Apolipoprotein E negatively regulates murine allergic airway inflammation via suppressing the activation of NLRP3 inflammasome and oxidative stress

Zhao, Cui-Cui; Xu, Jianming; Xie, Qiu-Meng; Fan, Xiaoning; Zhang, Xu; Wu, Hui-Mei

doi:10.1016/j.intimp.2020.106301

Cited by 18 publications

(10 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, NLRP3 inflammasome activation was associated with particulate matter induced pulmonary fibrosis, 10,30 and the activation of NLRP3 inflammasome can promote caspase‐1 activation and subsequently converting pro‐IL‐1β into its mature bioactive forms. Meanwhile, inactivation of NLRP3 inflammasome contributed to alleviating the progression of inflammatory diseases, including pulmonary fibrosis, 31 murine allergic airway inflammation, 32,33 myocardial dysfunction, 34 and cardiovascular diseases, 35 etc. Collectively, suppression of NLRP3 inflammasome activation may be a critical therapeutic target in PM2.5‐induced pulmonary injury.…”

Section: Discussionmentioning

confidence: 99%

PM2.5‐induced pulmonary inflammation via activating of the NLRP3/caspase‐1 signaling pathway

Jia

Liu

Guo

et al. 2020

Environmental Toxicology

View full text Add to dashboard Cite

Particulate matter 2.5 (PM2.5)‐induced pulmonary inflammation has become a public concern in recent years. In which, the activation of the NLRP3/caspase‐1 pathway was closely related to the inflammatory response of various diseases. However, the promotion effect of the NLRP3/caspase‐1 pathway on PM2.5‐induced pulmonary inflammation remains largely unclear. Here, our data showed that PM2.5 exposure caused lung injury in the mice by which inflammatory cell infiltration occurred in lung and alveolar structure disorder. Meanwhile, the exposure of human bronchial epithelial cells (16HBE) to PM2.5 resulted in suppressed cell viability, as well as elevated cell apoptosis. Moreover, a higher level of inflammatory cytokine and activation of the NLRP3/caspase‐1 pathway in PM2.5‐induced inflammation mice models and 16HBE cells. Mechanistically, pretreatment with MCC950, a NLRP3/caspase‐1 pathway inhibitor, prevented PM2.5‐induced lung injury, inflammatory response, and the number of inflammatory cells in BALFs, as well as promoted cell viability and decreased inflammatory cytokine secretion. Collectively, our findings indicated that the NLRP3/caspase‐1 pathway serves a vital role in the pathological changes of pulmonary inflammation caused by PM2.5 exposure. MCC950 was expected to be the therapeutic target of PM2.5 inhalation mediated inflammatory diseases.

show abstract

Section: Discussionmentioning

confidence: 99%

PM2.5‐induced pulmonary inflammation via activating of the NLRP3/caspase‐1 signaling pathway

Jia

Liu

Guo

et al. 2020

Environmental Toxicology

View full text Add to dashboard Cite

show abstract

“…Local or systematic inflammatory reactions can activate the NLRP3 inflammasome, which is widely distributed in different tissues and play a fundamental role in innate immunity. Inappropriate activation of NLRP3 inflammasome subsequently induces more proinflammatory cytokine release, such as tumor necrosis factor alpha (TNF-α) and interleukins, which, in turn, further aggravates inflammatory response and the progression of inflammatory disorders [8][9][10][11]. However, clinical drugs targeting the NLRP3 inflammasome are still unavailable [12].…”

Section: Introductionmentioning

confidence: 99%

Moxibustion Ameliorates Ovarian Reserve in Rats by Mediating Nrf2/HO-1/NLRP3 Anti-Inflammatory Pathway

Wang

Xie

et al. 2021

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

Diminished ovarian reserve (DOR) is an increasingly emerging reproductive disorder that disturbs reproductive-aged women, which is closely linked with inflammation. In clinic, moxibustion has already been applied for reproductive problems. In the present study, we examined the involvement of inflammation in DOR and investigated the effect of moxibustion for its anti-inflammatory activities. Methods. DOR rat model was established using tripterygium glycosides A tablets (TGs) suspension by intragastric administration and was then treated with either moxibustion or hormone replacement therapy (HRT), respectively. Estrus cycles were observed through vaginal cytology. Ovarian morphological alterations were observed by HE staining. The serum levels of follicle-stimulating hormone (FSH), estradiol (E2), anti-Müllerian hormone (AMH), tumor necrosis factor alpha (TNF-α), and interleukin-10 (IL-10) were measured through ELISA. The expression levels of Nrf2, HO-1, and NLRP3 were detected using immunohistochemistry. Nrf2, HO-1, and NLRP3 mRNA were examined by RT-PCR. Results. Moxibustion improved estrus cycles, FSH, E2, and AMH levels relative to DOR rats as well as HRT, while also inhibiting ovarian tissue injury. Anti-inflammatory cytokine IL-10 in peripheral blood was upregulated, and proinflammatory factor TNF-α was decreased after treatment with moxibustion. Moxibustion enhanced the expression of mRNA and protein of nuclear factor erythroid 2-related factor (Nrf2) and heme oxygenase-1 (HO-1); in the mean time, nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) was suppressed. Conclusions. We demonstrated that moxibustion could ameliorate the ovarian reserve in rats induced by TGs. Overall, the effect of moxibustion was comparable to that of HRT. The underlying mechanism could be attributed to the anti-inflammatory effects of moxibustion, which suppressed NLRP3 activation by upregulating Nrf2/HO-1 signaling pathway.

show abstract

“…In vivo experiments models show that ApoE-deficient mice demonstrated greater increases in lung lavage protein levels, neutrophil counts, and cytokine expression than wild-type animals [ 23 , 24 ]. These studies confirm the role of low levels of APOE expression in modulating inflammation in the setting of acute lung injury, which has been associated to an interleukin-6–dependent mechanism that increases endothelial cell permeability to oxidized LDL [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

Influence of APOE locus on poor prognosis of COVID-19

Rodrigues¹,

Pinto²,

Leitão³

et al. 2021

Heliyon

View full text Add to dashboard Cite

The COVID-19 pandemic has infected over 25 million of people worldwide, 5% of whom evolved to death and, among of the active cases, more than 60 thousand are classified as critical or severe. Recent studies revealed that ApoE, a protein encoded by APOE gene, may increase the risk of severe COVID-19 cases. ApoE has been involved with prevention of tissue damage and promotion of adaptative immune response in the lungs. This study investigated frequencies distribution of alleles that alter the ApoE expression in lung tissues to trace a profile of these variants and associate them to COVID-19 clinical outcomes. Data about APOE expression levels was obtained from the Genotype-Tissue Expression Project and the allele frequencies of APOE variants was acquired from the populations included in the phase 3 release of the 1000 Genomes Project. A total of 128 variants showed a significant impact on the APOE expression in lung tissues (p < 0.0001). Linkage Disequilibrium analysis revealed that 98 variants were closely grouped into seven distinct haplotype blocks, of which six were composed of variants that significantly decrease APOE gene expression in the lungs. Most of the haplotypes with higher impact on APOE expression showed greater frequencies in Europeans and lower in Africans, which implies that European populations might be more susceptible to SARS-CoV-2 infection. The present study indicates a potential genetic contribution of APOE expression-modifying variants in modulating the prognosis of COVID-19.

show abstract

Apolipoprotein E negatively regulates murine allergic airway inflammation via suppressing the activation of NLRP3 inflammasome and oxidative stress

Cited by 18 publications

References 49 publications

PM2.5‐induced pulmonary inflammation via activating of the NLRP3/caspase‐1 signaling pathway

PM2.5‐induced pulmonary inflammation via activating of the NLRP3/caspase‐1 signaling pathway

Moxibustion Ameliorates Ovarian Reserve in Rats by Mediating Nrf2/HO-1/NLRP3 Anti-Inflammatory Pathway

Influence of APOE locus on poor prognosis of COVID-19

Contact Info

Product

Resources

About