Mario R. Escobar

Macrophages and Lymphocytes

Background: Obesity is considered a low-grade inflammatory state that improves with weight loss. In addition to acute-phase proteins, other cytokines might contribute to systemic inflammation. Objective: Our objective was to compare serum concentrations of a large panel of inflammation-related factors in obese and normalweight subjects and to determine kinetic changes induced by caloric restriction. Design: The cohort comprised 14 normal-weight women and 51 obese women who were followed over 2 y after Roux-en-Y gastric bypass. Multiplexed proteomics were used to simultaneously assay 27 cytokines and growth factors in serum. Results: Concentrations of interleukin (IL)-9, IL-1-receptor antagonist, IL-10, interferon-c–inducible protein 10, macrophage inflammatory protein 1b, monocyte chemoattractant protein 1, IL-8, RANTES (regulated upon activation, normal T cell expressed and secreted), monokine induced by interferon-c, and vascular endothelial growth factor were found to be elevated in obesity. IL-10 was further elevated in diabetic obese patients, whereas eotaxin was found to be higher only in diabetic subjects. After surgery, many factors showed a biphasic pattern of variation, decreasing sharply at month 3 before rising back to presurgical values at month 6; these changes closely tracked similar kinetic changes in calorie and carbohydrate intake. After 1 y, an overall reduction in cytokines accompanied the reduction in body mass index and an amelioration in metabolic status. Conclusions: Obesity is associated with elevated circulating concentrations of a large panel of cytokines. Coordinated kinetic changes during weight loss suggest an early influence of calorie and carbohydrate intakes, whereas a longer-term reduction in corpulence might prevail in regulating circulating cytokine concentrations. This trial is registered at clincaltrials.gov as NCT00476658. Am J Clin Nutr 2011;94:450–8.

Immunomodulation by Hepatitis B and Related Viruses

Immunodeficiency disorders may occur as a result of one or more defects within the immune system spanning stem cell deficiencies, through immunoregulatory dysfunction, to a restricted failure to recognize or mount an immune response against certain antigens. The identification of these defects is complicated by their secondary effects, or by opportunistic infections in the immunocompromised host. Although the extent to which viral infections can initiate these deficits remains to be evaluated in most cases, the active role of many viruses in inducing immunosuppression is well established.