Promoting Neutrophil Apoptosis to Treat Acute Lung Injury

Kurdowska, Anna; Florence, Jon M.

doi:10.1164/rccm.201903-0707le

Cited by 6 publications

(2 citation statements)

References 7 publications

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“…Several studies prove its presence in endothelial cells [28] . Moreover, endothelial dysfunction and neutrophils migration are also associated with ALI’s pathological process [38] , [39] . We just explored the NLRP3-TREM-1-amplified inflammation response in macrophages.…”

Section: Discussionmentioning

confidence: 99%

Activation of NLRP3 inflammasome up-regulates TREM-1 expression in murine macrophages via HMGB1 and IL-18

Zhong

Duan

Tian

et al. 2020

International Immunopharmacology

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Highlights NLRP3 inflammasome inhibition reduces TREM-1 expression in the lungs of mice with ALI. Activation of NLRP3 inflammasome up-regulates TREM-1 expression in murine macrophages via HMGB1 and IL-18. NLRP3 inflammasome activation induces TREM-1 expression, contributing to the inflammatory network in the lungs of ALI mice.

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Section: Discussionmentioning

confidence: 99%

Activation of NLRP3 inflammasome up-regulates TREM-1 expression in murine macrophages via HMGB1 and IL-18

Zhong

Duan

Tian

et al. 2020

International Immunopharmacology

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“…ALI represents a pathological change due to pulmonary and systemic inflammatory responses. It has been demonstrated [26][27][28] that the production of lung inflammation in ALI is associated with excessive activation and aggregation of neutrophils in the lungs. Furthermore, excessive aggregation and activation of neutrophils can lead to the release of large quantities of reactive oxygen species (ROS) [29,30] which can further activate neutrophils and cause oxidative cellular damage, which aggravates the lung injury.…”

Section: Effects Of Eear On Neutrophils and Oxidative Stress Levels I...mentioning

confidence: 99%

Protective Effects of Atractylodis lancea Rhizoma on Lipopolysaccharide-Induced Acute Lung Injury via TLR4/NF-κB and Keap1/Nrf2 Signaling Pathways In Vitro and In Vivo

Shi

Xiao

Dong

et al. 2022

IJMS

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Acute lung injury (ALI) is a syndrome caused by an excessive inflammatory response characterized by intractable hypoxemia both inside and outside the lung, for which effective therapeutic drugs are lacking. Atractylodis rhizoma, a traditional Chinese medicine, has excellent anti-inflammatory and antiviral properties in addition to protecting the integrity of the cellular barrier. However, few studies of Atractylodis rhizoma for the treatment of ALI have been published, and its mechanism of action remains unclear. In the present study, the chemical composition of the ethanolic extract of Atractylodis rhizoma (EEAR) was initially clarified by high performance liquid chromatography (HPLC), after which it was studied in vivo using a lipopolysaccharide (LPS)-induced ALI rat model. Treatment with EEAR significantly reduced the lung wet/dry (W/D) ratio, neutrophil infiltration, and malondialdehyde (MDA) and myeloperoxidase (MPO) formation, and enhanced superoxide dismutase (SOD) and glutathione (GSH) depletion in rats with ALI, thereby improving lung barrier function and effectively reducing lung injury. In addition, EEAR significantly reduced histopathological changes, decreased the expression of inflammatory factors (such as tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β), inducible nitric oxide synthase (INOS), and cyclooxygenase-2 (COX-2)), and inhibited the activation of the NF-κB signaling pathway, thus reducing inflammation. In addition, EEAR was found to also reduce oxidative stress in ALI by upregulating the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream proteins heme oxygenase-1 (HO-1) and NADPH quinone acceptor oxidoreductase 1 (NQO-1). EEAR also reduced LPS-induced inflammatory factor expression in THP-1 cells in vitro by inhibition of the NF-κB signaling pathway, and reduced damage from lipopolysaccharide (LPS)-induced oxidative stress in THP-1 cells by promoting the expression of Nrf2 and its downstream targets HO-1 and NQO-1, the molecular mechanism of which was consistent with in vivo observations. Therefore, we conclude that EEAR attenuates oxidative stress and inflammatory responses via TLR4/NF-κB and Keap1/Nrf2 signaling pathways to alleviate LPS-induced ALI, suggesting that Atractylodis Rhizoma is a potential drug candidate for the treatment of ALI.

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Monocyte chemotactic protein (MCP)-1 (CCL2) and its receptor (CCR2) are elevated in chronic heart failure facilitating lung monocyte infiltration and differentiation which may contribute to lung fibrosis

et al. 2023

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Promoting Neutrophil Apoptosis to Treat Acute Lung Injury

Cited by 6 publications

References 7 publications

Activation of NLRP3 inflammasome up-regulates TREM-1 expression in murine macrophages via HMGB1 and IL-18

Activation of NLRP3 inflammasome up-regulates TREM-1 expression in murine macrophages via HMGB1 and IL-18

Protective Effects of Atractylodis lancea Rhizoma on Lipopolysaccharide-Induced Acute Lung Injury via TLR4/NF-κB and Keap1/Nrf2 Signaling Pathways In Vitro and In Vivo

Monocyte chemotactic protein (MCP)-1 (CCL2) and its receptor (CCR2) are elevated in chronic heart failure facilitating lung monocyte infiltration and differentiation which may contribute to lung fibrosis

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