Mechanisms of Sepsis-Induced Acute Lung Injury and Advancements of Natural Small Molecules in Its Treatment

Xu, Yaxi; Xin, Jianzeng; Sun, Yupei; Wang, Xuyan; Sun, Lili; Zhao, Feng; Niu, Changshan; Liu, Sheng

doi:10.3390/ph17040472

Cited by 6 publications

References 133 publications

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β-glucan reprograms alveolar macrophages via neutrophil/IFNγ axis to promote lung injury

Prével,

Pernet,

Tran

et al. 2024

Preprint

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Alveolar macrophages (AMs) reside in the lower airways and play a crucial role in lung health and response to sterile inflammation and infections. AMs possess remarkable adaptability to different environmental challenges that can persist through their memory capacity (trained immunity). β-glucan has been characterized as a potent inducer of trained immunity by reprogramming hematopoietic stem cells (HSCs) in the bone marrow generating trained innate cells with enhanced responsiveness. In the present study, we show that systemic administration of β-glucan reprograms alveolar macrophages (AMs) in the lung via neutrophils and IFNγ signalling, in a Dectin1-independent manner. We furthermore demonstrate that AM reprogramming at both the transcriptional and metabolic levels exacerbate lung injury following bacterial (LPS) or viral (polyI:C) challenges. These findings identify an additional facet of β-glucan in trained immunity involving AM reprogramming and shed light on the potential detrimental effects of trained immunity.

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β-glucan reprograms alveolar macrophages via neutrophil/IFNγ axis to promote lung injury

Prével,

Pernet,

Tran

et al. 2024

Preprint

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Role and mechanisms of autophagy, ferroptosis, and pyroptosis in sepsis-induced acute lung injury

Shen,

He,

Pan

et al. 2024

Front. Pharmacol.

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Sepsis-induced acute lung injury (ALI) is a major cause of death among patients with sepsis in intensive care units. By analyzing a model of sepsis-induced ALI using lipopolysaccharide (LPS) and cecal ligation and puncture (CLP), treatment methods and strategies to protect against ALI were discussed, which could provide an experimental basis for the clinical treatment of sepsis-induced ALI. Recent studies have found that an imbalance in autophagy, ferroptosis, and pyroptosis is a key mechanism that triggers sepsis-induced ALI, and regulating these death mechanisms can improve lung injuries caused by LPS or CLP. This article summarized and reviewed the mechanisms and regulatory networks of autophagy, ferroptosis, and pyroptosis and their important roles in the process of LPS/CLP-induced ALI in sepsis, discusses the possible targeted drugs of the above mechanisms and their effects, describes their dilemma and prospects, and provides new perspectives for the future treatment of sepsis-induced ALI.

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From Molecular Mechanisms to Clinical Therapy: Understanding Sepsis-Induced Multiple Organ Dysfunction

Srdić,

Đurašević,

Lakić

et al. 2024

IJMS

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Sepsis-induced multiple organ dysfunction arises from the highly complex pathophysiology encompassing the interplay of inflammation, oxidative stress, endothelial dysfunction, mitochondrial damage, cellular energy failure, and dysbiosis. Over the past decades, numerous studies have been dedicated to elucidating the underlying molecular mechanisms of sepsis in order to develop effective treatments. Current research underscores liver and cardiac dysfunction, along with acute lung and kidney injuries, as predominant causes of mortality in sepsis patients. This understanding of sepsis-induced organ failure unveils potential therapeutic targets for sepsis treatment. Various novel therapeutics, including melatonin, metformin, palmitoylethanolamide (PEA), certain herbal extracts, and gut microbiota modulators, have demonstrated efficacy in different sepsis models. In recent years, the research focus has shifted from anti-inflammatory and antioxidative agents to exploring the modulation of energy metabolism and gut microbiota in sepsis. These approaches have shown a significant impact in preventing multiple organ damage and mortality in various animal sepsis models but require further clinical investigation. The accumulation of this knowledge enriches our understanding of sepsis and is anticipated to facilitate the development of effective therapeutic strategies in the future.

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Mechanisms of Sepsis-Induced Acute Lung Injury and Advancements of Natural Small Molecules in Its Treatment

Cited by 6 publications

References 133 publications

β-glucan reprograms alveolar macrophages via neutrophil/IFNγ axis to promote lung injury

β-glucan reprograms alveolar macrophages via neutrophil/IFNγ axis to promote lung injury

Role and mechanisms of autophagy, ferroptosis, and pyroptosis in sepsis-induced acute lung injury

From Molecular Mechanisms to Clinical Therapy: Understanding Sepsis-Induced Multiple Organ Dysfunction

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