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Gestational exposure to mercury leads to persistent changes in T-cell phenotype and function in adult DBF1 mice.

Authors :
Pilones, Karsten
Tatum, Arthur
Gavalchin, Jerrie
Source :
Journal of Immunotoxicology; Sep2009, Vol. 6 Issue 3, p161-170, 10p, 4 Charts, 4 Graphs
Publication Year :
2009

Abstract

Previously, we showed that in utero exposure to mercury induced phenotypic changes in fetal immune cells. Here, we sought to determine whether the effects of in utero exposure on immune cells persisted in the adult. After overnight breeding to DBA/1 males, pregnant BALB/c dams were given either mercuric chloride in drinking water at 10 mg/L ad libitum for the duration of gestation or plain water. At the time of parturition, all dams were placed on regular drinking water. The pups (DBF<subscript>1</subscript>) were weaned and thymic and splenic tissues were harvested at 10 wk-of-age to assess T-cell phenotypes and function. Significant changes in the CD4/CD8 subsets in the thymus and spleen among mercury-exposed male and female mice were not observed. However, there was a significant reduction in splenic CD4<superscript>+</superscript>CD25<superscript>+</superscript> cells in mercury-exposed female, but not in male, mice. ConA-stimulated splenocytes from mercury-exposed mice showed significant increases in proliferative responses relative to cells from control mice, regardless of sex. Cytokine secretion was also modulated in the mercury-exposed mice. In particular, the production of IL-4 and IFN by ConA-stimulated splenocytes from mercury-exposed male and female mice was significantly increased, while IL-2 and IL-10 levels were unaffected. The results of our study revealed that exposure of the developing immune system to relatively low levels of inorganic mercury could lead to persistent alterations in adult immune cell phenotypes and functions. These changes could pose a relevant health risk, if they contribute to impaired responses to pathogens and/or an increased risk for the development of atopy, asthma or possibly autoimmune diseases. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
1547691X
Volume :
6
Issue :
3
Database :
Complementary Index
Journal :
Journal of Immunotoxicology
Publication Type :
Academic Journal
Accession number :
43670980
Full Text :
https://doi.org/10.1080/15476910903084021