Xue Cao

Polystyrene nanoplastics modulated sertraline hydrochloride responses in hydroponically rice, partly attenuating microbial responses in the root solution while enhancing selected oxidative stress responses in root tissues.

Summary: Neutrophils are important in the context of innate immunity and actively contribute to the progression of diverse autoimmune disorders. Distinct death mechanisms of neutrophils may exhibit specific and pivotal roles in autoimmune diseases and disease pathogenesis through the orchestration of immune homeostasis, the facilitation of autoantibody production, the induction of tissue and organ damage, and the incitement of pathological alterations. In recent years, more studies have provided in‐depth examination of various neutrophil death modes, revealing nuances that challenge conventional understanding and underscoring their potential clinical utility in diagnosis and treatment. This review explores the multifaceted processes and characteristics of neutrophil death, with a focus on tailored investigations within various autoimmune diseases. It also highlights the potential interplay between neutrophil death and the landscape of autoimmune disorders. The review encapsulates the pertinent pathways implicated in various neutrophil death mechanisms across diverse autoimmune diseases while also charts possible avenues for future research.

Autophagy pathways play an important role in immunity and inflammation via pathogen clearance mechanisms mediated by immune cells, such as macrophages and neutrophils. In particular, autophagic activity is essential for the release of neutrophil extracellular traps (NETs), a distinct form of active neutrophil death. The current study set out to elucidate the mechanism of the NFIL3/REDD1/mTOR axis in neutrophil autophagy and NET formation during gout inflammation. Firstly, NFIL3 expression patterns were determined in the peripheral blood neutrophils of gout patients and monosodium urate (MSU)-treated neutrophils. Interactions between NFIL3 and REDD1 were identified. In addition, gain- or loss-of-function approaches were used to manipulate NFIL3 and REDD1 in both MSU-induced neutrophils and mice. The mechanism of NFIL3 in inflammation during gout was evaluated both in vivo and in vitro via measurement of cell autophagy, NET formation, MPO activity as well as levels of inflammatory factors. NFIL3 was highly-expressed in both peripheral blood neutrophils from gout patients and MSU-treated neutrophils. NFIL3 promoted the transcription of REDD1 by binding to its promoter. REDD1 augmented neutrophil autophagy and NET formation by inhibiting the mTOR pathway. In vivo experimental results further confirmed that silencing of NFIL3 reduced the inflammatory injury of acute gouty arthritis mice by inhibiting the neutrophil autophagy and NET formation, which was associated with down-regulation of REDD1 and activation of the mTOR pathway. Taken together, NFIL3 can aggravate the inflammatory reaction of gout by stimulating neutrophil autophagy and NET formation via REDD1/mTOR, highlighting NFIL3 as a potential therapeutic target for gout.

It is well accepted that diesel exhaust particles (DEPs) are highly associated with improper function of organ systems. In this study, DEP toxicity was performed by using in vitro human BEAS-2B cell line and in vivo animal model, namely, Caenorhabditis elegans (C. elegans). The potential toxicity of DEP was assessed by the apical endpoints of BEAS-2B cell line and reflections of C. elegans under exposure scenarios of 0~50 μg mL^–1 DEP. With the increase of DEP exposure concentration, microscopic accumulations in the cytoplasm of cell line and intestine of C. elegans were observed. Such invasion of DEP impaired the behaviors of C. elegans as well as its un-exposed offspring and caused significant impeded locomotion. Moreover, the disorders of dopaminergic function were observed simultaneously under DEP exposure, specifically manifested by the decreased transcriptional expression of dat-1. The stress responses instructed by the expression of hsp-16.2 were also increased sharply in TJ375 strain of C. elegans at DEP concentrations of 1 and 10 μg mL^–1. In the case of cellular reactions to DEP exposure, the injuries of membrane integrity and the decreased viability of cell line were simultaneously identified, and reactive oxygen species (ROS), damaged DNA fragment, and upregulated apoptosis were monotonically elevated in cell lines with the increase of DEP concentrations. This study provided a systematic insight into toxicity of DEP both in vivo and vitro, demonstrating that DEP exposure could disturb the stability of cell system and further threat the stability of organism.

Contamination of the environment by toxic pesticides has become of great concern in agricultural countries. Chlorpyrifos (CP) is among the pesticides most commonly detected in the environment owing to its wide agricultural applications. The aim of this study was to compare potential changes in the toxicity of CP after irradiation. To this end, photolysis of CP was conducted under simulated sunlight, and neurotoxicity assessment was carried out at CP of 20 and 50 µg L-1 and its corresponding irradiated mixture solutions which contain a mixture of identified intermediates using the nematode, Caenorhabditis elegans as a model organism. Photodegradation of 20 µg L-1 CP for 1 h produced no obvious reduction of physiological damage, and more serious effects on animal movement were detected after exposure of the animals to a solution of 50 µg L-1 for 1 h compared with unirradiated solution. GABAergic and cholinergic neurons were selectively vulnerable to CP exposure, and maximal neuropathological alterations were observed after 1 h irradiation of the CP solutions in coherence with the behavioural impairment. The generation of photoproducts was considered to be responsible for the enhanced disturbance on those biological process. This work provided useful information on the toxicological assessments of chemicals that were produced during the environmental transformation of pesticides.