Exploring immune-related pathogenesis in lung injury: Providing new insights Into ALI/ARDS

Zheng, Jiajing; Li, Ying; Kong, Xianbin; Guo, Jinhe

doi:10.1016/j.biopha.2024.116773

Biomedicine & Pharmacotherapy

2024

DOI: 10.1016/j.biopha.2024.116773

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Exploring immune-related pathogenesis in lung injury: Providing new insights Into ALI/ARDS

Jiajing Zheng,

Ying Li,

Xianbin Kong

et al.

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2024

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Cited by 3 publications

References 84 publications

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Engineered mitochondrial ROS scavenger nanocomplex to enhance lung biodistribution and reduce inflammation for the treatment of ARDS

Hu,

Zhang,

Zhou

et al. 2024

Adv Compos Hybrid Mater

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Engineered mitochondrial ROS scavenger nanocomplex to enhance lung biodistribution and reduce inflammation for the treatment of ARDS

Hu,

Zhang,

Zhou

et al. 2024

Adv Compos Hybrid Mater

View full text Add to dashboard Cite

Interplay between pulmonary epithelial stem cells and innate immune cells contribute to the repair and regeneration of ALI/ARDS

Wang,

Peng,

Yuan

et al. 2024

Translational Research

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SS31 alleviates LPS-induced acute lung injury by inhibiting inflammatory responses through the S100A8/NLRP3/GSDMD signaling pathway

Luo,

Gu,

Wang

et al. 2024

Eur J Med Res

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Background Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is an acute, diffuse, inflammatory lung injury caused by various endogenous or exogenous factors. It is currently widely recognized that an excessive inflammatory response resulting from immune imbalance constitutes a crucial pathogenic mechanism in ALI/ARDS. SS31 is a novel mitochondria-targeted antioxidant peptide. This article validates the role of SS31 in lipopolysaccharide (LPS)-induced ALI. MethodsThe study applied transcriptome sequencing, immunofluorescence, PCR, immunofluorescence and other methods to explore the mechanism of SS31 in LPS induced ALI. ResultsTranscriptome sequencing results indicate that LPS-induced ALI is closely associated with immune regulatory processes, the Toll-like receptor pathway, and the NF-κB signaling pathway. The role of SS31 in acute lung injury is closely related to biological processes, such as immune regulation and cell death. This study demonstrated that SS31 can inhibit the expression of inflammatory factors IL-6, IL-1β, IL-18, and TNF-α, and reduce the expression of pyroptosis-related proteins NLRP3, and GSDMD-N. Further analysis revealed that S100A8 may be a key gene in the effect of SS31. LPS stimulation leads to increased expression of S100A8, while SS31 decreases its expression. Recombinant protein S100A8 can attenuate the inhibitory effect of SS31 on IL-1β, IL-18, NLRP3, and GSDMD-N. ConclusionsThe research results indicate that SS31 may inhibit the activation of the NLRP3 inflammasome and suppress inflammatory responses by regulating S100A8, thereby alleviating LPS-induced ALI in mice; this process may be related to pyroptosis.

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Exploring immune-related pathogenesis in lung injury: Providing new insights Into ALI/ARDS

Cited by 3 publications

References 84 publications

Engineered mitochondrial ROS scavenger nanocomplex to enhance lung biodistribution and reduce inflammation for the treatment of ARDS

Engineered mitochondrial ROS scavenger nanocomplex to enhance lung biodistribution and reduce inflammation for the treatment of ARDS

Interplay between pulmonary epithelial stem cells and innate immune cells contribute to the repair and regeneration of ALI/ARDS

SS31 alleviates LPS-induced acute lung injury by inhibiting inflammatory responses through the S100A8/NLRP3/GSDMD signaling pathway

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