New therapeutic strategies for IPF: Based on the “phagocytosis-secretion-immunization” network regulation mechanism of pulmonary macrophages

Liu, Guoxiu; Zhai, Huaqiang; Tian, Zengshan; Li, Siyu; Li, Ningning; Chen, Jiajia; Gu, Min; Qin, Zinan; Liu, Xin

doi:10.1016/j.biopha.2019.109230

Cited by 37 publications

(25 citation statements)

References 112 publications

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“…Tissue-resident AMs are the most numerous immune cells present in the lung and have a key role in lung homeostasis by protecting the lung during tissue damage (Higashimoto et al, 1993;Boyd et al, 2012;Hussell and Bell, 2014;Byrne et al, 2015;Wong et al, 2017;Angelidis et al, 2019). Specifically, M1 macrophages contribute to tissue injury after excessive production of proinflammatory mediators (e.g., TNF, IL-1B, and IL-6), and M2 macrophages lead to resolution of inflammation and tissue repair upon antiinflammatory cytokine activation (e.g., IL-4, IL-10, and IL-13;Zhang et al, 2018;Liu et al, 2019). M2 macrophages were reported to promote myofibroblast differentiation and are associated with pulmonary fibrogenesis (Hou et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Telomerase treatment prevents lung profibrotic pathologies associated with physiological aging

Piñeiro‐Hermida

Autilio

Martínez

et al. 2020

Journal of Cell Biology

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Short/dysfunctional telomeres are at the origin of idiopathic pulmonary fibrosis (IPF) in patients mutant for telomere maintenance genes. However, it remains unknown whether physiological aging leads to short telomeres in the lung, thus leading to IPF with aging. Here, we find that physiological aging in wild-type mice leads to telomere shortening and a reduced proliferative potential of alveolar type II cells and club cells, increased cellular senescence and DNA damage, increased fibroblast activation and collagen deposits, and impaired lung biophysics, suggestive of a fibrosis-like pathology. Treatment of both wild-type and telomerase-deficient mice with telomerase gene therapy prevented the onset of lung profibrotic pathologies. These findings suggest that short telomeres associated with physiological aging are at the origin of IPF and that a potential treatment for IPF based on telomerase activation would be of interest not only for patients with telomerase mutations but also for sporadic cases of IPF associated with physiological aging.

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Section: Discussionmentioning

confidence: 99%

Telomerase treatment prevents lung profibrotic pathologies associated with physiological aging

Piñeiro‐Hermida

Autilio

Martínez

et al. 2020

Journal of Cell Biology

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“…Thus, it is important to study the macrophages that reside in the lung to understand the role of macrophages in lung diseases. There are two subtypes based on anatomical position of pulmonary resident macrophages, alveolar macrophages (AMs) and interstitial macrophages (60).…”

Section: M2 Macrophagesmentioning

confidence: 99%

A crosstalk between type 2 innate lymphoid cells and alternative macrophages in lung development and lung diseases (Review)

Zhu

Lü

2021

Mol Med Rep

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Type 2 innate lymphoid cells (ILC2s) are important innate immune cells that are involved in type 2 inflammation, in both mice and humans. ILC2s are stimulated by factors, including interleukin (IL)-33 and IL-25, and activated ILC2s secrete several cytokines that mediate type 2 immunity by inducing profound changes in physiology, including activation of alternative (M2) macrophages. M2 macrophages possess immune modulatory, phagocytic, tissue repair and remodeling properties, and can regulate ILC2s under infection. The present review summarizes the role of ILC2s as innate cells and M2 macrophages as anti-inflammatory cells, and discusses current literature on their important biological significance. The present review also highlights how the crosstalk between ILC2s and M2 macrophages contributes to lung development, induces pulmonary parasitic expulsion, exacerbates pulmonary viral and fungal infections and allergic airway diseases, and promotes the development of lung diseases, such as pulmonary fibrosis, chronic obstructive pulmonary disease and carcinoma of the lungs. Contents

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“…These phenomena caused by immune cells seem to be closely associated with cytokines. A hypothesis called the "phagocytosis-secretion-immunity" network of macrophages explained the relationship between immune cells, cytokines, and pulmonary fibrosis 35 . Therefore, the unbalanced secretion of cytokines may be the key cause of aberrant cell function that results in immunologic derangement in pulmonary fibrosis.…”

Section: Introductionmentioning

confidence: 99%

Role of interleukins in the pathogenesis of pulmonary fibrosis

2021

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Interleukins, a group of cytokines participating in inflammation and immune response, are proved to be involved in the formation and development of pulmonary fibrosis. In this article, we reviewed the relationship between interleukins and pulmonary fibrosis from the clinical, animal, as well as cellular levels, and discussed the underlying mechanisms in vivo and in vitro. Despite the effects of interleukin-targeted treatment on experimental pulmonary fibrosis, clinical applications are lacking and unsatisfactory. We conclude that intervening in one type of interleukins with similar functions in IPF may not be enough to stop the development of fibrosis as it involves a complex network of regulation mechanisms. Intervening interleukins combined with other existing therapy or targeting interleukins affecting multiple cells/with different functions at the same time may be one of the future directions. Furthermore, the intervention time is critical as some interleukins play different roles at different stages. Further elucidation on these aspects would provide new perspectives on both the pathogenesis mechanism, as well as the therapeutic strategy and drug development.

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New therapeutic strategies for IPF: Based on the “phagocytosis-secretion-immunization” network regulation mechanism of pulmonary macrophages

Cited by 37 publications

References 112 publications

Telomerase treatment prevents lung profibrotic pathologies associated with physiological aging

Telomerase treatment prevents lung profibrotic pathologies associated with physiological aging

A crosstalk between type 2 innate lymphoid cells and alternative macrophages in lung development and lung diseases (Review)

Role of interleukins in the pathogenesis of pulmonary fibrosis

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