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Immunomodulatory Activities of Silver Nanoparticles (AgNPs) in Human Neutrophils
Published in Huiliang Cao, Silver Nanoparticles for Antibacterial Devices, 2017
We then performed another study using smaller AgNPs with a diameter of 15 nm, AgNP15. Similarly to AgNP20, AgNP15 were found to rapidly penetrate human PMNs (Liz et al. 2015). However, AgNP15 appears to induce unconventional apoptosis. Indeed, in contrast to the cell shrinkage and CD16 cell surface shedding (Dransfield et al. 1994) normally observed in human apoptotic PMNs that we routinely used in our laboratory as markers of apoptotic cells, we rather observed that AgNP15 increase the cell volume and do not induce CD16 shedding. This unconventional cell death was clearly distinct from cell necrosis and was reversed by the addition of a pan-caspase inhibitor known to mostly inhibit caspase-1, caspase-3, caspase-4 and caspase-7. Because of this, and since we previously published that the ER stress-induced cell apoptotic pathway was operational in human PMNs, including the fact that these cells were also found to express caspase-4 and that it could be activated (Binet et al. 2010), we then tried to inhibit AgNP15-induced atypical cell death by adding specific inhibitors to caspase-1 and to caspase-4. Interestingly, both of these inhibitors were found to prevent the effect of AgNP15. Knowing that these two inflammatory caspases are known to be involved in inflammasome activation and IL-1β production (Fernandes-Alnemri et al. 2007; Man and Kanneganti 2015), it was logical to verify if AgNP15 increase the IL-1β production and, if so, to determine if caspase-1 or caspase-4 is involved. We found that, indeed, AgNP15 increased the neutrophil IL-1β production and that both caspases are involved, although caspase-4 is more importantly implicated (Liz et al. 2015). In this study, we also demonstrated that AgNP15 increased ROS production and that ROS participate in AgNP15-induced cell death. Finally, we reported in this study that when PMNs were forced to adhere, AgNP15 induced the NET formation.
Latent Upregulation of Nlrp3, Nlrc4 and Aim2 Differentiates between Asymptomatic and Symptomatic Trichomonas vaginalis Infection
Published in Immunological Investigations, 2022
Sonal Yadav, Vivek Verma, Rakesh Singh Dhanda, Sumeeta Khurana, Manisha Yadav
Gene CASPASE-4 is an apoptosis-related cysteine peptidase, and its encoded protein has historically been called caspase 11. Recently studies reported IL-1β cleavage and secretion by caspase 11 in the mice and caspase 4/5 in humans due to LPS interaction; this mechanism is non-canonical inflammasomes activation (Knodler et al. 2014). High expression of CASPASE-4 was observed in vaginal tissues of the symptomatic group on the 8th dpi and on (4th dpi and 14th dpi) in the asymptomatic group as compared to the control group. In vaginal tissues of the asymptomatic group, significant levels of CASPASE-4 was measured on the 4th dpi as compared to the 2nd dpi, but no significant difference was observed between the symptomatic and asymptomatic groups (Figure 6c). In the cervical tissue of the symptomatic group, a high CASPASE-4 level was measured on the 4th dpi and 8th dpi as compared to the control.
Endothelial pyroptosis underlies systemic inflammatory response following radiofrequency ablation of hepatic hemangiomas
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2019
Shaohong Wang, Mengmeng Yang, Xu Yang, Li Xu, Shan Ke, Xuemei Ding, Wenbing Sun, Jun Gao
Pyroptosis is a form of programmed cell death and characterized by cell membrane rupture and release of inflammatory cytokines, such as IL-1β and IL-18 and intracellular contents. Pyroptosis is regulated via a caspase-1-dependent or caspase-1-independent mechanism. Caspase-1-independent pyroptosis is mediated caspase-4 and -5 in human or caspase-11 in mouse. Different inflammatory caspases can cause canonical or noncanonical activation of inflammasome pathway and the coexistence of the substrate gasdermin-D (GSDMD) causes the identical inflammatory process [15–19]. Studies have elucidated the role of endothelial pyroptosis in the development of inflammation in response to bacterial infection, hemorrhagic shock and traumatic brain injury [16,17], but whether endothelial pyroptosis involves in the incidence of SIR post RF ablation of hepatic hemangiomas has not been investigated.
Kaempferol alleviates LPS-ATP mediated inflammatory injury in splenic lymphocytes via regulation of the pyroptosis pathway in mice
Published in Immunopharmacology and Immunotoxicology, 2019
Changliang He, Jia Yang, Xiaolin Jiang, Xiaoxia Liang, Lizi Yin, Zhongqiong Yin, Yi Geng, Zhijun Zhong, Xu Song, Yuanfeng Zou, Lixia Li, Wei Zhang, Cheng Lv
Inflammation is a self-protective mechanism that defends the host organism from pathogens and signals to mobilize defensive resources. The initial immune response is generated by cell membrane and cytoplasmic pattern recognition receptors (PRRs) that can discern exogenous pathogen-associated molecular patterns (PAMPs) and endogenous danger-associated molecular patterns (DAMPs). Once triggered by PAMPs and DAMPs, membrane Toll-like receptor (TLR) and intracellular sensor NOD-like receptor 3 (NLRP3) signaling pathways start to operate. Then, NLRP3 recruits apoptosis-associated speck-like protein containing CARD (ASC) and procaspase-1 to assemble a supramolecular complex called inflammasome [1–4]. The process of assembly leads to the activation of caspase-1 via releasing its isoform p10, followed by the cleavage of gasdermin D (GSDMD) [5–7]. Caspase-1 enzymes are defined as one of the pro-inflammatory subfamilies of caspases which are expressed in both humans and mice, and contribute to an inflammatory cell death named pyroptosis. The subfamily of caspases also includes caspase-4 and -5 in humans, and caspase-11 in mice [8–10].