Malnutrition is a common cause of secondary immune deficiency and has been linked to an increased susceptibility to infection in humans. Malnutrition specifically affects T-cell-mediated immune responses. The aim of this study was to assess in lymphocytes from malnourished children the expression levels of IL-12, IL-18 and IL-21, molecules that induce the differentiation of T cells related to the immunological cellular response (Th1 response) and the production of cytokines related to the immunological cellular response (Th1 cytokines). We found that the expression levels of IL-12, IL-18 and IL-21 were significantly diminished in malnourished children compared to well-nourished children and were coincident with lower plasmatic levels of IL-2 and IFN-γ (Th1 cytokines). In this study, we show for the first time that the gene expression and intracellular production of cytokines responsible for Th1 cell differentiation (IL-12, IL-18 and IL-21) are diminished in malnourished children. As expected, this finding was related to lower plasmatic levels of IL-2 and IFN-γ. The decreased expression of Th1 cytokines observed in this study may contribute to the deterioration of the immunological Type 1 (cellular) response. We hypothesize that the decreased production of IL-12, IL-18 and IL-21 in malnourished children contributes to their inability to eradicate infections.

The development of obesity entails a chronic low-grade inflammatory state with increased pro-inflammatory cells, mainly in visceral adipose tissue (VAT). Additionally, dietary patterns have an influence on the regulation of chronic inflammation. Dietary Approaches to Stop Hypertension (DASH) include foods with an anti-inflammatory profile and that have positive impacts on body composition (BC), suggesting improvements in inflammatory processes. Objective: To analyze the impact of the DASH diet on cellular immunity, anthropometric, biochemical and BC parameters in patients with overweight and obesity, who could present metabolic syndrome. Methodology: Lymphocyte subpopulations, biochemical parameters, anthropometric parameters, and BC before and 8 weeks after intervention with the DASH diet in persons with overweight and obesity were measured. Results: Fifty-nine young adults participated in the study. After the intervention, no significant changes in biochemical parameters were observed, although a significant decrease in nearly all of the anthropometric and BC variables was found: waist circumference (p < 0.001), percentage and kilograms of fat (p < 0.001 and p < 0.025, respectively), VAT (p < 0.020), and weight (p < 0.001), as well as total lymphocytes and double-positive TCD4+ cells. A relation between changes in leukocyte subpopulations (monocytes, natural killer, helper and cytotoxic lymphocytes, and naive TCD4+ cells) and metabolic improvements (glucose, triglycerides, total cholesterol and LDL-c) was also found. Conclusions: The DASH diet promotes positive changes in lymphocyte subpopulations, anthropometric parameters and BC in persons with overweight and obesity. Future studies should elucidate the cellular and molecular mechanisms through which the DASH diet produces inmunometabolic improvement.

Objective: Tert-butylhydroquinone (t-BHQ) protective effect against oxidative damage in thymus from malnourished pops-rats was evaluated. Methods: Malnutrition in pops-rats was induced during the lactation period and first-, second-, and third-degree malnourished rats were studied (MN1, MN2, and MN3). To determine t-BHQ protective effect, lipid peroxidation (LPx) was assessed, as well as the carbonyl content. The reduced glutathione and glutathione disulfide content were determined and antioxidant enzyme activities were measured. Results: Oxidative protein damage, LPx, and Nuclear Factor-κB (NF-κB) content, increased in the MN2 and MN3 compared to well-nourished rats, associated with lower protein content and antioxidant activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase. Tert-butylhydroquinone treatment induced a protective effect against lipids and proteins oxidative damage, as well as decrease in NF-κB in MN rats and restored the antioxidant mechanisms, mostly GPx and SOD. No differences were found between male and female animals. Conclusions: Results show that higher body weight deficit leads to increased oxidative damage and probably inflammation, attributable to alterations in antioxidant mechanisms. These effects were reversed by the t-BHQ-treatment, which restores the antioxidant response. Our findings suggest that t-BHQ could be an interesting pharmacological intervention, but it needs to be studied further.