Experimental Murine Fascioliasis Derives Early Immune Suppression with Increased Levels of TGF-beta and IL-4.
- Author:
Joon Yong CHUNG
1
;
Young An BAE
;
Doo Hee YUN
;
Hyun Jong YANG
;
Yoon KONG
Author Information
1. Tissue Research Program, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland, USA.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Fasciola hepatica;
murine fascioliasis;
Mac 1+ cell;
T-lymphocyte;
IL-4;
TGF-beta
- MeSH:
Animals;
B-Lymphocytes/immunology;
CD4-Positive T-Lymphocytes/immunology;
CD8-Positive T-Lymphocytes/immunology;
Down-Regulation;
Fasciola hepatica/*immunology;
Fascioliasis/*immunology;
Immunophenotyping;
Immunosuppression;
Interleukin-4/blood/genetics/*immunology;
Male;
Mice;
Mice, Inbred BALB C;
Mice, Inbred C3H;
Mice, Inbred C57BL;
Spleen/immunology;
Transforming Growth Factor beta/blood/genetics/*immunology
- From:The Korean Journal of Parasitology
2012;50(4):301-308
- CountryRepublic of Korea
- Language:English
-
Abstract:
In fascioliasis, T-helper 2 (Th2) responses predominate, while little is known regarding early immune phenomenon. We herein analyzed early immunophenotype changes of BALB/c, C57BL/6, and C3H/He mice experimentally infected with 5 Fasciola hepatica metacercariae. A remarkable expansion of CD19+ B cells was observed as early as week 1 post-infection while CD4+/CD8+ T cells were down-regulated. Accumulation of Mac1+ cells with time after infection correlated well with splenomegaly of all mice strains tested. The expression of tumor necrosis factor (TNF)-alpha mRNA in splenocytes significantly decreased while that of IL-4 up-regulated. IL-1beta expression was down-modulated in BALB/c and C57BL/6 mice, but not in C3H/He. Serum levels of transforming growth factor (TGF)-beta were considerably elevated in all mice during 3 weeks of infection period. These collective results suggest that experimental murine fascioliasis might derive immune suppression with elevated levels of TGF-beta and IL-4 during the early stages of infection.
