Role of leukotriene B4 receptor-2 in mast cells in allergic airway inflammation

Sun Young Kwon; Jae Hong Kim

doi:10.3390/ijms20122897

Role of leukotriene B₄ receptor-2 in mast cells in allergic airway inflammation

Sun Young Kwon, Jae Hong Kim

Research output: Contribution to journal › Article › peer-review

14 Citations (Scopus)

Abstract

Mast cells are effector cells in the immune system that play an important role in the allergic airway inflammation. Recently, it was reported that BLT2, a low-affinity leukotriene (LT) B₄ receptor, plays a pivotal role in the pathogenesis of allergic airway inflammation through its action in mast cells. We observed that highly elevated expression levels of BLT2 are critical for the pathogenesis leading to allergic airway inflammation, and that if BLT2 expression is downregulated by siBLT2-mediated knockdown, allergic inflammation is dramatically alleviated. Furthermore, we demonstrated that BLT2 mediates the synthesis of vascular endothelial growth factor (VEGF) and Th2 cytokines, such as interleukin (IL)-13, in mast cells during allergic inflammation. Based on the critical roles of BLT2 in mast cells in allergic inflammation, anti-BLT2 strategies could contribute to the development of new therapies for allergic airway inflammation.

Original language	English
Article number	2897
Journal	International journal of molecular sciences
Volume	20
Issue number	12
DOIs	https://doi.org/10.3390/ijms20122897
Publication status	Published - 2019 Jun 2

Bibliographical note

Funding Information:
This work was supported by Bio and Medical Technology Development Program grants (2017M3A9D8063317) and a Mid-Career Researcher Program grant (2017R1A2B4002203) through the National Research Foundation (NRF) funded by the Ministry of Science, Information and Communication Technologies (ICT), and Future Planning, Republic of Korea. This work was also supported by the BK21 Plus Program (College of Life Sciences and Biotechnology, Korea University) and Korea University Grant.

Funding Information:
Funding: This work was supported by Bio and Medical Technology Development Program grants (2017M3A9D8063317) and a Mid-Career Researcher Program grant (2017R1A2B4002203) through the National Research Foundation (NRF) funded by the Ministry of Science, Information and Communication Technologies (ICT), and Future Planning, Republic of Korea. This work was also supported by the BK21 Plus Program (College of Life Sciences and Biotechnology, Korea University) and Korea University Grant.

Publisher Copyright:
© 2019 by the authors. Licensee MDPI, Basel, Switzerland.

Keywords

Allergic airway inflammation
Asthma
Leukotriene B receptor-2
Mast cells

ASJC Scopus subject areas

Catalysis
Molecular Biology
Spectroscopy
Computer Science Applications
Physical and Theoretical Chemistry
Organic Chemistry
Inorganic Chemistry

Access to Document

10.3390/ijms20122897

Cite this

@article{9cc7603404ea4e24bcc21701cf6c1383,

title = "Role of leukotriene B4 receptor-2 in mast cells in allergic airway inflammation",

abstract = "Mast cells are effector cells in the immune system that play an important role in the allergic airway inflammation. Recently, it was reported that BLT2, a low-affinity leukotriene (LT) B4 receptor, plays a pivotal role in the pathogenesis of allergic airway inflammation through its action in mast cells. We observed that highly elevated expression levels of BLT2 are critical for the pathogenesis leading to allergic airway inflammation, and that if BLT2 expression is downregulated by siBLT2-mediated knockdown, allergic inflammation is dramatically alleviated. Furthermore, we demonstrated that BLT2 mediates the synthesis of vascular endothelial growth factor (VEGF) and Th2 cytokines, such as interleukin (IL)-13, in mast cells during allergic inflammation. Based on the critical roles of BLT2 in mast cells in allergic inflammation, anti-BLT2 strategies could contribute to the development of new therapies for allergic airway inflammation.",

keywords = "Allergic airway inflammation, Asthma, Leukotriene B receptor-2, Mast cells",

author = "Kwon, {Sun Young} and Kim, {Jae Hong}",

note = "Funding Information: This work was supported by Bio and Medical Technology Development Program grants (2017M3A9D8063317) and a Mid-Career Researcher Program grant (2017R1A2B4002203) through the National Research Foundation (NRF) funded by the Ministry of Science, Information and Communication Technologies (ICT), and Future Planning, Republic of Korea. This work was also supported by the BK21 Plus Program (College of Life Sciences and Biotechnology, Korea University) and Korea University Grant. Funding Information: Funding: This work was supported by Bio and Medical Technology Development Program grants (2017M3A9D8063317) and a Mid-Career Researcher Program grant (2017R1A2B4002203) through the National Research Foundation (NRF) funded by the Ministry of Science, Information and Communication Technologies (ICT), and Future Planning, Republic of Korea. This work was also supported by the BK21 Plus Program (College of Life Sciences and Biotechnology, Korea University) and Korea University Grant. Publisher Copyright: {\textcopyright} 2019 by the authors. Licensee MDPI, Basel, Switzerland.",

year = "2019",

month = jun,

day = "2",

doi = "10.3390/ijms20122897",

language = "English",

volume = "20",

journal = "International journal of molecular sciences",

issn = "1661-6596",

publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",

number = "12",

}

TY - JOUR

T1 - Role of leukotriene B4 receptor-2 in mast cells in allergic airway inflammation

AU - Kwon, Sun Young

AU - Kim, Jae Hong

N1 - Funding Information: This work was supported by Bio and Medical Technology Development Program grants (2017M3A9D8063317) and a Mid-Career Researcher Program grant (2017R1A2B4002203) through the National Research Foundation (NRF) funded by the Ministry of Science, Information and Communication Technologies (ICT), and Future Planning, Republic of Korea. This work was also supported by the BK21 Plus Program (College of Life Sciences and Biotechnology, Korea University) and Korea University Grant. Funding Information: Funding: This work was supported by Bio and Medical Technology Development Program grants (2017M3A9D8063317) and a Mid-Career Researcher Program grant (2017R1A2B4002203) through the National Research Foundation (NRF) funded by the Ministry of Science, Information and Communication Technologies (ICT), and Future Planning, Republic of Korea. This work was also supported by the BK21 Plus Program (College of Life Sciences and Biotechnology, Korea University) and Korea University Grant. Publisher Copyright: © 2019 by the authors. Licensee MDPI, Basel, Switzerland.

PY - 2019/6/2

Y1 - 2019/6/2

N2 - Mast cells are effector cells in the immune system that play an important role in the allergic airway inflammation. Recently, it was reported that BLT2, a low-affinity leukotriene (LT) B4 receptor, plays a pivotal role in the pathogenesis of allergic airway inflammation through its action in mast cells. We observed that highly elevated expression levels of BLT2 are critical for the pathogenesis leading to allergic airway inflammation, and that if BLT2 expression is downregulated by siBLT2-mediated knockdown, allergic inflammation is dramatically alleviated. Furthermore, we demonstrated that BLT2 mediates the synthesis of vascular endothelial growth factor (VEGF) and Th2 cytokines, such as interleukin (IL)-13, in mast cells during allergic inflammation. Based on the critical roles of BLT2 in mast cells in allergic inflammation, anti-BLT2 strategies could contribute to the development of new therapies for allergic airway inflammation.

AB - Mast cells are effector cells in the immune system that play an important role in the allergic airway inflammation. Recently, it was reported that BLT2, a low-affinity leukotriene (LT) B4 receptor, plays a pivotal role in the pathogenesis of allergic airway inflammation through its action in mast cells. We observed that highly elevated expression levels of BLT2 are critical for the pathogenesis leading to allergic airway inflammation, and that if BLT2 expression is downregulated by siBLT2-mediated knockdown, allergic inflammation is dramatically alleviated. Furthermore, we demonstrated that BLT2 mediates the synthesis of vascular endothelial growth factor (VEGF) and Th2 cytokines, such as interleukin (IL)-13, in mast cells during allergic inflammation. Based on the critical roles of BLT2 in mast cells in allergic inflammation, anti-BLT2 strategies could contribute to the development of new therapies for allergic airway inflammation.

KW - Allergic airway inflammation

KW - Asthma

KW - Leukotriene B receptor-2

KW - Mast cells

UR - http://www.scopus.com/inward/record.url?scp=85068141475&partnerID=8YFLogxK

U2 - 10.3390/ijms20122897

DO - 10.3390/ijms20122897

M3 - Article

C2 - 31197082

AN - SCOPUS:85068141475

SN - 1661-6596

VL - 20

JO - International journal of molecular sciences

JF - International journal of molecular sciences

IS - 12

M1 - 2897

ER -