@article {101,
	title = {Effects of Eyjafjallajokull volcanic ash on innate immune system responses and bacterial growth in vitro},
	journal = {Environmental health perspectives},
	volume = {121},
	year = {2013},
	note = {MEDLINE AN 2013450089(Journal; Article; (JOURNAL ARTICLE); (RESEARCH SUPPORT, N.I.H., EXTRAMURAL); (RESEARCH SUPPORT, U.S. GOV{\textquoteright}T, NON-P.H.S.))},
	pages = {691 - 8},
	abstract = {BACKGROUND:  On 20 March 2010, the Icelandic volcano Eyjafjallajokull erupted for the first time in 190 years.  Despite many epidemiological reports showing effects of volcanic ash on the respiratory system, there are limited data evaluating cellular mechanisms involved in the response to ash.  Epidemiological studies have observed an increase in respiratory infections in subjects and populations exposed to volcanic eruptions.  METHODS:  We physicochemically characterized volcanic ash, finding various sizes of particles, as well as the presence of several transition metals, including iron.  We examined the effect of Eyjafjallajokull ash on primary rat alveolar epithelial cells and human airway epithelial cells (20-100 μg/cm(2)), primary rat and human alveolar macrophages (5-20 μg/cm(2)), and Pseudomonas aeruginosa (PAO1) growth (3 μg/104 bacteria).  RESULTS:  Volcanic ash had minimal effect on alveolar and airway epithelial cell integrity.  In alveolar macrophages, volcanic ash disrupted pathogen-killing and inflammatory responses.  In in vitro bacterial growth models, volcanic ash increased bacterial replication and decreased bacterial killing by antimicrobial peptides.  CONCLUSIONS:  These results provide potential biological plausibility for epidemiological data that show an association between air pollution exposure and the development of respiratory infections.  These data suggest that volcanic ash exposure, while not seriously compromising lung cell function, may be able to impair innate immunity responses in exposed individuals.[on SciFinder (R)]},
	isbn = {1552-9924},
	author = {Monick, Martha M. and Baltrusaitis, Jonas and Powers, Linda S. and Borcherding, Jennifer A. and Caraballo, Juan C. and Mudunkotuwa, Imali and Peate, David W. and Walters, Katherine and Thompson, Jay M. and Grassian, Vicki H. and Gudmundsson, Gunnar and Comellas, Alejandro P.}
}
@article {136,
	title = {Influenza A Viral Replication Is Blocked by Inhibition of the Inositol-requiring Enzyme 1 (IRE1) Stress Pathway.},
	journal = {Journal of Biological Chemistry},
	volume = {287},
	year = {2012},
	note = {CAPLUS AN 2012:212308(Journal; Online Computer File)},
	month = {2012///},
	pages = {4679 - 4689},
	publisher = {American Society for Biochemistry and Molecular Biology},
	abstract = {Known therapies for influenza A virus infection are complicated by the frequent emergence of resistance.  A therapeutic strategy that may escape viral resistance is targeting host cellular mechanisms involved in viral replication and pathogenesis.  The endoplasmic reticulum (ER) stress response, also known as the unfolded protein response (UPR), is a primitive, evolutionary conserved mol. signaling cascade that has been implicated in multiple biol. phenomena including innate immunity and the pathogenesis of certain viral infections.  We investigated the effect of influenza A viral infection on ER stress pathways in lung epithelial cells.  Influenza A virus induced ER stress in a pathway-specific manner.  We showed that the virus activates the IRE1 pathway with little or no concomitant activation of the PERK and the ATF6 pathways.  When we examd. the effects of modulating the ER stress response on the virus, we found that the mol. chaperone tauroursodeoxycholic acid (TUDCA) significantly inhibits influenza A viral replication.  In addn., a specific inhibitor of the IRE1 pathway also blocked viral replication.  Our findings constitute the first evidence that ER stress plays a role in the pathogenesis of influenza A viral infection.  Decreasing viral replication by modulating the host ER stress response is a novel strategy that has important therapeutic implications. [on SciFinder(R)]},
	keywords = {influenza viral replication IRE1 stress pathway inhibition},
	isbn = {0021-9258},
	author = {Hassan, Ihab H. and Zhang, Michael S. and Powers, Linda S. and Shao, Jian Q. and Baltrusaitis, Jonas and Rutkowski, D. Thomas and Legge, Kevin and Monick, Martha M.}
}
@article {153,
	title = {Induction of Inflammasome-dependent Pyroptosis by Carbon Black Nanoparticles.},
	journal = {Journal of Biological Chemistry},
	volume = {286},
	year = {2011},
	note = {CAPLUS AN 2011:737835(Journal)},
	month = {2011///},
	pages = {21844 - 21852},
	publisher = {American Society for Biochemistry and Molecular Biology},
	abstract = {Inhalation of nanoparticles has been implicated in respiratory morbidity and mortality.  In particular, carbon black nanoparticles are found in many different environmental exposures.  Macrophages take up inhaled nanoparticles and respond via release of inflammatory mediators and in some cases cell death.  Based on new data, we propose that exposure of macrophages (both a macrophage cell line and primary human alveolar macrophages) to carbon black nanoparticles induces pyroptosis, an inflammasome-dependent form of cell death.  Exposure of macrophages to carbon black nanoparticles resulted in inflammasome activation as defined by cleavage of caspase 1 to its active form and downstream IL-1β release.  The cell death that occurred with carbon black nanoparticle exposure was identified as pyroptosis by the protective effect of a caspase 1 inhibitor and a pyroptosis inhibitor.  These data demonstrate that carbon black nanoparticle exposure activates caspase 1, increases IL-1β release after LPS priming, and induces the proinflammatory cell death, pyroptosis.  The identification of pyroptosis as a cellular response to carbon nanoparticle exposure is novel and relates to environmental and health impacts of carbon-based particulates. [on SciFinder(R)]},
	keywords = {carbon black nanoparticle immunotoxicity inflammasome pyroptosis},
	isbn = {0021-9258},
	author = {Reisetter, Anna C. and Stebounova, Larissa V. and Baltrusaitis, Jonas and Powers, Linda and Gupta, Amit and Grassian, Vicki H. and Monick, Martha M.}
}
