The roles of Nrf2 and autophagy in modulating inflammation mediated by TLR4 - NFκB in A549 cell exposed to layer house particulate matter 2.5 (PM2.5)

Dai, Pengyuan; Shen, Dan; Shen, Jieliang; Tang, Qian; Xi, Mengxue; Li, Yansen; Li, Chunmei

doi:10.1016/j.chemosphere.2019.07.002

Cited by 38 publications

(20 citation statements)

References 79 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Nrf2-deficient mouse astrocytes exhibited increased DNA-binding activity and overproduction of pro-inflammatory cytokines [156]. The overexpression of Nrf2 decreased the level of p65 in inflammation reaction in human adenocarcinoma alveolar basal epithelial cells (A549 cell) [157]. p65 has a dual role in Nrf2 activation.…”

Section: Nf-κb Pathwaymentioning

confidence: 97%

The Role of Reactive Oxygen Species in Arsenic Toxicity

et al. 2020

View full text Add to dashboard Cite

Arsenic poisoning is a global health problem. Chronic exposure to arsenic has been associated with the development of a wide range of diseases and health problems in humans. Arsenic exposure induces the generation of intracellular reactive oxygen species (ROS), which mediate multiple changes to cell behavior by altering signaling pathways and epigenetic modifications, or cause direct oxidative damage to molecules. Antioxidants with the potential to reduce ROS levels have been shown to ameliorate arsenic-induced lesions. However, emerging evidence suggests that constructive activation of antioxidative pathways and decreased ROS levels contribute to chronic arsenic toxicity in some cases. This review details the pathways involved in arsenic-induced redox imbalance, as well as current studies on prophylaxis and treatment strategies using antioxidants.

show abstract

Section: Nf-κb Pathwaymentioning

confidence: 97%

The Role of Reactive Oxygen Species in Arsenic Toxicity

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Air borne PM2.5 induced the calcification of blood vessels through NFκB and p38 MAPK, thereby increasing smooth muscle cell proliferation [117,118]. As mentioned earlier, the activation of NFκB by PM2.5 might be mediated through TLR4 [101]. In human airway smooth muscle cells, exposure to PM2.5 increased cell migration and therefore may contribute to the increased mass of smooth muscle cells in asthma [119].…”

Section: Mechanisms To Explain How Air Pollution Triggers Remodeling mentioning

confidence: 86%

“…In animal models, the exposure to PM2.5 stimulated inflammation through TLR2/TLR4 and MyD88 signaling [99,100]. In human epithelial cells, the exposure to PM2.5 from indoor dust activated autophagy through activating TLR4 and Nuclear Factor kappa-B (NFκB) [101]. Interestingly, TLR4 was assumed to mediate the inflammatory and remodeling stimulating effect of HSP60 in vascular smooth muscle cells [102].…”

Section: Mechanisms To Explain How Air Pollution Triggers Remodeling mentioning

confidence: 99%

Immunologic and Non-Immunologic Mechanisms Leading to Airway Remodeling in Asthma

Fang

Sun

Roth

2020

IJMS

View full text Add to dashboard Cite

Asthma increases worldwide without any definite reason and patient numbers double every 10 years. Drugs used for asthma therapy relax the muscles and reduce inflammation, but none of them inhibited airway wall remodeling in clinical studies. Airway wall remodeling can either be induced through pro-inflammatory cytokines released by immune cells, or direct binding of IgE to smooth muscle cells, or non-immunological stimuli. Increasing evidence suggests that airway wall remodeling is initiated early in life by epigenetic events that lead to cell type specific pathologies, and modulate the interaction between epithelial and sub-epithelial cells. Animal models are only available for remodeling in allergic asthma, but none for non-allergic asthma. In human asthma, the mechanisms leading to airway wall remodeling are not well understood. In order to improve the understanding of this asthma pathology, the definition of “remodeling” needs to be better specified as it summarizes a wide range of tissue structural changes. Second, it needs to be assessed if specific remodeling patterns occur in specific asthma pheno- or endo-types. Third, the interaction of the immune cells with tissue forming cells needs to be assessed in both directions; e.g., do immune cells always stimulate tissue cells or are inflamed tissue cells calling immune cells to the rescue? This review aims to provide an overview on immunologic and non-immunologic mechanisms controlling airway wall remodeling in asthma.

show abstract

“…PM 2.5 significantly increased the levels of COX2 and p-p65/p65. COX2 is an important pro-inflammatory gene, and studies have shown that overexpression of coX2 promotes inflammation and adversely affects fibrosis (31). p65 belongs to the NF-κB family of proteins, and these proteins exist either as homologous or heterologous dimers formed between family members under normal conditions (31).…”

Section: Discussionmentioning

confidence: 99%

“…COX2 is an important pro-inflammatory gene, and studies have shown that overexpression of coX2 promotes inflammation and adversely affects fibrosis (31). p65 belongs to the NF-κB family of proteins, and these proteins exist either as homologous or heterologous dimers formed between family members under normal conditions (31). When cells were stimulated by different external factors, such as stress, lipopolysaccharide, viruses and free oxygen radicals, nF-κB immediately disassociates and translocates to the nucleus to enhance transcription of inflammatory genes (32).…”

Section: Discussionmentioning

confidence: 99%

Potential hazardous effects of printing room PM2.5 exposure include promotion of lung inflammation and subsequent injury

et al. 2020

View full text Add to dashboard Cite

There have been few studies investigating the potential effects of indoor sources of particulate matter on human health. in this study, the effect of different concentrations of fine particulate matter (PM 2.5) collected from a printing room on lung health was examined using cultured cells and a mouse model. Further, the mechanism of lung injury was examined. The results indicated that PM 2.5 significantly enhanced malondialdehyde activity (P<0.05), decreased superoxide dismutase activity (P<0.05), upregulated the expression of pro-inflammatory factors including interleukin (IL)-1β, tumor necrosis factor-, il-6 and downregulated the expression of the inflammatory factor IL-2 (P<0.05). Western blot analysis indicated that PM 2.5 significantly enhanced expression of phosphorylated (p)-ERK relative to total ERK, cyclooxygenase-2, p-anti-nuclear-factor-κB (p-NF-κB) relative to nF-κB, transforming growth factor-β1 and Bax relative to Bcl-2 in inflammation (P<0.05), fibrosis and apoptosis signaling pathways. Furthermore, the results revealed that exposure was associated with an increased abundance of pathogens including Burkholderiales, Coriobacteriia, and Betaproteobacteria in in the lungs. in conclusion, exposure to PM 2.5 from a printing room significantly increased inflammation, fibrosis, apoptosis and the abundance of pathogenic bacteria, indicating that exposure is potential threat to individuals who spend a significant amount of time in printing rooms.

show abstract

The roles of Nrf2 and autophagy in modulating inflammation mediated by TLR4 - NFκB in A549 cell exposed to layer house particulate matter 2.5 (PM2.5)

Cited by 38 publications

References 79 publications

The Role of Reactive Oxygen Species in Arsenic Toxicity

The Role of Reactive Oxygen Species in Arsenic Toxicity

Immunologic and Non-Immunologic Mechanisms Leading to Airway Remodeling in Asthma

Potential hazardous effects of printing room PM2.5 exposure include promotion of lung inflammation and subsequent injury

Contact Info

Product

Resources

About

The roles of Nrf2 and autophagy in modulating inflammation mediated by TLR4 - NFκB in A549 cell exposed to layer house particulate matter 2.5 (PM2.5)

Cited by 38 publications

References 79 publications

The Role of Reactive Oxygen Species in Arsenic Toxicity

The Role of Reactive Oxygen Species in Arsenic Toxicity

Immunologic and Non-Immunologic Mechanisms Leading to Airway Remodeling in Asthma

Potential hazardous effects of printing room PM2.5 exposure include promotion of lung inflammation and subsequent injury

Contact Info

Product

Resources

About

The roles of Nrf2 and autophagy in modulating inflammation mediated by TLR4 - NFκB in A549 cell exposed to layer house particulate matter 2.5 (PM2.5)