Inflammasomes, a critical component of the innate immune system, mediate much of the inflammatory response manifested by engineered nanomaterials. Iron oxide nanoparticles (IONPs), a type of nanoparticles that have gained widespread acceptance in preclinical and clinical settings, are known to induce inflammasome activation, but how morphology affects the inflammasome-activating property of IONPs has not been addressed. In this report, we have synthesized four morphologically distinct IONPs having the same aspect ratio and similar surface charge, thus offering an ideal system to assess the impact of morphology on nanoparticle-elicited biological effect. We show that morphology was a critical determinant for IONP-induced IL-1β release and pyroptosis, with the octapod and plate IONPs exhibiting significantly higher activity than the cube and sphere IONPs. The inflammasome-activating capacity of different IONPs correlated with their respective ability to elicit intracellular reactive oxygen species generation, lysosomal damage, and potassium efflux, three well-known mechanisms for nanoparticle-facilitated inflammasome activation. Furthermore, we demonstrate that the release of IL-1β induced by IONPs was only partly mediated by NLRP3, suggesting that inflammasomes other than NLRP3 are also involved in IONP-induced inflammasome activation. Our results may have implications for designing safer nanoparticles for in vivo applications.

The intestine, a high-turnover tissue, plays a critical role in regulating aging and health in both vertebrates and invertebrates. Maintaining the epithelial barrier function of the intestine by preserving innate immune homeostasis significantly delays aging and prevents mortality. In an effort to explore effective chemicals and materials that can improve intestinal integrity, we performed a nonbiased screen utilizing Drosophila as an animal model. We showed that long-term uptake of aspirin markedly prevented age-onset gut leakage, the over-proliferation of intestinal stem cells, and the dysbiosis of commensal microbiota in fruit flies. Mechanistically, aspirin efficiently downregulated chronic activation of intestinal immune deficiency signaling during aging. Furthermore, our in vivo and in vitro biochemical analyses indicated that aspirin is a negative modulator in control of the K63-linked ubiquitination of Imd. Our findings uncover a novel regulatory mechanism by which aspirin positively modulates intestinal homeostasis, thus delaying aging, in Drosophila .

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Negative regulators of the inflammatory responses are essential for the maintenance of immune homeostasis and organismal fitness. In Drosophila, the deubiquitinase (Dub) dTrbd selectively restricts the K63-linked ubiquitination modification of dTak1, a pivotal kinase of the IMD signaling pathway, to regulate the IMD innate immune response. However, which domain and how it functions to enable dTrbd’s activity remain unexplored. Here, we provide compelling evidence showing that the NZF domain of dTrbd is essential for its association with dTak1. Meanwhile, the Linker region of dTrbd is involved in modulating its condensation, a functional state representing the Dub enzymatical activity of dTrbd. Of interest, the activated IMD signals following bacterial stimuli enhance the dTrbd/dTak1 interaction, as well as the condensate assembly and Dub enzymatical activity of dTrbd. Collectively, our studies shed light on the dual mechanisms by which the IMD signaling-mediated feedback loop of dTrbd/dTak1 precisely regulates the innate immune response in Drosophila.

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In this paper, electrochemical corrosion tests and full immersion corrosion experiments were conducted in seawater at room temperature to investigate the electrochemical corrosion behavior and the corrosion mechanism of high-strength EH47. The polarization curve, EIS (electrochemical impedance spectroscopy), SEM (scanning electron microscope), and EDS analyses were employed to analyze the results of the electrochemical corrosion process. The electrochemical corrosion experiments showed that the open circuit potential of EH47 decreases and then increases with an increase in total immersion time, with the minimum value obtained at 28 days. With an increase in immersion time, the corrosion current density (Icorr) of EH47 steel first decreases and then increases, with the minimum at about 28 days. This 28-day sample also showed the maximum capacitance arc radius, the maximum impedance and the minimum corrosion rate. In the seawater immersion test in the laboratory, the corrosion mechanism of EH47 steel in the initial stage of corrosion is mainly pitting corrosion, accompanied by a small amount of crevice corrosion with increased corrosion time. The corrosion products of EH47 steel after immersion in seawater for 30 days are mainly composed of FeOOH, Fe3O4 and Fe2O3.

Nucleotide‐binding domain and leucine rich repeat family pyrin domain containing 3 (NLRP3) inflammasomes are implicated in diverse inflammatory diseases, so their activation needs to be tightly controlled. Over generation of reactive oxygen species (ROS) is a key factor in NLRP3 inflammasome activation. Consequently, nanozymes with ROS scavenging ability are potential inhibitors of NLRP3 activation and promising therapeutic agents for related inflammatory diseases. Herein, a type of 2D cobalt hydroxide oxide nanosheets (Co NSs), a nanozyme with excellent multienzyme‐like activity, possessing peroxidase (POD), catalase (CAT), and superoxide dismutase (SOD) activities, exhibits superior ROS scavenging properties and protects cells from oxidative damage. Density functional theory (DFT) calculations further reveal these enzyme‐like catalytic reactions of ROS eliminating are spontaneous and CAT is dominant under physiological conditions. Performing multienzyme properties, Co NSs present excellent anti‐inflammation activity by blocking NLRP3 oligomerization and ASC speck formation, thereby inhibiting NLRP3 inflammasome assembly and activation. Importantly, treatment with Co NSs attenuates the severity of LPS‐induced systemic inflammation and DSS‐induced colitis. This study highlights a successful strategy for utilizing cobalt‐based nanozymes to scavenge ROS and provides valuable insights into the underlying mechanism, demonstrating the potential therapeutic effects of nanozyme for the prevention and treatment of NLRP3‐associatied inflammatory diseases.