Bronchial epithelial pyroptosis promotes airway inflammation in a murine model of toluene diisocyanate-induced asthma

Zhuang, Jian; Cui, Haiyan; Zhuang, Lili; Zhai, Zeqing; Yang, Fengying; Luo, Guihu; He, Juan; Zhao, Haijin; Zhao, Wen Xiang; He, Yi; Sun, Erwei

doi:10.1016/j.biopha.2020.109925

Cited by 53 publications

(44 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The classical pyroptosis pathway is central to PM 2.5-induced injury. Previous studies have reported PM 2.5induced NLRP3 in ammasome activation and ocular injury in vivo and in vitro [15,23,24,25,26,27,28,29,30,31]. The NLRP3 in ammasome is a vital component of sterile-and infection-triggered in ammation as well as of the immune responses to various diseases [32].…”

Section: Discussionmentioning

confidence: 98%

“…Classical pyroptosis is mediated by the NLRP3 in ammasome, and caspase-1 activation promotes the cleavage of pro-IL-1β and GSDMD [33]. Previous studies have revealed that NLRP3 in ammasome activation greatly contributes to cardiovascular, neurological, and lung disease development [25,26,27,28,29,30,31]. In addition, ROS have been reported to activate the NLRP3 in ammasome in environment-induced dry eye and conjunctivitis, and a signi cant increase of in ammatory factors, such as IL-1β, was observed.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Airborne particulate matter (PM2.5) triggers ocular hypertension through pyroptosis

Xing

Niu

et al. 2021

Preprint

View full text Add to dashboard Cite

Background Particulate matter (PM) is strongly linked to human health and has detrimental effects on the eye. Studies have, however, focused on the ocular surface, with limited research on the impact of PM2.5 on intraocular pressure (IOP).Methods To investigate the impact of PM2.5 on IOP and the associated mechanism, C57BL/6 mouse eyes were topically exposed to a PM2.5 suspension for 3 months, and human trabecular meshwork (HTM) cells were subjected to various PM2.5 concentrations in vitro.Results The results revealed that the IOP increased gradually after PM2.5 exposure, and an upregulation of NLRP3 inflammasome, caspase-1, IL-1β, and GSDMD protein levels was observed in outflow tissues. PM2.5 exposure decreased HTM cell viability and affected contraction. Further, elevated ROS levels were observed as well as an activation of the NLRP3 inflammasome and downstream inflammatory factors caspase-1 and IL-1β. ROS scavenger or caspase-1 inhibitor treatment improved these PM2.5-induced changes.Conclusion This study provides novel evidence of the PM2.5-mediated development of ocular hypertension, which occurs as a result of increased oxidative stress and the subsequent induction of pyroptosis in trabecular meshwork cells.

show abstract

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Airborne particulate matter (PM2.5) triggers ocular hypertension through pyroptosis

Xing

Niu

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…Toluene diisocyanate (TDI) was found to exacerbate asthmatic airway inflammation by inducing NLRP3 inflammasome activation. Mechanistically, active NLRP3 inflammasome in epithelial cells activate caspase‐1 to cleave GSDMD, finally increasing the IL‐1β release and aggravating the airway inflammation in asthma 44 . Moreover, Zaslona et al 45 identified that caspase‐11‐driven pyroptosis in macrophages is a critical regulator of allergic airway inflammation.…”

Section: Pyroptosis In Noninfectious Diseasesmentioning

confidence: 99%

“…Mechanistically, active NLRP3 inflammasome in epithelial cells activate caspase‐1 to cleave GSDMD, finally increasing the IL‐1β release and aggravating the airway inflammation in asthma. 44 Moreover, Zaslona et al 45 identified that caspase‐11‐driven pyroptosis in macrophages is a critical regulator of allergic airway inflammation. Taken together, these studies advance our knowledge of the contributory role of pyroptosis in asthma.…”

Section: Pyroptosis In Noninfectious Diseasesmentioning

confidence: 99%

Pyroptosis: A promising therapeutic target for noninfectious diseases

Zheng

et al. 2021

Cell Proliferation

View full text Add to dashboard Cite

Pyroptosis, which is characterized by gasdermin family protein‐mediated pore formation, cellular lysis and the release of pro‐inflammatory cytokines, is a form of programmed cell death associated with intracellular pathogens‐induced infection. However, emerging evidence indicates that pyroptosis also contributes to sterile inflammation. In this review, we will first illustrate the biological process of pyroptosis. Then, we will focus on the pathogenic effects of pyroptosis on multiple noninfectious disorders. At last, we will characterize several specific pyroptotic inhibitors targeting the pyroptotic signalling pathway. These data demonstrate that pyroptosis plays a prominent role in sterile diseases, thereby providing a promising approach to the treatment of noninfective inflammatory disorders.

show abstract

“…Murine caspase-11 is an essential mediator of sepsis (8). Although originally limited to bacterial infection, pyroptosis has recently been implicated in the pathogenesis of disorders, including asthma and psoriasis (9)(10)(11)(12), in which caspase-11 plays an essential role (12,13). As caspase-4 expression is induced in asthmatic patients and correlates with disease severity, this suggests that its inhibition may have therapeutic potential (13,14).…”

Section: Introductionmentioning

confidence: 99%

Caspase-4: A Therapeutic Target for Peptic Ulcer Disease

et al. 2020

View full text Add to dashboard Cite

Peptic ulcers are caused by the interaction between bacterial and host factors. This study demonstrates enhanced expression of caspase-4 in peptic ulcer patient biopsies, indicating that pyroptosis and noncanonical inflammasome activity may be processes involved in peptic ulcer disease. We show that primary murine macrophages infected with Helicobacter pylori upregulate caspase-11 (the ortholog of human caspase-4), activate caspase-1, and secrete IL-1b. We demonstrate that misoprostol (a stable PGE 1 analogue) decreased IL-1b secretion and delayed lethality in vivo in a murine peritonitis model. PGE 2 was shown to inhibit caspase-11-driven pyroptosis and IL-1b secretion in macrophages. Overall, we provide evidence for a pathological role of caspase-4/11 in peptic ulcer disease and propose that targeting caspase-4 or inhibiting pyroptosis may have therapeutic potential in the management of peptic ulcers. ImmunoHorizons, 2020, 4: 627-633.

show abstract

Bronchial epithelial pyroptosis promotes airway inflammation in a murine model of toluene diisocyanate-induced asthma

Cited by 53 publications

References 35 publications

Airborne particulate matter (PM2.5) triggers ocular hypertension through pyroptosis

Airborne particulate matter (PM2.5) triggers ocular hypertension through pyroptosis

Pyroptosis: A promising therapeutic target for noninfectious diseases

Caspase-4: A Therapeutic Target for Peptic Ulcer Disease

Contact Info

Product

Resources

About