Autophagy Mediates Escherichia Coli-Induced Cellular Inflammatory Injury by Regulating Calcium Mobilization, Mitochondrial Dysfunction, and Endoplasmic Reticulum Stress

Liu, Jianguo; Qiu, Rendong; Liu, Ran; Song, Pengjie; Lin, Peng; Chen, Huatao; Zhou, Dong; Wang, Aihua; Jin, Yaping

doi:10.3390/ijms232214174

Cited by 7 publications

(13 citation statements)

References 62 publications

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“…47,48 In acute lung injury, LPS activates NF-κB signaling, which causes the overexpression of proinflammatory factors (IL-6 and IL-8), but inflammatory injury can be alleviated by inhibiting mTOR or activating autophagy. 37 In E. coli-infected BEECs, increasing autophagy levels could reduce inflammasome activation and the inflammatory response.. 36 Our results were consistent with these findings; the activation of the NF-κB pathway was increased by autophagy suppression, as was the expression of IL-6, IL-8, and TNF-α. In contrast, activating autophagy decreased activation of the NF-κB pathway, further reducing the expression levels of inflammatory factors and indicating that restoring autophagy decreases the inflammatory response in BEECs.…”

Section: Discussionsupporting

confidence: 85%

“…Consistent with our results, Liu et al showed that the autophagic activity of BEECs was inhibited when they were infected with E. coli. 36 LPS stimulation reduces the expression of LC3 II in human bronchial epithelial cells and the mouse lung epithelium. 37 Our study showed that the levels of LC3 II and p62 decreased and increased, respectively, in response to LPS.…”

Section: Discussionmentioning

confidence: 94%

“…In E. coli ‐infected BEECs, increasing autophagy levels could reduce inflammasome activation and the inflammatory response. 36 …”

Section: Discussionmentioning

confidence: 99%

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Autophagy activation alleviates the LPS‐induced inflammatory response in endometrial epithelial cells in dairy cows

Dong,

Ji,

Jiang

et al. 2024

American J Rep Immunol

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ProblemEndometritis is a common disease that affects dairy cow reproduction. Autophagy plays a vital role in cellular homeostasis and modulates inflammation by regulating interactions with innate immune signaling pathways. However, little is known about the regulatory relationship between autophagy and inflammation in bovine endometrial epithelial cells (BEECs). Thus, we aimed to determine the role of autophagy in the inflammatory response in BEECs.Methods of StudyIn the present study, the expression levels of proinflammatory cytokines were measured by quantitative real‐time polymerase chain reaction. Changes in the nuclear factor‐κB (NF‐κB) pathway and autophagy were determined using immunoblotting and immunocytochemistry. The induction of autophagosome formation was visualized by transmission electron microscopy.ResultsOur results demonstrated that autophagy activation was inhibited in LPS‐treated BEECs, while activation of the NF‐κB pathway and the mRNA expression of IL‐6, IL‐8, and TNF‐α were increased. Furthermore, blocking autophagy with the inhibitor chloroquine increased NF‐κB signaling pathway activation and proinflammatory factor expression in LPS‐treated BEECs. Conversely, activation of autophagy with the agonist rapamycin inhibited the NF‐κB signaling pathway and downregulated proinflammatory factors.ConclusionsThese data indicated that LPS‐induced inflammation was related to the inhibition of autophagy in BEECs. Thus, the activation of autophagy may represent a novel therapeutic strategy for eliminating inflammation in BEECs.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 94%

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Autophagy activation alleviates the LPS‐induced inflammatory response in endometrial epithelial cells in dairy cows

Dong,

Ji,

Jiang

et al. 2024

American J Rep Immunol

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“…This demonstrated that the TGF-β/Smad signal transduction pathway participated in the EMT process, and exosome therapy reversed the development of this transversion ( Yao et al, 2019 ). When the endometrium is damaged, the presence of excessive pro-inflammatory factors interferes with the level of calcium ions, and the latter abnormality causes mitochondrial dysfunction, resulting in endoplasmic reticulum misfolding or accumulation of unfolded proteins, triggering endoplasmic reticulum stress (ERS), eventually leading to cell death, and IUA also occurs under this condition ( Han et al, 2018 ; Liu J. et al, 2022 ). Further research showed that ERS may participated in the EMT process and promoted the occurrence of IUA through the TGF-β/SMAD pathway ( Bao et al, 2023 ).…”

Section: Exosome Combined With Hydrogel In the Treatment Of Iuamentioning

confidence: 99%

Treatment strategies for intrauterine adhesion: focus on the exosomes and hydrogels

Wu,

Lei,

Yang

et al. 2023

Front. Bioeng. Biotechnol.

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Intrauterine adhesion (IUA), also referred to as Asherman Syndrome (AS), results from uterine trauma in both pregnant and nonpregnant women. The IUA damages the endometrial bottom layer, causing partial or complete occlusion of the uterine cavity. This leads to irregular menstruation, infertility, or repeated abortions. Transcervical adhesion electroreception (TCRA) is frequently used to treat IUA, which greatly lowers the prevalence of adhesions and increases pregnancy rates. Although surgery aims to disentangle the adhesive tissue, it can exacerbate the development of IUA when the degree of adhesion is severer. Therefore, it is critical to develop innovative therapeutic approaches for the prevention of IUA. Endometrial fibrosis is the essence of IUA, and studies have found that the use of different types of mesenchymal stem cells (MSCs) can reduce the risk of endometrial fibrosis and increase the possibility of pregnancy. Recent research has suggested that exosomes derived from MSCs can overcome the limitations of MSCs, such as immunogenicity and tumorigenicity risks, thereby providing new directions for IUA treatment. Moreover, the hydrogel drug delivery system can significantly ameliorate the recurrence rate of adhesions and the intrauterine pregnancy rate of patients, and its potential mechanism in the treatment of IUA has also been studied. It has been shown that the combination of two or more therapeutic schemes has broader application prospects; therefore, this article reviews the pathophysiology of IUA and current treatment strategies, focusing on exosomes combined with hydrogels in the treatment of IUA. Although the use of exosomes and hydrogels has certain challenges in treating IUA, they still provide new promising directions in this field.

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“…Moreover, ERS is implicated in numerous inflammatory diseases [ 9 ]. Furthermore, a prolonged state of ERS not only affects uterine involution but also supports the appearance of endometritis in bovine endometrial epithelial cells (BEECs) during the postpartum period of dairy cows [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Transcription Factor Nrf2 Modulates Lipopolysaccharide-Induced Injury in Bovine Endometrial Epithelial Cells

Song

Liu

Sun

et al. 2023

IJMS

Self Cite

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Endometritis in high-yield dairy cows adversely affects lactation length, milk quality, and the economics of dairy products. Endoplasmic reticulum stress (ERS) in bovine endometrial epithelial cells (BEECs) occurs as a consequence of diverse post-natal stressors, and plays a key role in a variety of inflammatory diseases. Nuclear-factor-erythroid-2-related factor 2 (Nrf2) is an important protective regulatory factor in numerous inflammatory responses. However, the mechanism by which Nrf2 modulates inflammation by participating in ERS remains unclear. The objective of the present study was to explore the role of Nrf2 in lipopolysaccharide (LPS)-induced injury to BEECs and to decipher the underlying molecular mechanisms of this injury. The expression of Nrf2- and ERS-related genes increased significantly in bovine uteri with endometritis. Isolated BEECs were treated with LPS to stimulate the inflammatory response. The expression of Nrf2 was significantly higher in cells exposed to LPS, which also induced ERS in BEECs. Activation of Nrf2 led to enhanced expression of the genes for the inflammation markers TNF-α, p65, IL-6, and IL-8 in BEECs. Moreover, stimulation of Nrf2 was accompanied by activation of ERS. In contrast, Nrf2 knockdown reduced the expression of TNF-α, p65, IL-6, and IL-8. Additionally, Nrf2 knockdown decreased expression of ERS-related genes for the GRP78, PERK, eIF2α, ATF4, and CHOP proteins. Collectively, our findings demonstrate that Nrf2 and ERS are activated during inflammation in BEECs. Furthermore, Nrf2 promotes the inflammatory response by activating the PERK pathway in ERS and inducing apoptosis in BEECs.

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Autophagy Mediates Escherichia Coli-Induced Cellular Inflammatory Injury by Regulating Calcium Mobilization, Mitochondrial Dysfunction, and Endoplasmic Reticulum Stress

Cited by 7 publications

References 62 publications

Autophagy activation alleviates the LPS‐induced inflammatory response in endometrial epithelial cells in dairy cows

Autophagy activation alleviates the LPS‐induced inflammatory response in endometrial epithelial cells in dairy cows

Treatment strategies for intrauterine adhesion: focus on the exosomes and hydrogels

Transcription Factor Nrf2 Modulates Lipopolysaccharide-Induced Injury in Bovine Endometrial Epithelial Cells

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