GM-CSF & neonatal hypothyroidism

What is it about?

Hypothyroidisminduced bymethimazole (MMI), has a negative impact on the postnatal development. Neonatal GranulocyteMacrophage-Colony Stimulating Factor [GM-CSF; 50 μg/kg, intramuscular injection at postnatal day (PND) 17] had been tested to ameliorate the effects ofMMI [0.05%, (weight per volume; w/v), intraperitoneal injection at PND 15]-induced hypothyroidisminWistar rats. The hypothyroid conditions due to the administration of MMI produced inhibitory effects on neonatal serum thyroxine (T4), 3,5,3′-triiodothyronine (T3), neutrophil count in bone marrow and blood, cerebellar glutathione (GSH) and acetylcholinesterase (AchE), although it induced stimulatory actions on serum thyrotropin (TSH), growth hormone (GH), insulin growth factor-II (IGFII), tumor necrosis factor alpha (TNF-α), and cerebellar malondialdehyde (MDA) at PND 19. The treatment with GM-CSF could reverse the depressing and stimulating effects ofMMI on these markers except for cerebellar AchE where its enhancement was non-significant (P N 0.05) at tested PND. Thus, neonatal GM-CSF may be responsible for suppressing autoimmune responses and preventing hypothyroidism.

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Why is it important?

neonatal hypothyroidism might cause pathophysiological and patho-development states which impair HPTA, GH/ IGF axis and the development of cerebellum. Also, the deficiency of THs might be directly related to the impairment of the cellular immune system (neutropenia) and enhancement of cerebellar oxidative stress. Therefore, it is necessary to develop new anti-thyroid drugs without causing oxidative stress and cellular damage. Moreover, GM-CSF as a hematopoietic cytokine was an effective treatment against the neonatal hypothyroidism. These protective effectsmight be either directly or indirectly related to TH action, and depend on the intensity and nature of the dose, experimental duration, developmental period, and type of biological fraction studied

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