Journal of environmental immunology and toxicology最新文献

Inflammasome Activity in Non-Microbial Lung Inflammation. 非微生物性肺部炎症中的炎性小体活性。

Journal of environmental immunology and toxicology Pub Date : 2014-09-20

Jennifer L Ather, Rebecca A Martin, Karina Ckless, Matthew E Poynter

{"title":"Inflammasome Activity in Non-Microbial Lung Inflammation.","authors":"Jennifer L Ather, Rebecca A Martin, Karina Ckless, Matthew E Poynter","doi":"","DOIUrl":"","url":null,"abstract":"The understanding of interleukin-1 (IL-1) family cytokines in inflammatory disease has rapidly developed, due in part to the discovery and characterization of inflammasomes, which are multi-subunit intracellular protein scaffolds principally enabling recognition of a myriad of cellular stimuli, leading to the activation of caspase-1 and the processing of IL-1β and IL-18. Studies continue to elucidate the role of inflammasomes in immune responses induced by both microbes and environmental factors. This review focuses on the current understanding of inflammasome activity in the lung, with particular focus on the non-microbial instigators of inflammasome activation, including inhaled antigens, oxidants, cigarette smoke, diesel exhaust particles, mineral fibers, and engineered nanomaterials, as well as exposure to trauma and pre-existing inflammatory conditions such as metabolic syndrome. Inflammasome activity in these sterile inflammatory states contribute to diseases including asthma, chronic obstructive disease, acute lung injury, ventilator-induced lung injury, pulmonary fibrosis, and lung cancer.","PeriodicalId":90213,"journal":{"name":"Journal of environmental immunology and toxicology","volume":"1 3","pages":"108-117"},"PeriodicalIF":0.0,"publicationDate":"2014-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4308734/pdf/nihms655246.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33021752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Innate Immune Responses to Nanoparticle Exposure in the Lung. 纳米颗粒暴露在肺部的先天免疫反应。

Journal of environmental immunology and toxicology Pub Date : 2014-07-01 DOI: 10.7178/jeit.23

Elizabeth A Thompson, Brian C Sayers, Ellen E Glista-Baker, Kelly A Shipkowski, Alexia J Taylor, James C Bonner

{"title":"Innate Immune Responses to Nanoparticle Exposure in the Lung.","authors":"Elizabeth A Thompson, Brian C Sayers, Ellen E Glista-Baker, Kelly A Shipkowski, Alexia J Taylor, James C Bonner","doi":"10.7178/jeit.23","DOIUrl":"https://doi.org/10.7178/jeit.23","url":null,"abstract":"The nanotechnology revolution offers enormous societal and economic benefits for innovation in the fields of engineering, electronics, and medicine. Nevertheless, evidence from rodent studies show that biopersistent engineered nanomaterials (ENMs) stimulate immune, inflammatory, and fibroproliferative responses in the lung, suggesting possible risks for lung diseases or systemic immune disorders as a consequence of occupational, environmental, or consumer exposure. Due to their nanoscale dimensions and increased surface area per unit mass, ENMs have a much greater potential to reach the distal regions of the lung and generate ROS. High aspect ratio ENMs (e.g., nanotubes, nanofibers) activate inflammasomes in macrophages, triggering IL-1β release and neutrophilic infiltration into the lungs. Moreover, some ENMs alter allergen-induced eosinophilic inflammation by immunostimulation, immunosuppression, or modulating the balance between Th1, Th2, and Th17 cells, thereby influencing the nature of the inflammatory response. ENMs also migrate from the lungs across epithelial, endothelial, or mesothelial barriers to stimulate or suppress systemic immune responses.","PeriodicalId":90213,"journal":{"name":"Journal of environmental immunology and toxicology","volume":"1 3","pages":"150-156"},"PeriodicalIF":0.0,"publicationDate":"2014-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4437698/pdf/nihms690477.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33200870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 41

Dimethylarginine dimethylaminohydrolase (DDAH) overexpression attenuates agricultural organic dust extract-induced inflammation. 二甲基精氨酸二甲氨基水解酶（DDAH）过表达可减轻农业有机粉尘提取物诱发的炎症。

Journal of environmental immunology and toxicology Pub Date : 2014-03-01 DOI: 10.7178/jeit.15

Kl Bailey, Ta Wyatt, Sm Wells, Eb Klein, Je Robinson, Dj Romberger, Ja Poole

{"title":"Dimethylarginine dimethylaminohydrolase (DDAH) overexpression attenuates agricultural organic dust extract-induced inflammation.","authors":"Kl Bailey, Ta Wyatt, Sm Wells, Eb Klein, Je Robinson, Dj Romberger, Ja Poole","doi":"10.7178/jeit.15","DOIUrl":"10.7178/jeit.15","url":null,"abstract":"Modern, industrialized farming practices have lead to working conditions that include high levels of airborne dust. Agricultural workers inhale these complex organic dusts on a daily basis, leading to airway inflammation and higher risk for developing chronic obstructive pulmonary disease. The mechanisms regulating the organic dust-induced airway inflammatory response are not well-defined. We investigated whether overexpression of dimethylarginine dimethylaminohydrolase (DDAH) would lead to diminished pulmonary inflammation in an animal model of organic dust extract exposure. We instilled wild-type (WT) and DDAH overexpressing mice with an aqueous organic dust extract (ODE) collected from a swine confinement building. We found that inflammatory indices such as neutrophil influx and inflammatory cytokine production was lower in the DDAH overexpressing mice compared to WT after organic dust extract (ODE) instillation. We went on to determine how DDAH was mediating the decrease in inflammation induced by ODE. PKCα and PKCε play an essential role in the ODE inflammatory response. In a model of lung slices from WT and DDAH overexpressing mice, we demonstrated an increase in PKCα and PKCε in the WT mice exposed to ODE. This increase was diminished in the DDAH overexpressing mice exposed to ODE. We also tested an important component of the ODE, peptidoglycan (PGN). We noted a similar decrease in neutrophils and inflammatory cytokines in the DDAH overexpressing animals instilled with PGN compared to WT. In conclusion, our studies found a role for DDAH in regulating the ODE-triggered activation of epithelial PKCα and PKCε, a previously unrecognized mechanism of action. This ultimately results in diminished pulmonary inflammation.","PeriodicalId":90213,"journal":{"name":"Journal of environmental immunology and toxicology","volume":"2 2","pages":"72-78"},"PeriodicalIF":0.0,"publicationDate":"2014-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159103/pdf/nihms519728.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32667479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Environmental exposures and innate immunity in the lung. 环境暴露与肺部先天免疫

Journal of environmental immunology and toxicology Pub Date : 2014-01-01 DOI: 10.7178/jeit.25

Steve N Georas, John Upham

引用次数: 2