NLRP3 Inflammasome Activation Induced by Engineered Nanomaterials

Abstract

Engineered nanomaterials (ENMs) continue to attract significant attentions because they have novel physicochemical properties that can improve the functions of products that will benefit human lives. However, the physicochemical properties that make ENMs attractive could interact with biological systems and induce cascades of events that cause toxicological effects. Recently, there are more studies suggesting inflammasome activation may play an important role in ENMs-induced biological responses. Inflammasomes are a family of multi-protein complexes and are increasingly recognized as major mediators of host immune system. Among these, NLRP3 inflammasome is the most studied one that could directly interact with ENMs to generate inflammatory responses. In this review, we aim to link the ENM physicochemical properties to NLRP3 inflammasome activation. The understanding of the mechanisms of ENMs-NLRP3 inflammasome interaction will provide us strategies for safer nanomaterial design and therapy.

Oxidative Stress and Inflammation Induced by Environmental and Psychological Stressors: A Biomarker Perspective

“…Caspase-1 can also auto-activate and mediate cell death (151). Several studies have shown that ENM can activate the NLRP3 inflammasome (reviewed in (150)), similarly to other particulate agents (e.g. hydroxyapatite 11 crystals, cholesterol crystals, and aluminum hydroxide particles) (44,64,71).…”

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

“…15,16 In addition, recent studies have shown that NPs with various physicochemical properties activate the NLRP3 inflammasome, suggesting the important role of this inflammasome in mediating the host defense system against NP exposure. Activation of the NLRP3 inflammasome in macrophages, in addition to IL-1β signaling, has been shown to be necessary for CNT-induced inflammation.…”

Coculture with Low‐Dose SWCNT Attenuates Bacterial Invasion and Inflammation in Human Enterocyte‐like Caco‐2 Cells

“…[ 32 ] Importantly, new evidence has been found recently that particulate matters, including nanoparticles and CNTs that can stimulate the activation of NLRP3 infl ammasome. [ 8,[34][35][36] Therefore, we need to confi rm whether the restitution effect of low-dose SWCNT treatments on the infected cells is associated with the further inhibition of NLRP3 infl ammasome activation. As expected, the E. coli and S. aureus infection stimulated the expression of NLRP3 , Caspase-1 , and ASC mRNA and generated high IL-1β secretion in the host cells, moreover, the increased extracellular potassium level signifi cantly reduced IL-1β and NLRP3 mRNA expression, which were consistent with the reports of previous work, [ 32 ] indicating the activation of NLRP3 infl ammasome by the pathogenic infections.…”