@article{cesta_ryman-rasmussen_wallace_masinde_hurlburt_taylor_bonner_2010, title={Bacterial Lipopolysaccharide Enhances PDGF Signaling and Pulmonary Fibrosis in Rats Exposed to Carbon Nanotubes}, volume={43}, ISSN={["1535-4989"]}, DOI={10.1165/rcmb.2009-0113oc}, abstractNote={Engineered multi-walled carbon nanotubes (MWCNT) represent a possible health risk for pulmonary fibrosis due to their fiber-like shape and potential for persistence in the lung. We postulated that bacterial lipopolysaccharide (LPS), a ubiquitous agent in the environment that causes lung inflammation, would enhance fibrosis caused by MWCNT. Rats were exposed to LPS and then intratracheally instilled with MWCNT or carbon black (CB) nanoparticles 24 hours later. Pulmonary fibrosis was observed 21 days after MWCNT exposure, but not with CB. LPS alone caused no fibrosis but enhanced MWCNT-induced fibrosis. LPS plus CB did not significantly increase fibrosis. MWCNT increased platelet-derived growth factor-AA (PDGF-AA), a major mediator of fibrosis. PDGF-AA production in response to MWCNT, but not CB, was synergistically enhanced by LPS. Immunostaining showed PDGF-AA in bronchiolar epithelial cells and macrophages. Since macrophages engulfed MWCNT, were positive for PDGF-AA, and mediate fibroblast responses, experiments were performed with rat lung macrophages (NR8383 cells) and rat lung fibroblasts in vitro. LPS exposure increased PDGF-A mRNA levels in NR8383 cells and enhanced MWCNT-induced PDGF-A mRNA levels. Moreover, LPS increased MWCNT- or CB-induced PDGF receptor-alpha (PDGF-Ralpha) mRNA in fibroblasts. Our data suggest that LPS exacerbates MWCNT-induced lung fibrosis by amplifying production of PDGF-AA in macrophages and epithelial cells, and by increasing PDGF-Ralpha on pulmonary fibroblasts. Our findings also suggest that individuals with pre-existing pulmonary inflammation are at greater risk for the potential adverse effects of MWCNT.}, number={2}, journal={AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY}, author={Cesta, Mark F. and Ryman-Rasmussen, Jessica P. and Wallace, Duncan G. and Masinde, Tiwanda and Hurlburt, Geoffrey and Taylor, Alexia J. and Bonner, James C.}, year={2010}, month={Aug}, pages={142–151} }
 @article{ryman-rasmussen_tewksbury_moss_cesta_wong_bonner_2009, title={Inhaled Multiwalled Carbon Nanotubes Potentiate Airway Fibrosis in Murine Allergic Asthma}, volume={40}, ISSN={["1535-4989"]}, DOI={10.1165/rcmb.2008-0276OC}, abstractNote={Carbon nanotubes are gaining increasing attention due to possible health risks from occupational or environmental exposures. This study tested the hypothesis that inhaled multiwalled carbon nanotubes (MWCNT) would increase airway fibrosis in mice with allergic asthma. Normal and ovalbumin-sensitized mice were exposed to a MWCNT aerosol (100 mg/m(3)) or saline aerosol for 6 hours. Lung injury, inflammation, and fibrosis were examined by histopathology, clinical chemistry, ELISA, or RT-PCR for cytokines/chemokines, growth factors, and collagen at 1 and 14 days after inhalation. Inhaled MWCNT were distributed throughout the lung and found in macrophages by light microscopy, but were also evident in epithelial cells by electron microscopy. Quantitative morphometry showed significant airway fibrosis at 14 days in mice that received a combination of ovalbumin and MWCNT, but not in mice that received ovalbumin or MWCNT only. Ovalbumin-sensitized mice that did not inhale MWCNT had elevated levels IL-13 and transforming growth factor (TGF)-beta1 in lung lavage fluid, but not platelet-derived growth factor (PDGF)-AA. In contrast, unsensitized mice that inhaled MWCNT had elevated PDGF-AA, but not increased levels of TGF-beta1 and IL-13. This suggested that airway fibrosis resulting from combined ovalbumin sensitization and MWCNT inhalation requires PDGF, a potent fibroblast mitogen, and TGF-beta1, which stimulates collagen production. Combined ovalbumin sensitization and MWCNT inhalation also synergistically increased IL-5 mRNA levels, which could further contribute to airway fibrosis. These data indicate that inhaled MWCNT require pre-existing inflammation to cause airway fibrosis. Our findings suggest that individuals with pre-existing allergic inflammation may be susceptible to airway fibrosis from inhaled MWCNT.}, number={3}, journal={AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY}, author={Ryman-Rasmussen, Jessica P. and Tewksbury, Earl W. and Moss, Owen R. and Cesta, Mark F. and Wong, Brian A. and Bonner, James C.}, year={2009}, month={Mar}, pages={349–358} }
 @article{ryman-rasmussen_cesta_brody_shipley-phillips_everitt_tewksbury_moss_wong_dodd_andersen_et al._2009, title={Inhaled carbon nanotubes reach the subpleural tissue in mice}, volume={4}, ISSN={["1748-3395"]}, DOI={10.1038/NNANO.2009.305}, abstractNote={Carbon nanotubes are shaped like fibres and can stimulate inflammation at the surface of the peritoneum when injected into the abdominal cavity of mice, raising concerns that inhaled nanotubes may cause pleural fibrosis and/or mesothelioma. Here, we show that multiwalled carbon nanotubes reach the subpleura in mice after a single inhalation exposure of 30 mg m(-3) for 6 h. Nanotubes were embedded in the subpleural wall and within subpleural macrophages. Mononuclear cell aggregates on the pleural surface increased in number and size after 1 day and nanotube-containing macrophages were observed within these foci. Subpleural fibrosis unique to this form of nanotubes increased after 2 and 6 weeks following inhalation. None of these effects was seen in mice that inhaled carbon black nanoparticles or a lower dose of nanotubes (1 mg m(-3)). This work suggests that minimizing inhalation of nanotubes during handling is prudent until further long-term assessments are conducted.}, number={11}, journal={NATURE NANOTECHNOLOGY}, author={Ryman-Rasmussen, Jessica P. and Cesta, Mark F. and Brody, Arnold R. and Shipley-Phillips, Jeanette K. and Everitt, Jeffrey I. and Tewksbury, Earl W. and Moss, Owen R. and Wong, Brian A. and Dodd, Darol E. and Andersen, Melvin E. and et al.}, year={2009}, month={Nov}, pages={747–751} }
 @article{antao-menezes_turpin_bost_ryman-rasmussen_bonner_2008, title={STAT-1 signaling in human lung fibroblasts is induced by vanadium pentoxide through an IFN-beta autocrine loop}, volume={180}, ISSN={["1550-6606"]}, DOI={10.4049/jimmunol.180.6.4200}, abstractNote={Abstract}, number={6}, journal={JOURNAL OF IMMUNOLOGY}, author={Antao-Menezes, Aurita and Turpin, Elizabeth A. and Bost, Phillip C. and Ryman-Rasmussen, Jessica P. and Bonner, James C.}, year={2008}, month={Mar}, pages={4200–4207} }
 @article{rouse_yang_ryman-rasmussen_barron_monteiro-riviere_2007, title={Effects of mechanical flexion on the penetration of fullerene amino acid-derivatized peptide nanoparticles through skin}, volume={7}, ISSN={["1530-6992"]}, url={http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=ORCID&SrcApp=OrcidOrg&DestLinkType=FullRecord&DestApp=WOS_CPL&KeyUT=WOS:000243381300027&KeyUID=WOS:000243381300027}, DOI={10.1021/nl062464m}, abstractNote={Dermatomed porcine skin was fixed to a flexing device and topically dosed with 33.5 mg.mL-1 of an aqueous solution of a fullerene-substituted phenylalanine (Baa) derivative of a nuclear localization peptide sequence (Baa-Lys(FITC)-NLS). Skin was flexed for 60 or 90 min or left unflexed (control). Confocal microscopy depicted dermal penetration of the nanoparticles at 8 h in skin flexed for 60 and 90 min, whereas Baa-Lys(FITC)-NLS did not penetrate into the dermis of unflexed skin until 24 h. TEM analysis revealed fullerene-peptide localization within the intercellular spaces of the stratum granulosum.}, number={1}, journal={NANO LETTERS}, author={Rouse, Jillian G. and Yang, Jianzhong and Ryman-Rasmussen, Jessica P. and Barron, Andrew R. and Monteiro-Riviere, Nancy A.}, year={2007}, month={Jan}, pages={155–160} }
 @article{ryman-rasmussen_riviere_monteiro-riviere_2007, title={Surface coatings determine cytotoxicity and irritation potential of quantum dot nanoparticles in epidermal keratinocytes}, volume={127}, ISSN={["1523-1747"]}, url={http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=ORCID&SrcApp=OrcidOrg&DestLinkType=FullRecord&DestApp=WOS_CPL&KeyUT=WOS:000243192200021&KeyUID=WOS:000243192200021}, DOI={10.1038/sj.jid.5700508}, abstractNote={Quantum dot (QD) nanoparticles have potential applications in nanomedicine as drug delivery vectors and diagnostic agents, but the skin toxicity and irritation potential of QDs are unknown. Human epidermal keratinocytes (HEKs) were used to assess if QDs with different surface coatings would cause differential effects on HEK cytotoxicity, proinflammatory cytokine release, and cellular uptake. Commercially available QDs of two different sizes, QD 565 and QD 655, with neutral (polyethylene glycol (PEG)), cationic (PEG-amine), or anionic (carboxylic acid) coatings were utilized. Live cell imaging and transmission electron microscopy were used to determine that all QDs localized intracellularly by 24 hours, with evidence of QD localization in the nucleus. Cytotoxicity and release of the proinflammatory cytokines IL-1β, IL-6, IL-8, IL-10, and tumor necrosis factor-α were assessed at 24 and 48 hours. Cytotoxicity was observed for QD 565 and QD 655 coated with carboxylic acids or PEG-amine by 48 hours, with little cytotoxicity observed for PEG-coated QDs. Only carboxylic acid-coated QDs significantly increased release of IL-1β, IL-6, and IL-8. These data indicate that QD surface coating is a primary determinant of cytotoxicity and immunotoxicity in HEKs, which is consistent across size. However, uptake of QDs by HEKs is independent of surface coating. Quantum dot (QD) nanoparticles have potential applications in nanomedicine as drug delivery vectors and diagnostic agents, but the skin toxicity and irritation potential of QDs are unknown. Human epidermal keratinocytes (HEKs) were used to assess if QDs with different surface coatings would cause differential effects on HEK cytotoxicity, proinflammatory cytokine release, and cellular uptake. Commercially available QDs of two different sizes, QD 565 and QD 655, with neutral (polyethylene glycol (PEG)), cationic (PEG-amine), or anionic (carboxylic acid) coatings were utilized. Live cell imaging and transmission electron microscopy were used to determine that all QDs localized intracellularly by 24 hours, with evidence of QD localization in the nucleus. Cytotoxicity and release of the proinflammatory cytokines IL-1β, IL-6, IL-8, IL-10, and tumor necrosis factor-α were assessed at 24 and 48 hours. Cytotoxicity was observed for QD 565 and QD 655 coated with carboxylic acids or PEG-amine by 48 hours, with little cytotoxicity observed for PEG-coated QDs. Only carboxylic acid-coated QDs significantly increased release of IL-1β, IL-6, and IL-8. These data indicate that QD surface coating is a primary determinant of cytotoxicity and immunotoxicity in HEKs, which is consistent across size. However, uptake of QDs by HEKs is independent of surface coating. Hank's balanced salt solution human epidermal keratinocyte keratinocyte growth medium-2 polyethylene glycol quantum dot transmission electron microscopy 3-[4,5]dimethylthiazol-2,5 dephenyltetrazolium bromide}, number={1}, journal={JOURNAL OF INVESTIGATIVE DERMATOLOGY}, author={Ryman-Rasmussen, Jessica P. and Riviere, Jim E. and Monteiro-Riviere, Nancy A.}, year={2007}, month={Jan}, pages={143–153} }
 @article{ryman-rasmussen_riviere_monteiro-riviere_2007, title={Variables influencing interactions of untargeted quantum dot nanoparticles with skin cells and identification of biochemical modulators}, volume={7}, ISSN={["1530-6992"]}, url={http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=ORCID&SrcApp=OrcidOrg&DestLinkType=FullRecord&DestApp=WOS_CPL&KeyUT=WOS:000246313000041&KeyUID=WOS:000246313000041}, DOI={10.1021/nl070375j}, abstractNote={Skin cells (NHEK) take up untargeted quantum dots (QD) with surface polyethylene glycol (PEG), amines, and carboxylic acids, but the mechanisms are unknown. Time courses of QD-NHEK interactions were determined and effects of QD surface coating, temperature, culture medium supplements and inhibitors of the cell cycle and endocytosis identified. The magnitude of QD-NHEK interactions was coating dependent. Low-temperature or unsupplemented medium decreased QD-NHEK interactions. Biochemical inhibitors were identified that attenuate and potentiate QD-NHEK interactions. These results are important for understanding and controlling interactions of untargeted QD with cells.}, number={5}, journal={NANO LETTERS}, author={Ryman-Rasmussen, Jessica P. and Riviere, Jim E. and Monteiro-Riviere, Nancy A.}, year={2007}, month={May}, pages={1344–1348} }
 @inbook{monteiro-riviere_ryman-rasmussen_2006, title={Toxicology of nanomaterials}, ISBN={082472979X}, booktitle={Biological concepts and techniques in toxicology: An integrated approach}, publisher={New York: Taylor & Francis}, author={Monteiro-Riviere, N. A. and Ryman-Rasmussen, J. P.}, year={2006}, pages={217–233} }
 @article{agbasi-porter_ryman-rasmussen_franzen_feldheim_2006, title={Transcription inhibition using oligonucleotide-modified gold nanoparticles}, volume={17}, ISSN={["1043-1802"]}, DOI={10.1021/bc060100f}, abstractNote={The capture of T7 RNA polymerase using double-stranded promoter DNA on the surface of gold nanoparticles has been demonstrated. The competitive binding and inhibition of T7 RNA polymerase due to specific interactions on the nanoparticle surface represents a transcription factor decoy approach in a model system. The efficiency of inhibition was determined for various nanoparticle sizes, surface coverage, and linker length for double-stranded promoter DNA on gold nanoparticles. The experiments provide a basis for determining the accessibility of binding sites on nanoparticle surfaces for applications involving cell targeting or the use of nanoparticles as binding agents in solution.}, number={5}, journal={BIOCONJUGATE CHEMISTRY}, author={Agbasi-Porter, Chiamaka and Ryman-Rasmussen, Jessica and Franzen, Stefan and Feldheim, Daniel}, year={2006}, month={Sep}, pages={1178–1183} }