Characteristics of IL‐17 induction by Schistosoma japonicum infection in C57BL/6 mouse liver. Issue 4 (2nd July 2013)
- Record Type:
- Journal Article
- Title:
- Characteristics of IL‐17 induction by Schistosoma japonicum infection in C57BL/6 mouse liver. Issue 4 (2nd July 2013)
- Main Title:
- Characteristics of IL‐17 induction by Schistosoma japonicum infection in C57BL/6 mouse liver
- Authors:
- Chen, Dianhui
Luo, Xueping
Xie, Hongyan
Gao, Zhiyan
Fang, Huilong
Huang, Jun - Abstract:
- <abstract abstract-type="main" id="imm12105-abs-0001"> <title>Summary</title> <p>Schistosomiasis japonica is a severe tropical disease caused by the parasitic worm <italic>Schistosoma japonicum</italic>. Among the most serious pathological effects of <italic>S. japonicum</italic> infection are hepatic lesions (cirrhosis and fibrosis) and portal hypertension. Interleukin‐17 (IL‐17) is a pro‐inflammatory cytokine involved in the pathogenesis of many inflammatory and infectious conditions, including schistosomiasis. We infected C57BL/6 mice with <italic>S. japonicum</italic> and isolated lymphocytes from the liver to identify cell subsets with high IL‐17 expression and release using flow cytometry and ELISA. Expression and release of IL‐17 was significantly higher in hepatic lymphocytes from infected mice compared with control mice in response to both non‐specific stimulation with anti‐CD3 monoclonal antibody plus/anti‐CD28 monoclonal antibody and PMA plus ionomycin. We then compared IL‐17 expression in three hepatic T‐cell subsets, T helper, natural killer T and γδT cells, to determine the major source of IL‐17 during infection. Interleukin‐17 was induced in all three subsets by PMA + ionomycin, but γδT lymphocytes exhibited the largest increase in expression. We then established a mouse model to further investigate the role of IL‐17 in granulomatous and fibrosing inflammation against parasite eggs. Reducing IL‐17 activity using anti‐IL‐17A antibodies decreased infiltration of<abstract abstract-type="main" id="imm12105-abs-0001"> <title>Summary</title> <p>Schistosomiasis japonica is a severe tropical disease caused by the parasitic worm <italic>Schistosoma japonicum</italic>. Among the most serious pathological effects of <italic>S. japonicum</italic> infection are hepatic lesions (cirrhosis and fibrosis) and portal hypertension. Interleukin‐17 (IL‐17) is a pro‐inflammatory cytokine involved in the pathogenesis of many inflammatory and infectious conditions, including schistosomiasis. We infected C57BL/6 mice with <italic>S. japonicum</italic> and isolated lymphocytes from the liver to identify cell subsets with high IL‐17 expression and release using flow cytometry and ELISA. Expression and release of IL‐17 was significantly higher in hepatic lymphocytes from infected mice compared with control mice in response to both non‐specific stimulation with anti‐CD3 monoclonal antibody plus/anti‐CD28 monoclonal antibody and PMA plus ionomycin. We then compared IL‐17 expression in three hepatic T‐cell subsets, T helper, natural killer T and γδT cells, to determine the major source of IL‐17 during infection. Interleukin‐17 was induced in all three subsets by PMA + ionomycin, but γδT lymphocytes exhibited the largest increase in expression. We then established a mouse model to further investigate the role of IL‐17 in granulomatous and fibrosing inflammation against parasite eggs. Reducing IL‐17 activity using anti‐IL‐17A antibodies decreased infiltration of inflammatory cells and collagen deposition in the livers of infected C57BL/6 mice. The serum levels of soluble egg antigen (IL) ‐specific IgGs were enhanced by anti‐IL‐17A monoclonal antibody blockade, suggesting that IL‐17 normally serves to suppress this humoral response. These findings suggest that γδT cells are the most IL‐17‐producing cells and that IL‐17 contributes to granulomatous inflammatory and fibrosing reactions in <italic>S. japonicum‐</italic>infected C57BL/6 mouse liver.</p> </abstract> … (more)
- Is Part Of:
- Immunology. Volume 139:Issue 4(2013:Aug.)
- Journal:
- Immunology
- Issue:
- Volume 139:Issue 4(2013:Aug.)
- Issue Display:
- Volume 139, Issue 4 (2013)
- Year:
- 2013
- Volume:
- 139
- Issue:
- 4
- Issue Sort Value:
- 2013-0139-0004-0000
- Page Start:
- 523
- Page End:
- 532
- Publication Date:
- 2013-07-02
- Subjects:
- Immunology -- Periodicals
- Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1365-2567 ↗
http://www.blackwell-synergy.com/servlet/useragent?func=showIssues&code=imm&close=1997#C1997 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1111/imm.12105 ↗
- Languages:
- English
- ISSNs:
- 0019-2805
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 4369.700000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 3999.xml