Impaired thyroid function in murine toxoplasmosis

Abstract

A decline in serum thyroxine (T₄) occurs in Nya[ratio ]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.