Deregulated Nrf2-Keap1-BACH1 axis in autism spectrum disorder.

Autism Spectrum Disorder (ASD) is a group of neurodevelopmental disorders characterized by impairments in social communication, restricted interests, and repetitive behaviors. Although its etiology remains incompletely understood, increasing evidence suggests a multifactorial origin involving genetic alterations, immune dysregulation, and environmental exposures. The aim of this study was to investigate the redox-sensitive Nrf2 signaling pathway in primary dermal fibroblasts isolated from ASD patients.

Effect of Cu- and Fe- Isolated from Environmental Particulate Matter on Mitochondrial Dynamics in Human Colon CaCo-2 Cells.

Atmospheric particulate matter (PM) is one of the most dangerous air pollutants of anthropogenic origin; it consists of a heterogeneous mixture of inorganic and organic components, including transition metals and polycyclic aromatic hydrocarbons. Although previous studies have focused on the effects of exposure to highly concentrated PM on the respiratory and cardiovascular systems, emerging evidence supports a significant impact of air pollution on the gastrointestinal (GI) tract by linking exposure to external stressors with conditions such as appendicitis, colorectal cancer, and inflammatory bowel disease. In general, it has been hypothesized that the main mechanism involved in PM toxicity consists of an inflammatory response and this has also been suggested for the GI tract.

NLRP3 inflammasome-mitochondrion loop in autism spectrum disorder.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by deficits in social communication and the presence of restricted interests and repetitive behavior. To date, no single cause has been demonstrated but both genetic and environmental factors are believed to be involved in abnormal brain development. In recent years, immunological and mitochondrial dysfunctions acquired particular interest in the study of the molecular mechanisms underlying the pathophysiology of ASD.

Correction: Gut-derived wild blueberry phenolic acid metabolites modulate extrinsic cutaneous damage.

Correction for 'Gut-derived wild blueberry phenolic acid metabolites modulate extrinsic cutaneous damage' by John Ivarsson , , 2024, , 7849-7864, https://doi.org/10.1039/D4FO01874E.

Comparison of Pollutant Effects on Cutaneous Inflammasomes Activation.

The skin is the outermost layer of the body and, therefore, is exposed to a variety of stressors, such as environmental pollutants, known to cause oxinflammatory reactions involved in the exacerbation of several skin conditions. Today, inflammasomes are recognized as important modulators of the cutaneous inflammatory status in response to air pollutants and ultraviolet (UV) light exposure. In this study, human skin explants were exposed to the best-recognized air pollutants, such as microplastics (MP), cigarette smoke (CS), diesel engine exhaust (DEE), ozone (O), and UV, for 1 or 4 days, to explore how each pollutant can differently modulate markers of cutaneous oxinflammation.

Ox-inflammasome involvement in neuroinflammation.

Neuroinflammation plays a crucial role in the onset and the progression of several neuropathologies, from neurodegenerative disorders to migraine, from Rett syndrome to post-COVID 19 neurological manifestations. Inflammasomes are cytosolic multiprotein complexes of the innate immune system that fuel inflammation. They have been under study for the last twenty years and more recently their involvement in neuro-related conditions has been of great interest as possible therapeutic target.

The role of potassium current in the pulmonary response to environmental oxidative stress.

Exposure of human lung epithelial cells (A549 cell line) to the oxidant pollutant ozone (O) alters cell membrane currents inducing its decrease, when the cell undergoes to a voltage-clamp protocol ranging from -90 to +70mV. The membrane potential of these cells is mainly maintained by the interplay of potassium and chloride currents. Our previous studies indicated the ability of O to activate ORCC (Outward Rectifier Chloride Channel) and consequently increases the chloride current.

Ubiquitination as a key regulatory mechanism for O-induced cutaneous redox inflammasome activation.

NLRP1 is one of the major inflammasomes modulating the cutaneous inflammatory responses and therefore linked to a variety of cutaneous conditions. Although NLRP1 has been the first inflammasome to be discovered, only in the past years a significant progress was achieved in understanding the molecular mechanism and the stimuli behind its activation. In the past decades a crescent number of studies have highlighted the role of air pollutants as Particulate Matter (PM), Cigarette Smoke (CS) and Ozone (O) as trigger stimuli for inflammasomes activation, especially via Reactive Oxygen Species (ROS) mediators.