Regulatory T Cells Contribute to the Inhibition of Radiation-Induced Acute Lung Inflammation via Bee Venom Phospholipase A2 in Mice

Bibliographic Details
Title: Regulatory T Cells Contribute to the Inhibition of Radiation-Induced Acute Lung Inflammation via Bee Venom Phospholipase A2 in Mice
Authors: Dasom Shin, Gihyun Lee, Sung-Hwa Sohn, Soojin Park, Kyung-Hwa Jung, Ji Min Lee, Jieun Yang, Jaeho Cho, Hyunsu Bae
Source: Toxins, Vol 8, Iss 5, p 131 (2016)
Publisher Information: MDPI AG, 2016.
Publication Year: 2016
Collection: LCC:Medicine
Subject Terms: bee venom, phospholipase A2, inflammation, radiotherapy, regulatory T cells, Medicine
More Details: Bee venom has long been used to treat various inflammatory diseases, such as rheumatoid arthritis and multiple sclerosis. Previously, we reported that bee venom phospholipase A2 (bvPLA2) has an anti-inflammatory effect through the induction of regulatory T cells. Radiotherapy is a common anti-cancer method, but often causes adverse effects, such as inflammation. This study was conducted to evaluate the protective effects of bvPLA2 in radiation-induced acute lung inflammation. Mice were focally irradiated with 75 Gy of X-rays in the lung and administered bvPLA2 six times after radiation. To evaluate the level of inflammation, the number of immune cells, mRNA level of inflammatory cytokine, and histological changes in the lung were measured. BvPLA2 treatment reduced the accumulation of immune cells, such as macrophages, neutrophils, lymphocytes, and eosinophils. In addition, bvPLA2 treatment decreased inflammasome-, chemokine-, cytokine- and fibrosis-related genes’ mRNA expression. The histological results also demonstrated the attenuating effect of bvPLA2 on radiation-induced lung inflammation. Furthermore, regulatory T cell depletion abolished the therapeutic effects of bvPLA2 in radiation-induced pneumonitis, implicating the anti-inflammatory effects of bvPLA2 are dependent upon regulatory T cells. These results support the therapeutic potential of bvPLA2 in radiation pneumonitis and fibrosis treatments.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2072-6651
Relation: http://www.mdpi.com/2072-6651/8/5/131; https://doaj.org/toc/2072-6651
DOI: 10.3390/toxins8050131
Access URL: https://doaj.org/article/a87818832aac45bd827cc56038f19300
Accession Number: edsdoj.87818832aac45bd827cc56038f19300
Database: Directory of Open Access Journals
More Details
ISSN:20726651
DOI:10.3390/toxins8050131
Published in:Toxins
Language:English