that may lead to long-term alterations of the lung environment. The detrimental roles of increased ILC2 following these infections may include pathogenic chronic inflammation and/or alterations of the structural, repair, and even developmental processes of the lung. Respiratory viral infections in older adults and patients with established chronic pulmonary diseases often lead to exacerbated responses, likely due to previous exposures that leave the lung in a dysregulated functional and structural state. This review will focus on the role of ILC2 during respiratory viral exposures and their effects on the induction and regulation of lung pathogenesis. We aim to provide insight into ILC2-driven mechanisms that may enhance lung-associated diseases throughout life. Understanding these mechanisms will help identify better treatment options to limit not only viral infection severity but also protect against the development and/or exacerbation of other lung pathologies linked to severe respiratory viral infections.

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Tissue-Resident Type 2 Innate Lymphoid Cells Arrest Alveolarization in Bronchopulmonary Dysplasia

Cited by 9 publications

References 43 publications

IL‐33‐ST2 pathway regulates AECII transdifferentiation by targeting alveolar macrophage in a bronchopulmonary dysplasia mouse model

IL‐33‐ST2 pathway regulates AECII transdifferentiation by targeting alveolar macrophage in a bronchopulmonary dysplasia mouse model

Crosstalk between ILC2s and Th2 CD4+ T Cells in Lung Disease

Role of ILC2 in Viral-Induced Lung Pathogenesis

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