The biological effects of complete gasoline engine emissions exposure in a 3D human airway model (Mucilairtm) and in human bronchial epithelial cells (BEAS-2B)

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378041%3A_____%2F19%3A00518531" target="_blank" >RIV/68378041:_____/19:00518531 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68407700:21220/19:00335128 RIV/68407700:21230/19:00335128 RIV/00216208:11310/19:10409254 RIV/60460709:41310/19:81925

Výsledek na webu

<a href="https://www.mdpi.com/1422-0067/20/22/5710" target="_blank" >https://www.mdpi.com/1422-0067/20/22/5710</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3390/ijms20225710" target="_blank" >10.3390/ijms20225710</a>

Jazyk výsledku

angličtina

Název v původním jazyce

The biological effects of complete gasoline engine emissions exposure in a 3D human airway model (Mucilairtm) and in human bronchial epithelial cells (BEAS-2B)

Popis výsledku v původním jazyce

The biological effects induced by complete engine emissions in a 3D model of the human airway (MucilAir™) and in human bronchial epithelial cells (BEAS-2B) grown at the air–liquid interface were compared. The cells were exposed for one or five days to emissions generated by a Euro 5 direct injection spark ignition engine. The general condition of the cells was assessed by the measurement of transepithelial electrical resistance and mucin production. The cytotoxic effects were evaluated by adenylate kinase (AK) and lactate dehydrogenase (LDH) activity. Phosphorylation of histone H2AX was used to detect double-stranded DNA breaks. The expression of the selected 370 relevant genes was analyzed using next-generation sequencing. The exposure had minimal effects on integrity and AK leakage in both cell models. LDH activity and mucin production in BEAS-2B cells significantly increased after longer exposures, DNA breaks were also detected. The exposure affected CYP1A1 and HSPA5 expression in MucilAir™. There were no effects of this kind observed in BEAS-2B cells, in this system gene expression was rather affected by the time of treatment. The type of cell model was the most important factor modulating gene expression. In summary, the biological effects of complete emissions exposure were weak. In the specific conditions used in this study, the effects observed in BEAS-2B cells were induced by the exposure protocol rather than by emissions and thus this cell line seems to be less suitable for analyses of longer treatment than the 3D model.

Název v anglickém jazyce

The biological effects of complete gasoline engine emissions exposure in a 3D human airway model (Mucilairtm) and in human bronchial epithelial cells (BEAS-2B)

Popis výsledku anglicky

The biological effects induced by complete engine emissions in a 3D model of the human airway (MucilAir™) and in human bronchial epithelial cells (BEAS-2B) grown at the air–liquid interface were compared. The cells were exposed for one or five days to emissions generated by a Euro 5 direct injection spark ignition engine. The general condition of the cells was assessed by the measurement of transepithelial electrical resistance and mucin production. The cytotoxic effects were evaluated by adenylate kinase (AK) and lactate dehydrogenase (LDH) activity. Phosphorylation of histone H2AX was used to detect double-stranded DNA breaks. The expression of the selected 370 relevant genes was analyzed using next-generation sequencing. The exposure had minimal effects on integrity and AK leakage in both cell models. LDH activity and mucin production in BEAS-2B cells significantly increased after longer exposures, DNA breaks were also detected. The exposure affected CYP1A1 and HSPA5 expression in MucilAir™. There were no effects of this kind observed in BEAS-2B cells, in this system gene expression was rather affected by the time of treatment. The type of cell model was the most important factor modulating gene expression. In summary, the biological effects of complete emissions exposure were weak. In the specific conditions used in this study, the effects observed in BEAS-2B cells were induced by the exposure protocol rather than by emissions and thus this cell line seems to be less suitable for analyses of longer treatment than the 3D model.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30108 - Toxicology

Projekt

<a href="/cs/project/GA18-04719S" target="_blank" >GA18-04719S: Mechanismy toxicity emisí z benzinových motorů v 3D tkáňových kulturách a v modelové bronchiální epiteliální buněčné linii</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2019

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

International Journal of Molecular Sciences

ISSN

1422-0067

e-ISSN

—

Svazek periodika

20

Číslo periodika v rámci svazku

22

Stát vydavatele periodika

CH - Švýcarská konfederace

Počet stran výsledku

22

Strana od-do

5710

Kód UT WoS článku

000502786800192

EID výsledku v databázi Scopus

2-s2.0-85075115173