Aryl Hydrocarbon Receptor (AhR) Limits the Inflammatory Responses in Human Lung Adenocarcinoma A549 Cells via Interference with NF-kappa B Signaling

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68081707%3A_____%2F22%3A00555924" target="_blank" >RIV/68081707:_____/22:00555924 - isvavai.cz</a>

Alternative codes found

RIV/00159816:_____/22:00077580 RIV/00216224:14310/22:00128710

Result on the web

<a href="https://www.mdpi.com/2073-4409/11/4/707" target="_blank" >https://www.mdpi.com/2073-4409/11/4/707</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3390/cells11040707" target="_blank" >10.3390/cells11040707</a>

Result language

angličtina

Original language name

Aryl Hydrocarbon Receptor (AhR) Limits the Inflammatory Responses in Human Lung Adenocarcinoma A549 Cells via Interference with NF-kappa B Signaling

Original language description

Apart from its role in the metabolism of carcinogens, the aryl hydrocarbon receptor (AhR) has been suggested to be involved in the control of inflammatory responses within the respiratory tract. However, the mechanisms responsible for this are only partially known. In this study, we used A549 cell line, as a human model of lung alveolar type II (ATII)-like cells, to study the functional role of the AhR in control of inflammatory responses. Using IL-1 beta as an inflammation inducer, we found that the induction of cyclooxygenase-2 and secretion of prostaglandins, as well as expression and release of pro-inflammatory cytokines, were significantly higher in the AhR-deficient A549 cells. This was linked with an increased nuclear factor-kappa B (NF-kappa B) activity, and significantly enhanced phosphorylation of its regulators, IKK alpha/beta, and their target I kappa B alpha, in the AhR-deficient A549 cells. In line with this, when we mimicked the exposure to a complex mixture of airborne pollutants, using an organic extract of reference diesel exhaust particle mixture, an exacerbated inflammatory response was observed in the AhR-deficient cells, as compared with wild-type A549 cells. Together, the present results indicate that the AhR may act as a negative regulator of the inflammatory response in the A549 model, via a direct modulation of NF-kappa B signaling. Its role(s) in the control of inflammation within the lung alveoli exposed to airborne pollutants, especially those which simultaneously activate the AhR, thus deserve further attention.

Czech name

—

Czech description

—

Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

10601 - Cell biology

Project

<a href="/en/project/GA18-00145S" target="_blank" >GA18-00145S: Advanced in vitro models of lung epithelial cells for analysis of airborne pollutants</a><br>

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2022

Confidentiality

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

Name of the periodical

Cells

ISSN

2073-4409

e-ISSN

2073-4409

Volume of the periodical

11

Issue of the periodical within the volume

4

Country of publishing house

CH - SWITZERLAND

Number of pages

19

Pages from-to

707

UT code for WoS article

000763873200001

EID of the result in the Scopus database

—