TY - JOUR
T1 - Chronic exposure to trichloroethene causes early onset of SLE-like disease in female MRL +/+ mice
AU - Cai, Ping
AU - Konig, Rolf
AU - Boor, Paul
AU - Kondraganti, Shakuntala
AU - Kaphalia, Bhupendra S.
AU - Khan, M. Firoze
AU - Ansari, Ghulam
N1 - Funding Information:
This publication was made possible by grant ES11584 from the National Institute of Environmental Health Sciences (NIEHS), and its content are solely the responsibility of the authors and do not necessarily represent the views of the NIH or NIEHS. We gratefully acknowledge the Organic Synthesis Core at UTMB for the preparation of dichloroacetyl-albumin adducts supported by NIEHS center grant, P30ES06676.
PY - 2008/4/1
Y1 - 2008/4/1
N2 - Trichloroethene (TCE) exacerbates the development of autoimmune responses in autoimmune-prone MRL +/+ mice. Although TCE-mediated autoimmune responses are associated with an increase in serum immunoglobulins and autoantibodies, the underlying mechanism of autoimmunity is not known. To determine the progression of TCE-mediated immunotoxicity, female MRL +/+ mice were chronically exposed to TCE through the drinking water (0.5 mg/ml of TCE) for various periods of time. Serum concentrations of antinuclear antibodies increased after 36 and 48 weeks of TCE exposure. Histopathological analyses showed lymphocyte infiltration in the livers of MRL +/+ mice exposed to TCE for 36 or 48 weeks. Lymphocyte infiltration was also apparent in the pancreas, lungs, and kidneys of mice exposed to TCE for 48 weeks. Immunoglobulin deposits in kidney glomeruli were found after 48 weeks of exposure to TCE. Our results suggest that chronic exposure to TCE promotes inflammation in the liver, pancreas, lungs, and kidneys, which may lead to SLE-like disease in MRL +/+ mice.
AB - Trichloroethene (TCE) exacerbates the development of autoimmune responses in autoimmune-prone MRL +/+ mice. Although TCE-mediated autoimmune responses are associated with an increase in serum immunoglobulins and autoantibodies, the underlying mechanism of autoimmunity is not known. To determine the progression of TCE-mediated immunotoxicity, female MRL +/+ mice were chronically exposed to TCE through the drinking water (0.5 mg/ml of TCE) for various periods of time. Serum concentrations of antinuclear antibodies increased after 36 and 48 weeks of TCE exposure. Histopathological analyses showed lymphocyte infiltration in the livers of MRL +/+ mice exposed to TCE for 36 or 48 weeks. Lymphocyte infiltration was also apparent in the pancreas, lungs, and kidneys of mice exposed to TCE for 48 weeks. Immunoglobulin deposits in kidney glomeruli were found after 48 weeks of exposure to TCE. Our results suggest that chronic exposure to TCE promotes inflammation in the liver, pancreas, lungs, and kidneys, which may lead to SLE-like disease in MRL +/+ mice.
KW - Autoimmunity
KW - Cytokines
KW - Hepatitis
KW - Immunotoxicity
KW - MRL +/+ mice
KW - Trichloroethene (TCE)
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U2 - 10.1016/j.taap.2007.11.031
DO - 10.1016/j.taap.2007.11.031
M3 - Article
C2 - 18234256
AN - SCOPUS:40849126568
SN - 0041-008X
VL - 228
SP - 68
EP - 75
JO - Toxicology and Applied Pharmacology
JF - Toxicology and Applied Pharmacology
IS - 1
ER -