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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
Abstract:
A decline in serum thyroxine (T4) occurs in Nya: NYLAR female mice infected with Toxoplasma gondii. To ascertain whether the hypothyroxinaemia might be the result of primary thyroid dysfunction, 2 parameters of thyrofollicular cell function were monitored to determine (a) if the cell surface membrane receptors for thyroid-stimulating hormone (TSH) were operative, and (b) whether the cyclic adenosine monophosphate (cAMP)-dependent cascade of intracellular events leading to the release of T4 was responsive to exogenous cAMP. Our results indicated that both parameters were intact and functional in the infected-mouse thyrocytes. However, the elicited T4 responses were distinctly diminished in magnitude, reflecting a lack of readily available thyroidal T4 reserves. Because the continuing synthesis, storage, and release of T4 is dependent on the pulsatile stimulation of the thyroid by TSH, we suggest that the depletion of T4 reserves is likely due to perturbation of the pulsatile release of TSH from the pituitary, rather than to primary thyroid malfunction.
Insights
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.