DOI . ORG {}

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We began analyzing https://www.dovepress.com/lung-inflammation-caused-by-inhaled-toxicants-a-review-peer-reviewed-fulltext-article-COPD, but it redirected us to https://www.dovepress.com/lung-inflammation-caused-by-inhaled-toxicants-a-review-peer-reviewed-fulltext-article-COPD. The analysis below is for the second page.

Title[redir]:
Lung inflammation caused by inhaled toxicants: a review | COPD
Description:
Lung inflammation caused by inhaled toxicants: a review John Wong, Bruce E Magun, Lisa J Wood School of Nursing, MGH Institute of Health Professions, Boston, MA, USA Abstract: Exposure of the lungs to airborne toxicants from different sources in the environment may lead to acute and chronic pulmonary or even systemic inflammation. Cigarette smoke is the leading cause of chronic obstructive pulmonary disease, although wood smoke in urban areas of underdeveloped countries is now recognized as a leading cause of respiratory disease. Mycotoxins from fungal spores pose an occupational risk for respiratory illness and also present a health hazard to those living in damp buildings. Microscopic airborne particulates of asbestos and silica (from building materials) and those of heavy metals (from paint) are additional sources of indoor air pollution that contributes to respiratory illness and is known to cause respiratory illness in experimental animals. Ricin in aerosolized form is a potential bioweapon that is extremely toxic yet relatively easy to produce. Although the aforementioned agents belong to different classes of toxic chemicals, their pathogenicity is similar. They induce the recruitment and activation of macrophages, activation of mitogen-activated protein kinases, inhibition of protein synthesis, and production of interleukin-1 beta. Targeting either macrophages (using nanoparticles) or the production of interleukin-1 beta (using inhibitors against protein kinases, NOD-like receptor protein-3, or P2X7) may potentially be employed to treat these types of lung inflammation without affecting the natural immune response to bacterial infections. Keywords: cigarette, mycotoxin, trichothecene, ricin, inflammasome, macrophage, inhibitors

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Health & Fitness
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Custom-built

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🌟 Strong Traffic: 100k - 200k visitors per month

Based on our best estimate, this website will receive around 100,019 visitors per month in the current month.
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We don't see any clear sign of profit-making.

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Keywords {🔍}

inflammation, lung, ricin, cells, pulmonary, cigarette, disease, smoke, macrophages, chronic, inflammasome, inflammatory, kinase, protein, activation, copd, obstructive, response, cell, ilβ, expression, toxicol, mycotoxins, airway, respir, human, biol, receptor, med, immunol, effects, signaling, exposure, production, role, cytokine, toxicants, inhibitors, epithelial, mapk, nlrp, inhalation, alveolar, mol, immune, pathways, cytokines, review, health, kinases,

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tumor necrosis factor-alpha il-1r1/myd88 signaling dependent multi-walled carbon nanotubes multi-wall carbon nanotubes transforming growth factor-beta1 mitogen-activated protein kinase nf-kappab-dependent gene expression pre-adaptive pharmacophores stress-activated map kinases unique structure-based rationales mitogen-activated protein kinases tnf-alpha-converting enzyme aryl-substituted dihydropyrrolopyrazole quinoline src-erk/ap-1 pathways enzyme-linked immunosorbent assay anti-proline-glycine-proline silica-induced tnf-alpha nucleotide-binding oligomerization domain 164 5-chloro-2-methoxy-n-[2 dove medical press reduce nf-kappab activation toluene diisocyanate-induced asthma mapk-activated protein kinases cigarette smoke-induced emphysema toxicant-induced lung inflammation ligand-bound receptor forms effector t-cell dysfunction manuscript login dysregulated nf-κb activity inhibit tnf-α signaling nf-kappab signaling inflammasome-caspase1/11-il-1/18 axis inhibits tnf-α signaling mapk kinase kinase mature il-1β product effective anti-inflammatory treatments including fast-track processing chrysotile asbestos protein complex called anti-inflammatory compounds parthenolide national center nlrp3-inflammasome-dependent manner favored authors cytokine induced jnk ricin-mediated gene expression nf-κb pathway anti-tnf-α therapy murine cd4+ t-cells reactive oxygen species mapk kinase kinases

Questions {❓}

Do lower respiratory tract infections in early childhood cause chronic obstructive pulmonary disease?
Is alveolar destruction and emphysema in chronic obstructive pulmonary disease an immune disease?
Review: Is lung inflammation associated with microbes and microbial toxins in cigarette tobacco smoke?
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