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. 2008 Apr 1;228(1):68-75.
doi: 10.1016/j.taap.2007.11.031. Epub 2007 Dec 14.

VSports最新版本 - Chronic exposure to trichloroethene causes early onset of SLE-like disease in female MRL +/+ mice

Ping Cai  1 , Rolf König, Paul J Boor, Shakuntala Kondraganti, Bhupendra S Kaphalia, M Firoze Khan, G A S Ansari
Affiliations

Chronic exposure to trichloroethene causes early onset of SLE-like disease in female MRL +/+ mice

Ping Cai et al. Toxicol Appl Pharmacol. .

Abstract

Trichloroethene (TCE) exacerbates the development of autoimmune responses in autoimmune-prone MRL +/+ mice VSports手机版. 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. .

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Figures

Figure 1
Figure 1
Antinuclear antibodies (ANA) in the serum of female MRL +/+ mice exposed to vehicle (filled circles) or TCE (open circles) in the drinking water. Each circle is an individual measurement and the horizontal bars indicate the means (n = 6).
Figure 2
Figure 2
IFN-γ secretion by ex vivo cultured splenocytes from untreated, age-matched control MRL +/+ mice (diamonds) or MRL +/+ mice treated with TCE for 36 weeks (stars). IFN-γ was measured in supernatants after 48 h of culture without stimulation (none) or following stimulation with 25 µg/ml of dichloroacetylated-albumin (DCAC-Alb) or unmodified albumin (Alb). The horizontal bars indicate the means (n = 5).
Figure 3
Figure 3
Morphological changes in the liver of female MRL +/+ mice treated with TCE for 48 weeks. A. Control, H&E stain; B. TCE-treated: the arrow indicates inflammatory infiltration of portal triads extending into lobules; also present was focal piece-meal necrosis of hepatocytes; C. Control PCNA stain; D. TCE-treated: the arrows indicate PCNA-positive hepatocellular nuclei. E. Control CD3-stain; F. TCE-treated: note the infiltrate of CD3-positive lymphocytes. (A–D, x100; E–F, x200).
Figure 4
Figure 4
Morphological changes in the lungs of MRL +/+ mice treated with TCE for 48 weeks. A. Control, H&E stain; B. TCE-treated: the arrow indicates perivascular inflammatory infiltrates. C. Control CD3-stain; D. TCE-treated: the arrow indicates CD3-positive lymphocytes (A–B, x100; C–D, x200).
Figure 5
Figure 5
Morphological changes in the kidneys of MRL +/+ mice treated with TCE for 48 weeks. A. Control, H&E stain. B. TCE-treated: the arrow indicates perivascular inflammatory infiltrates. C. Control, CD3-stain. D. TCE-treated: the arrow indicates CD3-positive lymphocytes (A–D, x200).
Figure 6
Figure 6
Immunoglobulin deposits in the kidney glomeruli (in the mesangial areas and the walls of adjacent capillaries) of mice treated with TCE for 48 weeks (B). In contrast, vehicle control-treated mice did not show immunoglobulin deposits in the glomeruli (A).
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References

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