- Title Information
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- A
- Title
- safer alternative? Investigating the impact of e-cigarettes on pulmonary
inflammation, tissue repair, and infectious disease
- Name:
Personal
- Name Part
- Yu, Tammy
- Role
- Role Term:
Text
- creator
- Name:
Personal
- Name Part
- Jamieson, Amanda
- Role
- Role Term:
Text
- advisor
- affiliation
- Brown University. Department of Molecular Microbiology and
Immunology
- Name:
Corporate
- Name Part
- Brown University. Summer Research Assistantship in Biomedical
Sciences
- Role
- Role Term:
Text
- research program
- Type of Resource
- still image
- Genre (aat)
- posters
- Origin Information
- Place
- Place Term:
Text
- Providence
- Publisher
- Brown University
- Date Created
(encoding="w3cdtf")
- 2015-08-07
- Physical Description
- Extent
- 1 poster
- digitalOrigin
- reformatted digital
- Abstract
- E-cigarettes (e-cigs) are often marketed and perceived as safer substitutes for
traditional tobacco products. These devices use batteries to aerosolize and deliver
nicotine, avoiding the formation of toxic combustion compounds that occurs when conventional
cigarettes are burned. Nevertheless, both known and potential toxins have been identified in
e-cig vapor. Some of these, such as volatile carbon compounds and nitrosamines, are also
found in tobacco smoke. Others may be derived from the solvent and flavoring components of
e-cig fluid. Little conclusive data exist on the safety of e-cigarettes, particularly when
exposure occurs repeatedly over many years. Given that annual e-cig use in the US is now
growing exponentially, particularly among adolescents and young adults, comprehensive
studies of the health effects of these devices are urgently needed. Environmental stressors
like tobacco smoke and e-cigarette vapor can have multiple effects on the respiratory
system. Cytotoxicity, whether immediate or delayed, is one of these. In addition, changes in
gene transcription may occur as the lung activates various stress, inflammatory, and tissue
repair pathways. Resident alveolar macrophage (MΦ) cells are key players in these responses.
Depending on environmental cues, they can assume pro- or anti-inflammatory phenotypes (M1
and M2 respectively), regulating the delicate balance between inflammation and tissue
repair. Over time, exposure to toxins can dysregulate these functions, leading to
pathological inflammation, increased susceptibility to infections, and carcinogenesis. We
hypothesized that components in e-cigarette vapor induce cytotoxicity and cell damage in the
lung. Exposure to e-cigs was also predicted to upregulate inflammatory and stress responses,
especially when acting synergistically with common respiratory infectious agents. Bone
marrow macrophages were used as in vitro models of alveolar macrophages. We assessed the
effects of treatment with e-cigarette extract (ECE), both alone and in conjunction with
influenza virus or Streptococcus pneumoniae, on cell viability, transcriptional activity,
and phenotype.
- Subject (LCSH)
- Topic
- Electronic cigarettes
- Subject (LCSH)
- Topic
- Smoking
- Subject (LCSH)
- Topic
- Respiratory infections
- Subject (LCSH)
- Topic
- Lungs
- Subject (LCSH)
- Topic
- Inflammation
- Identifier:
DOI
- 10.26300/v1eh-6z97