Alveolar Macrophages Play a Key Role in Cockroach-Induced Allergic Inflammation via TNF-alpha Pathwayopen access
- Authors
- Kim, Joo Young; Sohn, Jung Ho; Choi, Je-Min; Lee, Jae-Hyun; Hong, Chein-Soo; Lee, Joo-Shil; Park, Jung-Won
- Issue Date
- Oct-2012
- Publisher
- PUBLIC LIBRARY SCIENCE
- Citation
- PLOS ONE, v.7, no.10, pp.1 - 12
- Indexed
- SCIE
SCOPUS
- Journal Title
- PLOS ONE
- Volume
- 7
- Number
- 10
- Start Page
- 1
- End Page
- 12
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/164598
- DOI
- 10.1371/journal.pone.0047971
- ISSN
- 1932-6203
- Abstract
- The activity of the serine protease in the German cockroach allergen is important to the development of allergic disease. The protease-activated receptor (PAR)-2, which is expressed in numerous cell types in lung tissue, is known to mediate the cellular events caused by inhaled serine protease. Alveolar macrophages express PAR-2 and produce considerable amounts of tumor necrosis factor (TNF)-alpha. We determined whether the serine protease in German cockroach extract (GCE) enhances TNF-alpha production by alveolar macrophages through the PAR-2 pathway and whether the TNF-alpha production affects GCE-induced pulmonary inflammation. Effects of GCE on alveolar macrophages and TNF-alpha production were evaluated using in vitro MH-S and RAW264.6 cells and in vivo GCE-induced asthma models of BALB/c mice. GCE contained a large amount of serine protease. In the MH-S and RAW264.7 cells, GCE activated PAR-2 and thereby produced TNF-alpha. In the GCE-induced asthma model, intranasal administration of GCE increased airway hyperresponsiveness (AHR), inflammatory cell infiltration, productions of serum immunoglobulin E, interleukin (IL)-5, IL-13 and TNF-alpha production in alveolar macrophages. Blockade of serine proteases prevented the development of GCE induced allergic pathologies. TNF-alpha blockade also prevented the development of such asthma-like lesions. Depletion of alveolar macrophages reduced AHR and intracellular TNF-alpha level in pulmonary cell populations in the GCE-induced asthma model. These results suggest that serine protease from GCE affects asthma through an alveolar macrophage and TNF-alpha dependent manner, reflecting the close relation of innate and adaptive immune response in allergic asthma model.
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