The role of ROS-pyroptosis in PM induced air-blood barrier destruction.

Fine particulate matter (PM) has attracted increasing attention due to its health-threatening effects. Although numerous studies have investigated the impact of PM on lung injuries, the specific mechanisms underlying the damage to the air-blood barrier after exposure to PM remain unclear. In this study, we established an in vitro co-culture system using lung epithelial cells and capillary endothelial cells.

PM induce myocardial injury in hyperlipidemic mice through ROS-pyroptosis signaling pathway.

Exposure to particulate matters with diameters below 2.5 µm (PM) is considered a major risk factor for cardiovascular diseases (CVDs). The closest associations between PM and CVDs have been observed in hyperbetalipoproteinemia cases, although the detailed underpinning mechanism remains undefined.

Pyroptosis participates in PM-induced air-blood barrier dysfunction.

Epidemiological studies have shown that particulate matters with diameter less than 2.5 μm (PM) play an important role in inducing and promoting respiratory diseases, but its underlying mechanism remains to be explored. The air-blood barrier, also known as the alveolar-capillary barrier, is the key element of the lung, working as the site of oxygen and carbon dioxide exchange between pulmonary vasculatures.

Oxidative stress activates Ryr2-Ca and apoptosis to promote PM-induced heart injury of hyperlipidemia mice.

The increased cases of hyperlipemia in China and the crucial role of PM in inducing and promoting cardiovascular diseases have attracting more and more researchers' attention. However, the effects and mechanisms of PM on cardiovascular system of hyperlipidemia people are still unclear. In this study, hyperlipidemia mice model was established by high-fat diet.

Differential expression of long non-coding RNAs in the hippocampus of mice exposed to PM in Dalian, China.

Evidence is mounting that PM exposure could lead to learning disability, memory deficits, and cognitive impairment; however, the underlying mechanisms are still not well demonstrated yet. Long non-coding RNAs (LncRNAs) play a crucial role in many human diseases. Although the relationship of Alzheimer's disease (AD) and lncRNAs have been discovered, the role of lncRNA in AD-like phenotype induced by PM needs further exploration.

Oxidative stress activates the TRPM2-Ca-NLRP3 axis to promote PM-induced lung injury of mice.

PM, a main particulate air pollutant, poses a serious hazard to human health. The exposure to PM increases mortality and morbidity of many respiratory diseases such as asthma, chronic obstructive pulmonary diseases and even lung cancer. The contribution of reactive oxygen species (ROS) in the PM-induced acute lung injury process was confirmed in our previous research, but the molecular mechanism based for it remains unclarified.

The harmful effects of acute PM exposure to the heart and a novel preventive and therapeutic function of CEOs.

Epidemiological researches have demonstrated the relationship between PM exposure and increased morbidity and mortality of cardiovascular injury. However, no effective therapeutic method was established. The purpose of this study is to investigate the effect of acute PM exposure on the mice heart tissue and explore the therapeutic effects of compound essential oils (CEOs) in this model.

The acute airway inflammation induced by PM exposure and the treatment of essential oils in Balb/c mice.

PM is the main particulate air pollutant whose aerodynamic diameter is less than 2.5 micron. The inflammation of various respiratory diseases are associated with PM inhalation.

A Cross-Validation Design Using Age and HLA Alleles for the Assessment of Clinical Schizophrenia Risk.

Background: Schizophrenia (SCH) is a highly heritable disease that occurs mostly in young adults. Genetic factors usually play important roles in the onset of SCH. Human leukocyte antigen complex (HLA) genes are considered to be the important genetic predisposition factor and the genetic markers in SCH and other diseases.

Th17 can regulate silica-induced lung inflammation through an IL-1β-dependent mechanism.

Silicosis is an occupational lung disease caused by the inhalation of silica dust and characterized by lung inflammation and fibrosis. Interleukin (IL)-1β is induced by silica and functions as the key pro-inflammatory cytokine in this process. The Th17 response, which is induced by IL-1β, has been reported very important in chronic human lung inflammatory diseases.

Reduction of IL-17A might suppress the Th1 response and promote the Th2 response by boosting the function of Treg cells during silica-induced inflammatory response in vitro.

Silica inhalation can induce chronic lung inflammation and fibrosis. Upon silica stimulation, activated macrophages trigger the T-lymphocyte which can differentiate into many different types of Th cells, including the recently discovered Th17 cells. IL-17A, the typical Th17 cytokine, is reported in some inflammatory diseases.

Neutralization of interleukin-17A delays progression of silica-induced lung inflammation and fibrosis in C57BL/6 mice.

Silica exposure can cause lung inflammation and fibrosis, known as silicosis. Interleukin-17A (IL-17A) and Th17 cells play a pivotal role in controlling inflammatory diseases. However, the roles of IL-17A and Th17 cells in the progress of silica-induced inflammation and fibrosis are poorly understood.

1,3-β-glucan affects the balance of Th1/Th2 cytokines by promoting secretion of anti-inflammatory cytokines in vitro.

1,3-β-glucan is considered a fungal biomarker and exposure to this agent induces lung inflammation. Previous studies have shown that 1,3-β-glucan affects Th1 and Th2 immune responses. Interleukin (IL)-10 and transforming growth factor (TGF)-β, as typical anti-inflammatory cytokines, suppress the Th1 immune response.

T(reg) cells may regulate interlukin-17 production by modulating TH1 responses in 1,3-β-glucan-induced lung inflammation in mice.

1,3-β-glucan is considered a fungal biomarker and exposure to this agent can induce lung inflammation. Complement activation plays an important role in early immune responses to β-glucan. Previous studies showed that T-regulatory cells (Tregs) regulated 1,3-β-glucan-induced lung inflammation by modulating the maintenance of immune homeostasis in the lung.

Tregs promote the differentiation of Th17 cells in silica-induced lung fibrosis in mice.

Background: Silicosis is an occupational lung disease caused by inhalation of silica dust and characterized by lung inflammation and fibrosis. Previous study showed that Tregs regulate the process of silicosis by modulating the maintenance of immune homeostasis in the lung. Th17 cells share reciprocal developmental pathway with Tregs and play a pivotal role in the immunopathogenesis of many lung diseases by recruiting and activating neutrophils, but the regulatory function of Tregs on Th17 response in silica induced lung fibrosis remains to be explored.

Depletion of CD4+CD25+Foxp3+ regulatory T cells with anti-CD25 antibody may exacerbate the 1,3-β-glucan-induced lung inflammatory response in mice.

1,3-β-Glucan was a major cell wall component of fungus. The existing studies showed that 1,3-β-glucan exposure could induce lung inflammation that involved both Th1 and Th2 cytokines. Regulatory T cells (Treg cells) played a critical role in regulating immune homeostasis by adjusting the Th1/Th2 balance.

CD4+CD25+Foxp3+ regulatory T cells depletion may attenuate the development of silica-induced lung fibrosis in mice.

Background: Silicosis is an occupational lung disease caused by inhalation of silica dust characterized by lung inflammation and fibrosis. Previous study showed that Th1 and Th2 cytokines are involved in silicosis, but Th1/Th2 polarization during the development of silicosis is still a matter of debate. Regulatory T cells (Treg cells) represent a crucial role in modulation of immune homeostasis by regulating Th1/Th2 polarization, but their possible implication in silicosis remains to be explored.