Alveolar macrophages play a key role in cockroach-induced allergic inflammation via TNF-α pathway.

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. Alve...

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Autores principales: Joo Young Kim, Jung Ho Sohn, Je-Min Choi, Jae-Hyun Lee, Chein-Soo Hong, Joo-Shil Lee, Jung-Won Park
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Publicado: Public Library of Science (PLoS) 2012
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spelling oai:doaj.org-article:c43fe6883e0c46a694f95b0c72500e442021-11-18T08:11:27ZAlveolar macrophages play a key role in cockroach-induced allergic inflammation via TNF-α pathway.1932-620310.1371/journal.pone.0047971https://doaj.org/article/c43fe6883e0c46a694f95b0c72500e442012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23094102/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203The 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)-α. We determined whether the serine protease in German cockroach extract (GCE) enhances TNF-α production by alveolar macrophages through the PAR-2 pathway and whether the TNF-α production affects GCE-induced pulmonary inflammation. Effects of GCE on alveolar macrophages and TNF-α 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-α. 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-α production in alveolar macrophages. Blockade of serine proteases prevented the development of GCE induced allergic pathologies. TNF-α blockade also prevented the development of such asthma-like lesions. Depletion of alveolar macrophages reduced AHR and intracellular TNF-α 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-α dependent manner, reflecting the close relation of innate and adaptive immune response in allergic asthma model.Joo Young KimJung Ho SohnJe-Min ChoiJae-Hyun LeeChein-Soo HongJoo-Shil LeeJung-Won ParkPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 10, p e47971 (2012)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Joo Young Kim
Jung Ho Sohn
Je-Min Choi
Jae-Hyun Lee
Chein-Soo Hong
Joo-Shil Lee
Jung-Won Park
Alveolar macrophages play a key role in cockroach-induced allergic inflammation via TNF-α pathway.
description 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)-α. We determined whether the serine protease in German cockroach extract (GCE) enhances TNF-α production by alveolar macrophages through the PAR-2 pathway and whether the TNF-α production affects GCE-induced pulmonary inflammation. Effects of GCE on alveolar macrophages and TNF-α 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-α. 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-α production in alveolar macrophages. Blockade of serine proteases prevented the development of GCE induced allergic pathologies. TNF-α blockade also prevented the development of such asthma-like lesions. Depletion of alveolar macrophages reduced AHR and intracellular TNF-α 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-α dependent manner, reflecting the close relation of innate and adaptive immune response in allergic asthma model.
format article
author Joo Young Kim
Jung Ho Sohn
Je-Min Choi
Jae-Hyun Lee
Chein-Soo Hong
Joo-Shil Lee
Jung-Won Park
author_facet Joo Young Kim
Jung Ho Sohn
Je-Min Choi
Jae-Hyun Lee
Chein-Soo Hong
Joo-Shil Lee
Jung-Won Park
author_sort Joo Young Kim
title Alveolar macrophages play a key role in cockroach-induced allergic inflammation via TNF-α pathway.
title_short Alveolar macrophages play a key role in cockroach-induced allergic inflammation via TNF-α pathway.
title_full Alveolar macrophages play a key role in cockroach-induced allergic inflammation via TNF-α pathway.
title_fullStr Alveolar macrophages play a key role in cockroach-induced allergic inflammation via TNF-α pathway.
title_full_unstemmed Alveolar macrophages play a key role in cockroach-induced allergic inflammation via TNF-α pathway.
title_sort alveolar macrophages play a key role in cockroach-induced allergic inflammation via tnf-α pathway.
publisher Public Library of Science (PLoS)
publishDate 2012
url https://doaj.org/article/c43fe6883e0c46a694f95b0c72500e44
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