Fine Particulate Matter-Induced Exacerbation of Allergic Asthma via Activation of T-cell Immunoglobulin and Mucin Domain 1

Zhao, Yi‐Fang; Zhang, Huiran; Yang, Xiuna; Zhang, Yuhao; Feng, Shan; Yu, Fei; Yan, Xixin

doi:10.4103/0366-6999.243551

Cited by 24 publications

(16 citation statements)

References 38 publications

(42 reference statements)

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“…Previous studies have confirmed that PM2.5 exposure could cause acute airway inflammation 15,16 . In the present study, we explore the effect of PM2.5 on pulmonary inflammation in vivo.…”

Section: Resultsmentioning

confidence: 82%

PM2.5‐induced pulmonary inflammation via activating of the NLRP3/caspase‐1 signaling pathway

Jia

Liu

Guo

et al. 2020

Environmental Toxicology

105

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Particulate matter 2.5 (PM2.5)‐induced pulmonary inflammation has become a public concern in recent years. In which, the activation of the NLRP3/caspase‐1 pathway was closely related to the inflammatory response of various diseases. However, the promotion effect of the NLRP3/caspase‐1 pathway on PM2.5‐induced pulmonary inflammation remains largely unclear. Here, our data showed that PM2.5 exposure caused lung injury in the mice by which inflammatory cell infiltration occurred in lung and alveolar structure disorder. Meanwhile, the exposure of human bronchial epithelial cells (16HBE) to PM2.5 resulted in suppressed cell viability, as well as elevated cell apoptosis. Moreover, a higher level of inflammatory cytokine and activation of the NLRP3/caspase‐1 pathway in PM2.5‐induced inflammation mice models and 16HBE cells. Mechanistically, pretreatment with MCC950, a NLRP3/caspase‐1 pathway inhibitor, prevented PM2.5‐induced lung injury, inflammatory response, and the number of inflammatory cells in BALFs, as well as promoted cell viability and decreased inflammatory cytokine secretion. Collectively, our findings indicated that the NLRP3/caspase‐1 pathway serves a vital role in the pathological changes of pulmonary inflammation caused by PM2.5 exposure. MCC950 was expected to be the therapeutic target of PM2.5 inhalation mediated inflammatory diseases.

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“…Previous studies have confirmed that PM2.5 exposure could cause acute airway inflammation 15,16 . In the present study, we explore the effect of PM2.5 on pulmonary inflammation in vivo.…”

Section: Resultsmentioning

confidence: 82%

PM2.5‐induced pulmonary inflammation via activating of the NLRP3/caspase‐1 signaling pathway

Jia

Liu

Guo

et al. 2020

Environmental Toxicology

105

View full text Add to dashboard Cite

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“…Fine particulate matter (PM 2.5 , particle size < 2.5 μ m) generally has greater toxicity than other particles due to its smaller diameter and larger surface-to-mass ratio, thus allowing it to enter into the lower respiratory tract and even penetrate into the alveolar space and ultimately into the blood circulation [1]. PM 2.5 exposure can induce lung inflammation and airway hyperresponsiveness (AHR) and can even increase the risk of developing asthma [2, 3]. The underlying mechanisms of PM 2.5 toxicity may be partly explained by its ability to cause oxidative stress and mitochondrial damage [4], a process that involves the activation of pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs) and nucleotide binding domain leucine-rich repeat-containing receptors (NLRs) [5].…”

Section: Introductionmentioning

confidence: 99%

TRPV1 and TRPA1 in Lung Inflammation and Airway Hyperresponsiveness Induced by Fine Particulate Matter (PM_2.5)

Zhang

Wang

et al. 2019

Oxidative Medicine and Cellular Longevity

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Exposure to fine particulate matter (PM2.5) has been associated with lung inflammation and airway hyperresponsiveness (AHR). Transient receptor potential (TRP) vanilloid 1 (TRPV1) and ankyrin 1 (TRPA1) both may play important roles in lung inflammation and AHR. We investigated whether PM2.5-induced lung inflammation and AHR could be prevented by blocking TRPV1 and TRPA1 channels. Mice were injected intraperitoneally with AMG9810 (30 mg/kg, a TRPV1 antagonist) or A967079 (30 mg/kg, a TRPA1 antagonist) or their combination or vehicle (PBS) one hour before intranasal instillation of PM2.5 (7.8 mg/kg) or vehicle (PBS) for two consecutive days, and then the mice were studied 24 h later. All pretreatments inhibited PM2.5-induced AHR and inflammatory infiltration in the lung tissue and decreased inflammatory cytokine levels in the bronchoalveolar lavage fluid, together with oxidant levels in the lung. AMG9810 inhibited MFF expression and increased MFN2 expression while A967079 inhibited DRP1 expression and increased OPA1 expression; combined pretreatment reduced MFF and DPR1 expression and increased MFN2 and OPA1 expression. All pretreatments inhibited the activation of the TLR4/NF-κB pathway, while A967079 alone, and combined with AMG9810 also reduced the activation of the NLRP3/caspase-1 pathway. Both TRPV1 and TRPA1 channels play an important role in PM2.5-induced lung inflammation and AHR. However, inhibition of the TRPA1 channel or combined inhibition of TRPA1 and TRPV1 channels resulted in greater inhibitory effect on PM2.5-induced lung injury through regulating the mitochondrial fission/fusion proteins and inhibiting the TLR4/NF-κB and NLRP3/caspase-1 pathways.

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“…PM 2.5 had been obtained by filtering ambient air followed by up-concentration, however, the exact chemical composition was not elucidated. One of the studies attributed the elevated AHR to an increase in apoptosis and TIM-1 activation, which was also witnessed in the OVA/PM 2.5 group (156). Another study has shown that prolonged exposure to high concentrations of PM 2.5 leads to an increase in AHR, which was linked to necroptosis-induced neutrophils as well as IL-17 production (158).…”

Section: Aggravation Of Allergic Asthma By Inhaled Aerosolsmentioning

confidence: 94%

Mechanisms of Particles in Sensitization, Effector Function and Therapy of Allergic Disease

et al. 2020

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Humans have always been in contact with natural airborne particles from many sources including biologic particulate matter (PM) which can exhibit allergenic properties. With industrialization, anthropogenic and combustion-derived particles have become a major fraction. Currently, an ever-growing number of diverse and innovative materials containing engineered nanoparticles (NPs) are being developed with great expectations in technology and medicine. Nanomaterials have entered everyday products including cosmetics, textiles, electronics, sports equipment, as well as food, and food packaging. As part of natural evolution humans have adapted to the exposure to particulate matter, aiming to protect the individual's integrity and health. At the respiratory barrier, complications can arise, when allergic sensitization and pulmonary diseases occur in response to particle exposure. Particulate matter in the form of plant pollen, dust mites feces, animal dander, but also aerosols arising from industrial processes in occupational settings including diverse mixtures thereof can exert such effects. This review article gives an overview of the allergic immune response and addresses specifically the mechanisms of particulates in the context of allergic sensitization, effector function and therapy. In regard of the first theme (i), an overview on exposure to particulates and the functionalities of the relevant immune cells involved in allergic sensitization as well as their interactions in innate and adaptive responses are described. As relevant for human disease, we aim to outline (ii) the potential effector mechanisms that lead to the aggravation of an ongoing immune deviation (such as asthma, chronic obstructive pulmonary disease, etc.) by inhaled particulates, including NPs. Even though adverse effects can be exerted by (nano)particles, leading to allergic sensitization, and the exacerbation of allergic symptoms, promising potential has been shown for their use in (iii) therapeutic approaches of allergic disease, for example as adjuvants. Hence, allergen-specific immunotherapy (AIT) is introduced and the role of adjuvants such as alum as well as the current understanding of their mechanisms of action is reviewed. Finally, future prospects of nanomedicines in allergy treatment are described, which involve modern platform technologies combining immunomodulatory effects at several (immuno-)functional levels.

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Fine Particulate Matter-Induced Exacerbation of Allergic Asthma via Activation of T-cell Immunoglobulin and Mucin Domain 1

Cited by 24 publications

References 38 publications

PM2.5‐induced pulmonary inflammation via activating of the NLRP3/caspase‐1 signaling pathway

PM2.5‐induced pulmonary inflammation via activating of the NLRP3/caspase‐1 signaling pathway

TRPV1 and TRPA1 in Lung Inflammation and Airway Hyperresponsiveness Induced by Fine Particulate Matter (PM_2.5)

Mechanisms of Particles in Sensitization, Effector Function and Therapy of Allergic Disease

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Fine Particulate Matter-Induced Exacerbation of Allergic Asthma via Activation of T-cell Immunoglobulin and Mucin Domain 1

Cited by 24 publications

References 38 publications

PM2.5‐induced pulmonary inflammation via activating of the NLRP3/caspase‐1 signaling pathway

PM2.5‐induced pulmonary inflammation via activating of the NLRP3/caspase‐1 signaling pathway

TRPV1 and TRPA1 in Lung Inflammation and Airway Hyperresponsiveness Induced by Fine Particulate Matter (PM2.5)

Mechanisms of Particles in Sensitization, Effector Function and Therapy of Allergic Disease

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TRPV1 and TRPA1 in Lung Inflammation and Airway Hyperresponsiveness Induced by Fine Particulate Matter (PM_2.5)