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

J 2022

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

VAZQUEZ-GOMEZ, Gerardo, Martina KARASOVÁ, Zuzana TYLICHOVA, Marketa KABATKOVA, Aleš HAMPL et. al.

Basic information

Original name

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

Authors

VAZQUEZ-GOMEZ, Gerardo (guarantor), Martina KARASOVÁ (203 Czech Republic, belonging to the institution), Zuzana TYLICHOVA (203 Czech Republic), Marketa KABATKOVA (203 Czech Republic), Aleš HAMPL (203 Czech Republic, belonging to the institution), Jason MATTHEWS, Jiri NECA (203 Czech Republic), Miroslav CIGANEK (203 Czech Republic), Miroslav MACHALA (203 Czech Republic) and Jan VONDRACEK (203 Czech Republic)

Edition

Cells, BASEL, MDPI, 2022, 2073-4409

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

10601 Cell biology

Country of publisher

Switzerland

Confidentiality degree

není předmětem státního či obchodního tajemství

References:

URL

Impact factor

Impact factor: 6.000

RIV identification code

RIV/00216224:14310/22:00128710

Organization unit

Faculty of Science

DOI

http://dx.doi.org/10.3390/cells11040707

UT WoS

000763873200001

Keywords in English

AhR; inflammation; alveolar epithelial type II cellsNF-kappa B; prostaglandins; cytokines

Abstract

V originále

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.

Citovat

VAZQUEZ-GOMEZ, Gerardo, Martina KARASOVÁ, Zuzana TYLICHOVA, Marketa KABATKOVA, Aleš HAMPL, Jason MATTHEWS, Jiri NECA, Miroslav CIGANEK, Miroslav MACHALA and Jan VONDRACEK. Aryl Hydrocarbon Receptor (AhR) Limits the Inflammatory Responses in Human Lung Adenocarcinoma A549 Cells via Interference with NF-kappa B Signaling. Cells. BASEL: MDPI, 2022, vol. 11, No 4, p. 1-19. ISSN 2073-4409. Available from: https://dx.doi.org/10.3390/cells11040707.

@article{2260377,
   author = {VazquezandGomez, Gerardo and Karasová, Martina and Tylichova, Zuzana and Kabatkova, Marketa and Hampl, Aleš and Matthews, Jason and Neca, Jiri and Ciganek, Miroslav and Machala, Miroslav and Vondracek, Jan},
   article_location = {BASEL},
   article_number = {4},
   doi = {http://dx.doi.org/10.3390/cells11040707},
   keywords = {AhR; inflammation; alveolar epithelial type II cellsNF-kappa B; prostaglandins; cytokines},
   language = {eng},
   issn = {2073-4409},
   journal = {Cells},
   title = {Aryl Hydrocarbon Receptor (AhR) Limits the Inflammatory Responses in Human Lung Adenocarcinoma A549 Cells via Interference with NF-kappa B Signaling},
   url = {https://www.mdpi.com/2073-4409/11/4/707},
   volume = {11},
   year = {2022}
}

TY  - JOUR
ID  - 2260377
AU  - Vazquez-Gomez, Gerardo - Karasová, Martina - Tylichova, Zuzana - Kabatkova, Marketa - Hampl, Aleš - Matthews, Jason - Neca, Jiri - Ciganek, Miroslav - Machala, Miroslav - Vondracek, Jan
PY  - 2022
TI  - Aryl Hydrocarbon Receptor (AhR) Limits the Inflammatory Responses in Human Lung Adenocarcinoma A549 Cells via Interference with NF-kappa B Signaling
JF  - Cells
VL  - 11
IS  - 4
SP  - 1-19
EP  - 1-19
PB  - MDPI
SN  - 20734409
KW  - AhR
KW  - inflammation
KW  - alveolar epithelial type II cellsNF-kappa B
KW  - prostaglandins
KW  - cytokines
UR  - https://www.mdpi.com/2073-4409/11/4/707
N2  - 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.
ER  -

VAZQUEZ-GOMEZ, Gerardo, Martina KARASOVÁ, Zuzana TYLICHOVA, Marketa KABATKOVA, Aleš HAMPL, Jason MATTHEWS, Jiri NECA, Miroslav CIGANEK, Miroslav MACHALA and Jan VONDRACEK. Aryl Hydrocarbon Receptor (AhR) Limits the Inflammatory Responses in Human Lung Adenocarcinoma A549 Cells via Interference with NF-kappa B Signaling. \textit{Cells}. BASEL: MDPI, 2022, vol.~11, No~4, p.~1-19. ISSN~2073-4409. Available from: https://dx.doi.org/10.3390/cells11040707.

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