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Objective:The precise role of iron in immune regulation especially in children vulnerable to iron deficiency is not fully known. Hence, this study was conducted to evaluate the effects of iron deficiency anemia (IDA) and its treatment with oral iron supplementation on cell-mediated immunity (CMI) and humoral immunity (HMI) in children.Materials and Methods:A total of 40 children (<15 years) with IDA and 40 age-matched healthy children after satisfying the inclusion criteria were enrolled for this case-control study. Flow cytometric evaluation of absolute and relative numbers of cluster of differentiation 4 (CD4) and CD8 (cluster of differentiation 8) lymphocyte subgroups was carried out to assess the CMI and serum Immunoglobulin G (IgG), Immunoglobulin A (IgA), Immunoglobulin M (IgM) were measured to assess the HMI at baseline and 3 months post oral iron supplementation.Results:Significantly lower levels (P < 0.05) of CD4+ T-cells and decreased CD4:CD8 ratios were observed in the iron deficient children. Iron supplementation significantly improved the CD4+ cell counts and CD4:CD8 ratios. However, immunoglobulin levels weren’t different between the two groups.Conclusions:Although IDA did not influence HMI, it significantly impaired CMI, which was improved following iron supplementation for 3 months.

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Acephate, an organophosphate (OP) pesticide, was used to investigate the effects of its chronic exposure on hemocyte abundance in a non-target dipteran insect Drosophila melanogaster. For this purpose, six graded concentrations ranging from 1 to 6 μg/ml were selected, which are below the reported residual values (up to 14 μg/ml) of the chemical. 1st instar larvae were fed with these concentrations up to the 3rd instar stage and accordingly hemolymph smears from these larvae were prepared for differential hemocyte count. Three types of cells are found in Drosophila hemolymph, namely, plasmatocytes, lamellocytes and crystal cells. Plasmatocyte count was found to decrease with successive increase in treatment concentrations. Crystal cells showed an increasing trend in their number. Though the number of lamellocytes was very low, a bimodal response was noticed. Lamellocyte number was found to increase with the initial three concentrations, followed by a dose dependent reduction in their number. As hemocytes are directly linked to the immune system of fruit flies, fluctuations in normal titer of these cells may affect insect immunity. Hemocytes share homologies in their origin and mode of action with the immune cells of higher organisms including man. Thus the present findings suggest that immune cells of humans and other organisms may be affected adversely under chronic exposure to Acephate.

During adult-onset peripheral hypothyroidism, the brain maintains normal levels of thyroid hormone for some time through a mechanism of ‘central homeostasis’. Although onset, duration, and termination of such a homeostatic phenomenon have been recently evaluated in rat models, the mechanism behind remains unknown. During our investigation to understand the mechanism further, we injected the protein synthesis blockers actinomycin D and cycloheximide along with propylthiouracil to adult male rats during the days of onset (day 2) and termination (day 20) of the homeostatic mechanism. We evaluated synaptosomal T₃ level and neuronal Na⁺-K⁺-ATPase and acetylcholinesterase activities along with deiodinase II activity and cyclic adenosine monophosphate level in the cerebral cortex. The results indicated prevalence of unchanged or lower levels of synaptosomal T₃ on the 2nd and on the 20th day, respectively. Such a condition has been parallely supported by reflections in cerebrocortical deiodinase II activity and cyclic adenosine monophosphate levels. The activities of cerebrocortical synaptosomal Na⁺-K⁺-ATPase and acetylcholinesterase, which are the two important physiological parameters for neuronal function, have been found to be supportive of the involvement of a neuronal protein-mediated factor in the ‘on’ and ‘off’ reactions in central homeostasis during peripheral hypothyroidism. The results of our study indicate that the expression of ‘central thyroid hormone homeostasis’ is a genomic nuclear-mediated mechanism.

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