Marta Cristaldi's research while affiliated with Fondazione Ri.MED and other places
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Publications (8)
Airway epithelium represents a physical barrier against toxic substances and pathogens but also presents pattern recognition receptors on the epithelial cells that detect pathogens leading to molecule release and sending signals that activate both the innate and adaptive immune responses. Thus, impaired airway epithelial function and poor integrity...
Cigarette smoking impairs the lung innate immune response making smokers more susceptible to infections and severe symptoms. Dysregulation of cell death is emerging as a key player in chronic inflammatory conditions. We have recently reported that short exposure of human monocyte-derived macrophages (hMDMs) to cigarette smoke extract (CSE) altered...
Mechanisms and consequences of gasdermin D (GSDMD) activation in cigarette smoke (CS)‐associated inflammation and lung disease are unknown. GSDMD is a downstream effector of caspase‐1, ‐8, and ‐4. Upon cleavage, GSDMD generates pores into cell membranes. Different degrees of GSDMD activation are associated with a range of physiological outputs rang...
Exposure of the airways epithelium to environmental insults, including cigarette smoke, results in increased oxidative stress due to unbalance between oxidants and antioxidants in favor of oxidants. Oxidative stress is a feature of inflammation and promotes the progression of chronic lung diseases, including Chronic Obstructive Pulmonary Disease (C...
Citations
... Whether the NLRP3 inflammasome pathway is activated in COPD and/or response to cigarette smoke exposure remains a debatable issue (see review [26]). While multiple evidence from human [22; 59] and animal studies [59][60][61] lends support for a "Yes" answer, other studies present opposite results [62][63][64][65][66], As a potent protective mechanism but potentially detrimental at excessive activation, the NLRP3 inflammasome pathway is tightly controlled by multiple regulatory pathways acting on post-translational modifications of proteins as well as transcription and translation levels [67][68][69]. In this relation cigarette smoke could inhibit the inflammasome by upregulated catabolism of NLRP3 [64]. ...
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... EM appears to counteract the oxidative stress instigated by smoking by attenuating ROS levels. Notably, smoking-induced oxidative stress is instrumental in COPD pathogenesis (27). Existing literature underscores the phenomenon that the lung parenchyma of COPD patients releases a multitude of inflammatory cells, predominantly macrophages. ...
![[object Object]](https://i1.rgstatic.net/ii/profile.image/1171899522527232-1656414027211_Q64/Andreina-Bruno-3.jpg)
