MatTek Poster Sessions at ATS 2016
MatTek is attending and hosting poster discussion sessions at the American Thoracic Society (ATS) 2016 International Conference. Attend our poster sessions to see the latest we’ve been working on and our plans for the future!
Poster Session:
A26-SMOKE, POLLUTANTS, AND TOXINS: INSIGHTS FROM BENCH STUDIES
Poster Discussion Session
Sunday, May 15, 2016
9:00 AM-11:00 AM
Room 2010/2012 (West Building, Level 2), MOSCONE CENTER
Poster Details:
Development of an In Vitro Test to Assess the Inhalation Toxicity of Nanomaterials
Patrick Hayden4, Monita Sharma1, Hana Barosova2, Savvina Chortarea2, Fikad Zerimariam2, Martin Clift2, Vicki Stone3, Anna Maione4, Amy Clippinger1, Barbara Rothen-Rutishauser2
1PETA International Science Consortium Ltd., UK, 2Adolphe Merkle Institute, University of Fribourg, CH, 3Heriot-Watt University, UK, 4MatTek Corporation, USA.
Poster Board Number: 420 | Abstract Number: A1200
Viewing Time: 9:00-9:45 | Discussion Time: 9:45-11:00
RATIONALE: The increasing use of multi-walled carbon nanotubes (MWCNTs) in consumer products and their potential to induce adverse lung effects following inhalation has lead to much interest in better understanding the hazard associated with these nanomaterials (NMs). While the current regulatory requirement for substances of concern in many jurisdictions is a 90-day rodent inhalation test, the monetary, ethical, and scientific concerns associated with this assay led an international expert group to convene in February 2015 to discuss the approaches to evaluate inhalation toxicity of MWCNTs (https://www.thepsci.eu/pulmonary_fibrosis/). Pulmonary fibrosis was identified as a key adverse outcome linked to MWCNT exposure and recommendations were made on the design of an in vitro assay that is predictive of the (pro-)fibrotic potential of MWCNTs. Subsequently, work began to develop and optimize in vitro co-culture systems using relevant lung cells exposed to MWCNTs at the air-liquid interface (ALI) while considering human-relevant CONCLUSIONS: First experiments showed that The long-term goal of this work is to develop an in vitro testing strategy using human-relevant methods to predict pulmonary toxicity and to enable effective risk assessment of substances including MWCNTs. FUNDING: This work was funded by the PETA International Science Consortium.
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Be sure to also check out this work by Boston University, UCLA and MatTek using EpiAirway:
Poster Session:
A26-SMOKE, POLLUTANTS, AND TOXINS: INSIGHTS FROM BENCH STUDIES
Poster Discussion Session
Sunday, May 15, 2016
9:00 AM-11:00 AM
Room 2010/2012 (West Building, Level 2), MOSCONE CENTER
Poster Details:
Molecular Impact of Electronic Cigarette Exposure on Airway Epithelium
S Corbett1, M Nitzberg1, ES Moses1, T Wang1, GR Jackson2, E Drizik1, C Perdomo1, C Perdomo3, E Kleerup3, D Brooks1, GT O’Connor1, SM Dubinett3, P Hayden2, ME Lenburg1 and A Spira1
1BU, Boston MA. 2MaTek Corp, Ashland MA. 3UCLA, Los Angeles CA.
Rationale: Electronic cigarettes (ECIGs) simulate cigarette smoking by delivering nicotine via an aerosol and are advertised as an alternative to tobacco cigarette (TCIG) smoking. However, there are few studies evaluating the physiological impact of ECIG use. Our objective was to determine the cellular and molecular impact of ECIG aerosol on human bronchial epithelial cells (1) in vivo and (2) in vitro. Methods: For the in vivo arm of this study, we profiled bronchial epithelial cells from the mainstem bronchus of former TCIG smokers (n=16) and former smokers who have transitioned to ECIGs for at least 1 month (n=17), as well as current TCIG smokers (n=9). For the in vitro arm, human bronchial epithelial cells (HBECs) differentiated at an Air Liquid Interface (ALI) were directly exposed to ECIG vapor or TCIG smoke. ECIG exposures varied by dose, flavorings, and nicotine content. Gene expression of both in vivo and in vitro samples was measured using Affymetrix HuGene ST 1.0 microarrays. Results: In vivo, we demonstrated that previously published gene sets associated with TCIG smoking were enriched in the airways of both TCIG smokers and ECIG users, suggesting that the transcriptional effects of TCIGs and ECIGs have some similarity in vivo. We also demonstrated that genes differentially expressed between ECIG and air exposed samples in vitro are enriched in ECIG users in vivo, suggesting that our in vitro model is useful for modeling this exposure’s effects. Further investigation into the mechanisms of TCIG and ECIG exposure in vitro revealed that ECIG exposure, like TCIG exposure, induces genes involved in response to oxidative and xenobiotic stress, and downregulates genes involved in cilia assembly and movement. We also found similar functional enrichment in our in vivo samples. Conclusions: Together, these results indicate that ECIG vapor can induce cellular stress and molecular alterations within airway epithelium that share similarities with the effects of TCIG smoke. These findings underscore the urgent need for long-term studies of ECIG users to better determine the type and magnitude of the cellular and molecular response to ECIG exposure.
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