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Impaired thyroid function in murine toxoplasmosis
1Department of Infectious Diseases, Tokai University School of Medicine, Kanagawa, Japan. stahl@is.icc.u-tokai.ac.jp
Parasitology
|October 17, 1998
Summary
Toxoplasma gondii infection in mice causes low thyroxine (T4) by affecting pituitary thyroid-stimulating hormone (TSH) release, not primary thyroid issues. This impacts T4 reserves and overall thyroid function.
Area of Science:
- Endocrinology
- Immunology
- Parasitology
Background:
- Toxoplasma gondii infection is known to cause physiological changes.
- A decline in serum thyroxine (T4) has been observed in infected Nya:NYLAR female mice.
Purpose of the Study:
- To investigate if hypothyroxinemia in Toxoplasma gondii-infected mice results from primary thyroid dysfunction.
- To assess thyroidal T4 reserve and responsiveness to thyroid-stimulating hormone (TSH) and cyclic adenosine monophosphate (cAMP).
Main Methods:
- Monitored TSH receptor function on thyrofollicular cells.
- Assessed the cAMP-dependent intracellular cascade response to exogenous cAMP.
- Evaluated T4 release in response to stimulation in infected mice.
Main Results:
- Thyroidal TSH receptor and cAMP-mediated pathways were functional in infected mice.
- Elicited T4 responses were diminished, indicating depleted thyroidal T4 reserves.
- Thyroidal T4 synthesis, storage, and release are dependent on pulsatile TSH stimulation.
Conclusions:
- The hypothyroxinemia is likely due to perturbed pulsatile TSH release from the pituitary.
- Primary thyroid malfunction is not the cause of diminished T4 levels in this model.
- Toxoplasma gondii infection disrupts the hypothalamic-pituitary-thyroid axis regulation.