@article{shipkowski_taylor_thompson_glista-baker_sayers_messenger_bauer_jaspers_bonner_2015, title={An allergic lung microenvironment suppresses carbon nanotube-induced inflammasome activation via STAT6-dependent inhibition of caspase-1}, volume={10}, number={6}, journal={PLoS One}, author={Shipkowski, K. A. and Taylor, A. J. and Thompson, E. A. and Glista-Baker, E. E. and Sayers, B. C. and Messenger, Z. J. and Bauer, R. N. and Jaspers, I. and Bonner, J. C.}, year={2015} }
 @article{thompson_sayers_glista-baker_shipkowski_ihrie_duke_taylor_bonner_2015, title={Role of Signal Transducer and Activator of Transcription 1 in Murine Allergen-Induced Airway Remodeling and Exacerbation by Carbon Nanotubes}, volume={53}, ISSN={["1535-4989"]}, DOI={10.1165/rcmb.2014-0221oc}, abstractNote={Asthma is characterized by a T helper type 2 phenotype and by chronic allergen-induced airway inflammation (AAI). Environmental exposure to air pollution ultrafine particles (i.e., nanoparticles) exacerbates AAI, and a concern is possible exacerbation posed by engineered nanoparticles generated by emerging nanotechnologies. Signal transducer and activator of transcription (STAT) 1 is a transcription factor that maintains T helper type 1 cell development. However, the role of STAT1 in regulating AAI or exacerbation by nanoparticles has not been explored. In this study, mice with whole-body knockout of the Stat1 gene (Stat1(-/-)) or wild-type (WT) mice were sensitized to ovalbumin (OVA) allergen and then exposed to multiwalled carbon nanotubes (MWCNTs) by oropharygneal aspiration. In Stat1(-/-) and WT mice, OVA increased eosinophils in bronchoalveolar lavage fluid, whereas MWCNTs increased neutrophils. Interestingly, OVA sensitization prevented MWCNT-induced neutrophilia and caused only eosinophilic inflammation. Stat1(-/-) mice displayed increased IL-13 in bronchoalveolar lavage fluid at 1 day compared with WT mice after treatment with OVA or OVA and MWCNTs. At 21 days, the lungs of OVA-sensitized Stat1(-/-) mice displayed increased eosinophilia, goblet cell hyperplasia, airway fibrosis, and subepithelial apoptosis. MWCNTs further increased OVA-induced goblet cell hyperplasia, airway fibrosis, and apoptosis in Stat1(-/-) mice at 21 days. These changes corresponded to increased levels of profibrogenic mediators (transforming growth factor-β1, TNF-α, osteopontin) but decreased IL-10 in Stat1(-/-) mice. Finally, fibroblasts isolated from the lungs of Stat1(-/-) mice produced significantly more collagen mRNA and protein in response to transforming growth factor-β1 compared with WT lung fibroblasts. Our results support a protective role for STAT1 in chronic AAI and exacerbation of remodeling caused by MWCNTs.}, number={5}, journal={AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY}, author={Thompson, Elizabeth A. and Sayers, Brian C. and Glista-Baker, Ellen E. and Shipkowski, Kelly A. and Ihrie, Mark D. and Duke, Katherine S. and Taylor, Alexia J. and Bonner, James C.}, year={2015}, month={Nov}, pages={625–636} }
 @article{glista-baker_taylor_sayers_thompson_bonner_2014, title={Nickel Nanoparticles cause exaggerated lung and airway remodeling in mice lacking the T-box transcription factor, TBX21 (T-bet)}, volume={11}, journal={Particle and Fibre Toxicology}, author={Glista-Baker, E. E. and Taylor, A. J. and Sayers, B. C. and Thompson, E. A. and Bonner, J. C.}, year={2014} }
 @article{sayers_taylor_glista-baker_shipley-phillips_dackor_edin_lih_tomer_zeldin_langenbach_et al._2013, title={Role of Cyclooxygenase-2 in Exacerbation of Allergen-Induced Airway Remodeling by Multiwalled Carbon Nanotubes}, volume={49}, ISSN={["1535-4989"]}, DOI={10.1165/rcmb.2013-0019oc}, abstractNote={The emergence of nanotechnology has produced a multitude of engineered nanomaterials such as carbon nanotubes (CNTs), and concerns have been raised about their effects on human health, especially for susceptible populations such as individuals with asthma. Multiwalled CNTs (MWCNTs) have been shown to exacerbate ovalbumin (OVA)-induced airway remodeling in mice. Moreover, cyclooxygenase-2 (COX-2) has been described as a protective factor in asthma. We postulated that COX-2-deficient (COX-2(-/-)) mice would be susceptible to MWCNT-induced exacerbations of allergen-induced airway remodeling, including airway inflammation, fibrosis, and mucus-cell metaplasia (i.e., the formation of goblet cells). Wild-type (WT) or COX-2(-/-) mice were sensitized to OVA to induce allergic airway inflammation before a single dose of MWCNTs (4 mg/kg) delivered to the lungs by oropharyngeal aspiration. MWCNTs significantly increased OVA-induced lung inflammation and mucus-cell metaplasia in COX-2(-/-) mice compared with WT mice. However, airway fibrosis after exposure to allergen and MWCNTs was no different between WT and COX-2(-/-) mice. Concentrations of certain prostanoids (prostaglandin D2 and thromboxane B2) were enhanced by OVA or MWCNTs in COX-2(-/-) mice. No differences in COX-1 mRNA concentrations were evident between WT and COX-2(-/-) mice treated with OVA and MWCNTs. Interestingly, MWCNTs significantly enhanced allergen-induced cytokines involved in Th2 (IL-13 and IL-5), Th1 (CXCL10), and Th17 (IL-17A) inflammatory responses in COX-2(-/-) mice, but not in WT mice. We conclude that exacerbations of allergen-induced airway inflammation and mucus-cell metaplasia by MWCNTs are enhanced by deficiencies in COX-2, and are associated with the activation of a mixed Th1/Th2/Th17 immune response.}, number={4}, journal={AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY}, author={Sayers, Brian C. and Taylor, Alexia J. and Glista-Baker, Ellen E. and Shipley-Phillips, Jeanette K. and Dackor, Ryan T. and Edin, Matthew L. and Lih, Fred B. and Tomer, Kenneth B. and Zeldin, Darryl C. and Langenbach, Robert and et al.}, year={2013}, month={Oct}, pages={525–535} }
 @article{lee_sayers_chun_lao_shipley-phillips_bonner_langenbach_2012, title={Multi-walled carbon nanotubes induce COX-2 and iNOS expression via MAP Kinase-dependent and -independent mechanisms in mouse RAW264.7 macrophages}, volume={9}, journal={Particle and Fibre Toxicology}, author={Lee, J. K. and Sayers, B. C. and Chun, K. S. and Lao, H. C. and Shipley-Phillips, J. K. and Bonner, J. C. and Langenbach, R.}, year={2012} }
 @article{glista-baker_taylor_sayers_thompson_bonner_2012, title={Nickel Nanoparticles Enhance Platelet-Derived Growth Factor-Induced Chemokine Expression by Mesothelial Cells via Prolonged Mitogen-Activated Protein Kinase Activation}, volume={47}, ISSN={["1535-4989"]}, DOI={10.1165/rcmb.2012-0023oc}, abstractNote={Pleural diseases (fibrosis and mesothelioma) are a major concern for individuals exposed by inhalation to certain types of particles, metals, and fibers. Increasing attention has focused on the possibility that certain types of engineered nanoparticles (NPs), especially those containing nickel, might also pose a risk for pleural diseases. Platelet-derived growth factor (PDGF) is an important mediator of fibrosis and cancer that has been implicated in the pathogenesis of pleural diseases. In this study, we discovered that PDGF synergistically enhanced nickel NP (NiNP)-induced increases in mRNA and protein levels of the profibrogenic chemokine monocyte chemoattractant protein-1 (MCP-1 or CCL2), and the antifibrogenic IFN-inducible CXC chemokine (CXCL10) in normal rat pleural mesothelial 2 (NRM2) cells in vitro. Carbon black NPs (CBNPs), used as a negative control NP, did not cause a significant increase in CCL2 or CXCL10 in the absence or presence of PDGF. NiNPs prolonged PDGF-induced phosphorylation of the mitogen-activated protein kinase family termed extracellular signal-regulated kinases (ERK)-1 and -2 for up to 24 hours, and NiNPs also synergistically increased PDGF-induced hypoxia-inducible factor (HIF)-1α protein levels in NRM2 cells. Inhibition of ERK-1,2 phosphorylation with the mitogen-activated protein kinase kinase (MEK) inhibitor, PD98059, blocked the synergistic increase in CCL2, CXCL10, and HIF-1α levels induced by PDGF and NiNPs. Moreover, the antioxidant, N-acetyl-L-cysteine (NAC), significantly reduced HIF-1α, ERK-1,2 phosphorylation, and CCL2 protein levels that were synergistically increased by the combination of PDGF and NiNPs. These data indicate that NiNPs enhance the activity of PDGF in regulating chemokine production in NRM2 cells through a mechanism involving reactive oxygen species generation and prolonged activation of ERK-1,2.}, number={4}, journal={AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY}, author={Glista-Baker, Ellen E. and Taylor, Alexia J. and Sayers, Brian C. and Thompson, Elizabeth A. and Bonner, James C.}, year={2012}, month={Oct}, pages={552–561} }