The role of the NLRP3 inflammasome in pulmonary diseases

Hosseinian, Nima; Cho, Young; Lockey, Richard F.; Kolliputi, Narasaiah

doi:10.1177/1753465815586335

Cited by 123 publications

(72 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Both NF-κB activation and Mt-ROS generation have been implicated in the activation of NLRP3 inflammasomes (16,35,47,65,74,75), with emerging data suggesting a role for inflammasomes in a variety of lung diseases (16,31,(44)(45)(46)(76)(77)(78). In a model of house dust mite-induced asthma, airway epithelial NLRP3 expression correlates with enhanced asthma phenotypes, which can be reduced by scavenging Mt-ROS (16).…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial CaMKII inhibition in airway epithelium protects against allergic asthma

et al. 2017

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Mitochondrial CaMKII inhibition in airway epithelium protects against allergic asthma

et al. 2017

View full text Add to dashboard Cite

“…14,40,41 This inflammasome consists of a complex of proteins that oligomerize and activate the caspase-1 cascade, which induces production of the active pro-inflammatory cytokines, IL-1β and IL-18, when triggered by various environmental, pathogenic, or endogenous danger signals. Full activation of the NLRP3 inflammasome generally requires a two-step mechanism.…”

mentioning

confidence: 99%

Exposure to nickel oxide nanoparticles induces pulmonary inflammation through NLRP3 inflammasome activation in rats

Cao¹,

Fang²,

Lu³

et al. 2016

IJN

View full text Add to dashboard Cite

With recent advances in the manufacture and application of nickel oxide nanoparticles (NiONPs), concerns about their adverse effects on the respiratory system are increasing. However, the underlying cellular and molecular mechanisms of NiONP-induced pulmonary toxicity remain unclear. In this study, we focused on the impacts of NiONPs on pulmonary inflammation and investigated whether the NLRP3 inflammasome is involved in NiONP-induced pulmonary inflammation and injury. NiONP suspensions were administered by single intratracheal instillation to rats, and inflammatory responses were evaluated at 3 days, 7 days, or 28 days after treatment. NiONP exposure resulted in sustained pulmonary inflammation accompanied by inflammatory cell infiltration, alveolar proteinosis, and cytokine secretion. Expression of Nlrp3 was markedly upregulated by the NiONPs, which was accompanied by overexpression of the active form of caspase-1 (p20) and interleukin (IL)-1β secretion in vivo. NiONP-induced IL-1β secretion was partially prevented by co-treatment with a caspase-1 inhibitor in macrophages. Moreover, siRNA-mediated Nlrp3 knockdown completely attenuated NiONP-induced cytokine release and caspase-1 activity in macrophages in vitro. In addition, NiONP-induced NLRP3 inflammasome activation requires particle uptake and reactive oxygen species production. Collectively, our findings suggest that the NLRP3 inflammasome participates in NiONP-induced pulmonary inflammation and offer new strategies to combat the pulmonary toxicity induced by NiONPs.

show abstract

“…In various renal diseases, TLR4 was confirmed to induce NLRP3 inflammasome activation and hence promote kidney injury [23-25]. Although significant effect of NLRP3 inflammasome has been characterized in various renal diseases [26-28], its role in CNAKI remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Involvement of S100A8/A9-TLR4-NLRP3 Inflammasome Pathway in Contrast-Induced Acute Kidney Injury

Tan

Zheng

Huang

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

Background: Contrast-induced acute kidney injury (CIAKI) is a common cause of hospital-acquired acute kidney injury (AKI). S100A8/A9-TLR4-NLRP3 inflammasome pathway triggers inflammation, apoptosis and tissue injury in several AKI models. Nevertheless, the underlying mechanism of S100A8/A9-TLR4-NLRP3 inflammasome pathway in CIKAI is not clear. We aimed to investigate the possible role of S100A8/A9-TLR4-NLRP3 inflammasome in the pathophysiology of CIAKI. Methods: We treated male rats and NRK-52E cells by iopromide to establish in vivo and in vitro models of CIAKI. We collected serum and urine samples to detect renal function. We obtained kidney tissue for histological analysis and detection of protein concentration. We used inhibitor of TLR4 and NLRP3-siRNA to further testify their role in CIAKI in NRK-52E cells. Results: Iopromide caused elevation of SCr, BUN and NGAL level, decrease of endogenous creatinine clearance, morphological injury and tubular apoptosis, enhanced IL-1β and IL-18 expression, and increased expression of S100A8/A9, TLR4 and NLRP3 inflammsome. In NRK-52E cells, iopromide caused enhanced apoptotic rates and ROS generation, which could be ameliorated by inhibitor of TLR4 and NLRP3-siRNA. Moreover, inhibition of TLR4 dampened NLRP3 expression. Conclusion: S100A8/A9-TLR4-NLRP3 inflammasome pathway represented a key mechanism of CI-AKI, which provided a potential therapeutic target.

show abstract

The role of the NLRP3 inflammasome in pulmonary diseases

Cited by 123 publications

References 57 publications

Mitochondrial CaMKII inhibition in airway epithelium protects against allergic asthma

Mitochondrial CaMKII inhibition in airway epithelium protects against allergic asthma

Exposure to nickel oxide nanoparticles induces pulmonary inflammation through NLRP3 inflammasome activation in rats

Involvement of S100A8/A9-TLR4-NLRP3 Inflammasome Pathway in Contrast-Induced Acute Kidney Injury

Contact Info

Product

Resources

About