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Prenatal HgCl(2) Exposure Alters Fetal Cell Phenotypes
Karsten Pilones1, Zhi-Wei Lai, Jerrie Gavalchin
1Department of Microbiology & Immunology, SUNY Upstate Medical University, Syracuse, New York.
Prenatal exposure to inorganic mercury altered fetal immune cell development in mice. This exposure increased double negative T-cells and altered B-cell development, potentially impacting autoimmune disease risk.
Area of Science:
- Immunology
- Developmental Toxicology
- Environmental Health
Background:
- Prenatal exposure to environmental toxins can impact immune system development.
- Inorganic mercury is a known neurotoxin with potential immunomodulatory effects.
- The developing immune system may be particularly vulnerable to toxic insults.
Purpose of the Study:
- To investigate the effects of subtoxic prenatal inorganic mercury exposure on the fetal immune repertoire in mice.
- To identify specific immunophenotypic changes in the fetal thymus and liver following mercury exposure.
- To explore potential links between mercury-induced immune alterations and autoimmune disease susceptibility.
Main Methods:
- BALB/c and DBA/1 mice were bred, and pregnant females received 10 mg/l mercuric chloride in drinking water.
- Fetal pups (DBF(1)) were examined at day 16 of gestation.
- Immunophenotyping of fetal thymus and liver cells was performed using flow cytometry.
- Lymphocyte reactivity to the Id(LN)F(1) idiotype was assessed.
Main Results:
- Mercury exposure did not alter total thymocyte counts but modulated immune cell populations.
- Increased percentages of double negative (DN) thymocytes (CD4(-)CD8(-)) were observed.
- Reduced numbers of activated T-cells (CD4(+)CD25(+)) and altered B220(+) cell development in the liver were noted.
- Increased populations of thymic and splenic lymphocytes reactive to the Id(LN)F(1) idiotype were found.
Conclusions:
- Subtoxic prenatal inorganic mercury exposure alters fetal immune cell development in mice.
- These alterations include changes in T-cell subsets and B-cell development, potentially affecting immune homeostasis.
- The observed immune modulation and increased reactivity to a pathogenic idiotype suggest a potential for increased susceptibility to autoimmune diseases post-natally.
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