Corylin Ameliorates LPS-Induced Acute Lung Injury via Suppressing the MAPKs and IL-6/STAT3 Signaling Pathways

Chen, I-Chen; Wang, Shu-Chi; Chen, Yi-Ting; Tseng, Hsin-Han; Liu, Po-Len; Lin, Tzu-Chieh; Wu, Hsin‐Lung; Chen, Yuan-Ru; Tseng, Yu‐Hsin; Hsu, Jong‐Hau; Dai, Zen‐Kong; Suen, Jau‐Ling; Li, Chia-Yang

doi:10.3390/ph14101046

Cited by 18 publications

(11 citation statements)

References 46 publications

(57 reference statements)

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“…Although these cells are closest to primary cultures, IL-6 secretion and mucociliary differentiation are also impaired compared to primary airway epithelium [ 71 ]. Furthermore, this line lacks inflammatory characteristics such as the absence of LPS-induced secretion of pro-inflammatory cytokines (e.g., tumor necrosis factor α [TNFα], interleukin [IL]-1β, IL-12) [ 72 ]. While the ease of passaging and growing oncogenic and immortalized cells has led to these lines being widely utilized, they lack key features of primary epithelium, limiting the ability to make generalized conclusions using this system.…”

Section: Viewing Human Airway Epithelium As a Monomorphic Barrier Is ...mentioning

confidence: 99%

Human Airway Epithelium Responses to Invasive Fungal Infections: A Critical Partner in Innate Immunity

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Ward

Reedy

et al. 2022

JoF

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The lung epithelial lining serves as the primary barrier to inhaled environmental toxins, allergens, and invading pathogens. Pulmonary fungal infections are devastating and carry high mortality rates, particularly in those with compromised immune systems. While opportunistic fungi infect primarily immunocompromised individuals, endemic fungi cause disease in immune competent and compromised individuals. Unfortunately, in the case of inhaled fungal pathogens, the airway epithelial host response is vastly understudied. Furthering our lack of understanding, very few studies utilize primary human models displaying pseudostratified layers of various epithelial cell types at air-liquid interface. In this review, we focus on the diversity of the human airway epithelium and discuss the advantages and disadvantages of oncological cell lines, immortalized epithelial cells, and primary epithelial cell models. Additionally, the responses by human respiratory epithelial cells to invading fungal pathogens will be explored. Future investigations leveraging current human in vitro model systems will enable identification of the critical pathways that will inform the development of novel vaccines and therapeutics for pulmonary fungal infections.

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Section: Viewing Human Airway Epithelium As a Monomorphic Barrier Is ...mentioning

confidence: 99%

Human Airway Epithelium Responses to Invasive Fungal Infections: A Critical Partner in Innate Immunity

Crossen

Ward

Reedy

et al. 2022

JoF

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“…In addition, ZEB1 is increased in LPS-induced pulmonary fibrosis, which is associated with the p38 MAPK signaling pathway ( 27 ). JNK and ERK pathways, the other MAPK pathways, also play vital roles in triggering the production of pro-inflammatory cytokines in response to LPS stimulation ( 41 ). In the present study, it was determined that p38, JNK, and ERK phosphorylation levels were downregulated when miR-374a-5p was overexpressed in LPS-treated HPMVECs, while ZEB1 overexpression led to the activation of p38 MAPK, JNK and ERK signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

miR‑374a‑5p alleviates sepsis‑induced acute lung injury by targeting ZEB1 via the p38 MAPK pathway

Shen

2022

Exp Ther Med

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The aim of the present study was to investigate the effects of microRNA (miR)-374a-5p on sepsis-induced acute lung injury (ALI) and the associated mechanism. Lipopolysaccharide (LPS)-induced human pulmonary microvascular endothelial cells (HPMVECs) were used to construct the cellular model of sepsis. A luciferase reporter assay was performed to confirm the association between miR-374a-5p and zinc finger E-box binding homeobox 1 (ZEB1). Reverse transcription-quantitative polymerase chain reaction and western blot analysis were performed to assess the relative expression of miR-374a-5p, ZEB1 and apoptosis-related proteins. Cell viability and apoptosis were determined by Cell Counting Kit-8 assay and flow cytometry, respectively. Enzyme-linked immunosorbent assays were used to evaluate inflammatory cytokines. The results revealed that miR-374a-5p was downregulated in sepsis patients and LPS-treated HPMVECs. Upregulation of miR-374a-5p alleviated LPS-triggered cell injury in HPMVECs, as evidenced by restoration of cell viability, and inhibition of apoptosis and the production of proinflammatory cytokines. In addition, ZEB1 was revealed to be a downstream target of miR-374a-5p, and overexpression of ZEB1 could reverse the anti-apoptotic and anti-inflammatory effects of miR-374a-5p on an LPS-induced sepsis cell model. Moreover, miR-374a-5p-induced protective effects involved the p38 MAPK signaling pathway. Collectively, miR-374a-5p exerted a protective role in sepsis-induced ALI by regulating the ZEB1-mediated p38 MAPK signaling pathway, providing a potential target for the diagnosis and treatment of sepsis.

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“…However, this gene is also involved in coronavirus biology, immune response, and antiviral activity. Previous studies have shown that LPS-induced ALI can be improved by regulating the MAPK and IL-6/STAT3 signaling pathways [ 47 , 48 ]. The MAPK kinase family is involved in various cellular processes such as cell proliferation, differentiation, and cell cycle progression.…”

Section: Discussionmentioning

confidence: 99%

Integrated metabolomics, network pharmacology and biological verification to reveal the mechanisms of Nauclea officinalis treatment of LPS-induced acute lung injury

Han

et al. 2022

Chin Med

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Background Acute lung injury (ALI) is a severe inflammatory disease, underscoring the urgent need for novel treatments. Nauclea officinalis Pierre ex Pitard (Danmu in Chinese, DM) is effective in treating inflammatory respiratory diseases. However, there is still no evidence of its protective effect against ALI. Methods Metabolomics was applied to identify the potential biomarkers and pathways in ALI treated with DM. Further, network pharmacology was introduced to predict the key targets of DM against ALI. Then, the potential pathways and key targets were further verified by immunohistochemistry and western blot assays. Results DM significantly improved lung histopathological characteristics and inflammatory response in LPS-induced ALI. Metabolomics analysis showed that 16 and 19 differential metabolites were identified in plasma and lung tissue, respectively, and most of these metabolites tended to recover after DM treatment. Network pharmacology analysis revealed that the PI3K/Akt pathway may be the main signaling pathway of DM against ALI. The integrated analysis of metabolomics and network pharmacology identified 10 key genes. These genes are closely related to inflammatory response and cell apoptosis of lipopolysaccharide (LPS)-induced ALI in mice. Furthermore, immunohistochemistry and western blot verified that DM could regulate inflammatory response and cell apoptosis by affecting the PI3K/Akt pathway, and expression changes in Bax and Bcl-2 were also triggered. Conclusion This study first integrated metabolomics, network pharmacology and biological verification to investigate the potential mechanism of DM in treating ALI, which is related to the regulation of inflammatory response and cell apoptosis. And the integrated analysis can provide new strategies and ideas for the study of traditional Chinese medicines in the treatment of ALI. Graphical Abstract

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Corylin Ameliorates LPS-Induced Acute Lung Injury via Suppressing the MAPKs and IL-6/STAT3 Signaling Pathways

Cited by 18 publications

References 46 publications

Human Airway Epithelium Responses to Invasive Fungal Infections: A Critical Partner in Innate Immunity

Human Airway Epithelium Responses to Invasive Fungal Infections: A Critical Partner in Innate Immunity

miR‑374a‑5p alleviates sepsis‑induced acute lung injury by targeting ZEB1 via the p38 MAPK pathway

Integrated metabolomics, network pharmacology and biological verification to reveal the mechanisms of Nauclea officinalis treatment of LPS-induced acute lung injury

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