Toll-like receptor 9 mediates paraquat-induced acute lung injury: an in vitro and in vivo study

Shen, Haitao; Wu, Na; Wang, Yu; Zhang, Lichun; Hu, Xiao; Chen, Zhiguang; Zhao, Min

doi:10.1016/j.lfs.2017.03.021

Cited by 12 publications

(3 citation statements)

References 29 publications

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“…For tumor diseases, the expression of TLR9 is higher in lung cancer tissue versus in normal lung tissue (28)(29). For ALI, TLR9 can be activated by mitochondrial DNA and cause secondary lung injury (30).…”

Section: Discussionmentioning

confidence: 99%

Analysis of Macrophage Chemotactic Activity and TLR9 Signaling Pathway in the Mouse Model of Viral Acute Lung Injury

Li¹,

Xiong²,

Ye³

2022

Cell Mol Biol (Noisy-le-grand)

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This study focused on the chemotactic activity of macrophages and the role of the TLR9 signaling pathway in the pathogenesis of viral Acute Lung Injury (ALI). For this purpose, a total of 40 male SPF mice were used, aged 5-8 weeks. They were randomly divided into an experimental group and a control group. The experimental group was further divided into S1 and S2, and the control group was further divided into D1 and D2, with 10 in each. The different groups were detected for the expression of inflammatory cytokines and chemokines and the expression of alveolar macrophages. Results showed that as for the weight, survival status, arterial blood gas analysis, lung index and wet-to-dry value of lung tissue, and lung histopathological analysis results, the S2 group showed more obvious changes versus the D2 group, and the difference was statistically significant (P<0.05). S2 had higher levels of the inflammatory factors TNF-α, IL-1β, IL-6 and the chemokine CCL3 in the BALF supernatant versus the D2 Group, and the difference is statistically significant (P<0.05). S2 had higher expression levels of chemokines CCR5, TLR9, and JMJD1A mRNA versus the D2 group, and the difference was statistically significant (P<0.05). In conclusion, the establishment of a mouse ALI model induced by poly l:C was successful; AM has a certain chemotactic activity on CCL3; polyI:C can promote the expression activity and chemotactic activity of macrophages CCR5 through signal pathways, such as TLR9.

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Section: Discussionmentioning

confidence: 99%

Analysis of Macrophage Chemotactic Activity and TLR9 Signaling Pathway in the Mouse Model of Viral Acute Lung Injury

Li¹,

Xiong²,

Ye³

2022

Cell Mol Biol (Noisy-le-grand)

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“…Injury caused by cell-free mtDNA via the TLR9-p38 MAPK pathway has also been confirmed in some organs (59,107,108). In ALI, in vivo experiments demonstrated that TLR9 contributes to the development of ALI and systemic inflammation, and inhibition of TLR9 prominently attenuated histopathological changes and pro-inflammatory mediators, including interleukin-1 beta (IL-1b), interleukin-6 (IL-6), and tumor necrosis factor-a (TNF-a) (50,(109)(110)(111)(112)(113)(114). Meanwhile, enhanced levels of mtDNA have been found in BALF and plasma from ALI patients and animal models (22,25,115).…”

Section: The Tlr9 Signalingmentioning

confidence: 99%

Role of released mitochondrial DNA in acute lung injury

et al. 2022

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Acute lung injury(ALI)/acute respiratory distress syndrome(ARDS) is a form of acute-onset hypoxemic respiratory failure characterised by an acute, diffuse, inflammatory lung injury, and increased alveolar-capillary permeability, which is caused by a variety of pulmonary or nonpulmonary insults. Recently, aberrant mitochondria and mitochondrial DNA(mtDNA) level are associated with the development of ALI/ARDS, and plasma mtDNA level shows the potential to be a promising biomarker for clinical diagnosis and evaluation of lung injury severity. In mechanism, the mtDNA and its oxidised form, which are released from impaired mitochondria, play a crucial role in the inflammatory response and histopathological changes in the lung. In this review, we discuss mitochondrial outer membrane permeabilisation (MOMP), mitochondrial permeability transition pore(mPTP), extracellular vesicles (EVs), extracellular traps (ETs), and passive release as the principal mechanisms for the release of mitochondrial DNA into the cytoplasm and extracellular compartments respectively. Further, we explain how the released mtDNA and its oxidised form can induce inflammatory cytokine production and aggravate lung injury through the Toll-like receptor 9(TLR9) signalling, cytosolic cGAS-stimulator of interferon genes (STING) signalling (cGAS-STING) pathway, and inflammasomes activation. Additionally, we propose targeting mtDNA-mediated inflammatory pathways as a novel therapeutic approach for treating ALI/ARDS.

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“…Different from ALI, BPD has a chronic course. Although the pathogenesis of the two diseases is not yet fully understood, a large number of studies have shown that there is a certain overlapping genetic background between the two diseases ( 50 , 51 ), and both can develop and progress in response to adverse factors such as infection and inflammatory reactions. ALI and BPD may be the manifestation of the same disease at different stages.…”

Section: Mechanisms Of Necroptosis and Lung Diseasesmentioning

confidence: 99%

The role of necroptosis in common respiratory diseases in children

Ning

Qiao

2022

Front. Pediatr.

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Studies have shown that necroptosis (NEC) relies on a unique gene-regulated molecular pathway to cause cell death. With the development of knockout mouse models and specific molecular inhibitors of necrotic proteins, this cell death pathway has been considered one of the important causes of the pathogenesis of human diseases. In this review, we explored the possible roles and mechanisms of NEC in common respiratory diseases in children, such as acute lung injury, acute respiratory distress syndrome, pulmonary infection, childhood asthma, pulmonary hypertension, etc., in order to provide new ideas for the prevention and treatment of such diseases.

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Toll-like receptor 9 mediates paraquat-induced acute lung injury: an in vitro and in vivo study

Cited by 12 publications

References 29 publications

Analysis of Macrophage Chemotactic Activity and TLR9 Signaling Pathway in the Mouse Model of Viral Acute Lung Injury

Analysis of Macrophage Chemotactic Activity and TLR9 Signaling Pathway in the Mouse Model of Viral Acute Lung Injury

Role of released mitochondrial DNA in acute lung injury

The role of necroptosis in common respiratory diseases in children

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