The descrease of the in vitro proliferative response of zinc-treated stressed mice's thymic lymphocytes.

Area of Science:

• Immunology
• Neonatal Research
• Oxidative Stress

Background:

• Prolonged stimulation of newborn mice with inactivated staphylococci causes chronic inflammation and oxidative stress.
• This condition leads to anorexia, reduced body weight, and suppressed immune functions, including antibody synthesis and T-lymphocyte proliferation.
• Stressed mice exhibit adrenal hyperplasia, hypozincemia, and thymic hypoplasia, yet thymic T-lymphocytes show increased proliferation.

Purpose of the Study:

• To investigate the effects of zinc acetate administration on immune parameters in chronically stressed neonatal mice.
• To determine if zinc supplementation can mitigate the negative impacts of stress on the immune system.

Main Methods:

• Newborn mice were subjected to prolonged intraperitoneal injections with inactivated staphylococci.
• Stressed mice received intramuscular injections of zinc acetate (5 microg) every other day for two weeks.
• Immune responses, including antibody synthesis, T-lymphocyte proliferation (Con A-stimulated splenic and thymic), zinc concentration, and thymus gland characteristics, were assessed.

Main Results:

• Zinc acetate treatment reduced zinc concentration in the thymus gland of stressed mice.
• The in vitro proliferative response of Con A-stimulated T-lymphocytes from stressed mice treated with zinc acetate was reduced.
• Despite thymic involution due to stress, zinc supplementation showed potential benefits for immune function.

Conclusions:

• Prophylactic administration of zinc acetate in chronically stressed mice impacts thymus gland zinc levels and T-lymphocyte proliferation.
• Zinc supplementation may offer beneficial consequences for the immunity of chronically stressed neonatal mice.
• Further research is warranted to fully elucidate the mechanisms and therapeutic potential of zinc in stress-induced immune dysfunction.