Though we know much about development of obesity and its associated complications like type II diabetes, cardiovascular diseases, hypertension and cancer, our knowledge is very limited about the impact of this metabolic syndrome on immune functions per se. Studies in obese humans and animal models have earlier shown, altered lymphocyte numbers, and reduced lymphocyte responsiveness to mitogen stimulation, dysregulated cytokine expression, decreased natural killer cells, macrophage and dendritic cell functions, leading to reduced resistance to infections involving a number of organisms such as Mycobacterium tuberculosis, Coxsackie virus, Helicobacter pyroli and influenza. Several obesity-associated hormonal changes such as leptin resistance, hyperinsulinemia, and metabolic changes such as excessive inflammation and altered glucose, amino acid and fatty acid metabolism which are required for the functionality of T cells could affect the immune response. This review tries to explore these possibilities and project them as plausible mechanism(s), which could affect the response to infectious diseases and vaccine in obese conditions.
Aim: Role of leptin in bringing about systemic immune response under obesity has so far been speculative. In the present study we addressed this question using genetically obese rats developed at our centre-WNIN/Ob and WNIN/ GR-Ob. Methodology: Both the lean (+/+) and homozygous obese animals (-/-) received either phosphate buffered saline or leptin. While another set of fed lean and obese served as controls. Effect of leptin on immune function was assessed in terms of splenic lymphocyte proliferative response to Concavalin A (Con A), splenic CD4/CD8 ratio and Nitric oxide (NO) production by macrophages. Further, we also studied if the effect of leptin on immune function was associated with changes in receptor OBR (Leptin receptor) and or JAK2 (Janus tyrosine kinase 2) total protein expression. Results: Lean animals of both the strains (WNIN/GR-Ob & WNIN/Ob lean) responded to leptin treatment, in terms of increased CD4/CD8 ratio and lipopolysaccharide stimulated peritoneal macrophage Nitric Oxide (NO) production (P<0.05), while splenic lymphocyte proliferative response (P<0.05) to Concavalin A upon leptin treatment was observed only in WNIN/GR-Ob lean animals. Furthermore, significant increase in obese receptor (OBR) protein expression and a trend for JAK2 protein expression (P=0.06) upon leptin treatment were seen in WNIN/GR-Ob and WNIN/Ob lean animals respectively. Conclusion: The data thus show that leptin resistance could be one of the factors associated with immune dysfunction in obese condition.
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