The effects of BRL-50481 on ovalbumin-induced asthmatic lung inflammation exacerbated by co-exposure to Asian sand dust in the murine modelThe effects of BRL-50481 on ovalbumin-induced asthmatic lung infl ammation exacerbated by co-exposure to Asian sand dust in the murine model
- Authors
- Kim, Hong Jo; Song, Jin Yong; Park, Tae Il; Choi, Won Seok; Kim, Jong Heon; Kwon, Oh Seong; Lee, Ji-Yun
- Issue Date
- Jan-2022
- Publisher
- PHARMACEUTICAL SOC KOREA
- Keywords
- Asthma; Asian sand dust; PDE7 inhibitor; IL-13; Mucin
- Citation
- ARCHIVES OF PHARMACAL RESEARCH, v.45, no.1, pp 51 - 62
- Pages
- 12
- Journal Title
- ARCHIVES OF PHARMACAL RESEARCH
- Volume
- 45
- Number
- 1
- Start Page
- 51
- End Page
- 62
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/54602
- DOI
- 10.1007/s12272-021-01367-x
- ISSN
- 0253-6269
1976-3786
- Abstract
- Asian sand dust (ASD), which mainly originates in China and Mongolia in the spring and blows into Korea, can exacerbate respiratory and immunological diseases. This study aims to observe effects of co-exposure to ASD on ovalbumin (OVA)-induced asthmatic lung inflammation and of treatment with a phosphodiesterase 7 (PDE7) inhibitor in a mouse model. The challenge with OVA increased airway hyperresponsiveness (AHR) and inflammatory cell infiltration into the lung tissue. Interleukin (IL)-13, tumor necrosis factor-alpha, monocyte-protein-1, mucin, and antigen-specific IgE and IgG1 production increased in mouse serum. The co-exposure of ASD significantly exacerbated these effects in this asthma model. Notably, the administration of a PDE7 inhibitor, BRL-50481 (BRL), significantly reduced AHR, infiltration of inflammatory cells into the lungs, and the levels of type 2 T helper cell-related cytokines, antigen-specific immunoglobulins, and mucin. Thus, the administration of BRL ameliorated OVA-induced allergic asthmatic responses exacerbated by co-exposure to ASD. This study suggests that PDE7 inhibition can be a therapeutic strategy for inflammatory lung diseases and asthma via the regulation of T lymphocytes and reduction of IL-13, and, consequently, mucin production.
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