Department of Food and Nutrition, College of Human Ecology, Seoul National University, Seoul, South Korea.
Nutr Res. 2011 May;31(5):362-9. doi: 10.1016/j.nutres.2011.04.002.
Obesity accompanies various metabolic and immunologic changes. Evidence from epidemiological, animal, and human studies has linked obesity to impaired immunity. However, human studies that have investigated the immunocompetence of the obese are still limited. We studied the immune and inflammatory responses of obese (body mass index [BMI], 28.3 ± 0.5 kg/m²; n = 30) and normal-weight (BMI, 21.2 ± 0.3 kg/m²; n = 15) young adults to test the hypothesis that obesity is associated with an impaired immune function and dysregulated inflammatory response. Serum levels of adipokines and subpopulations of immune cells were examined. In vitro proliferative response of whole blood lymphocytes, the production of inflammatory cytokines (interleukin [IL] 1β, IL-6, and tumor necrosis factor α) and T helper 1/T helper 2 cytokines (IL-2, interferon γ, IL-4, and IL-10) were determined. Serum leptin levels were significantly higher (P < .001) and CD8+ T-cell subpopulation was significantly lower (P = .044) in the obese than normal-weight subjects. There was no difference in the proliferative response of whole-blood lymphocytes to T-cell mitogens between 2 groups. Phytohemagglutinin-stimulated peripheral blood mononuclear cells from the obese group produced significantly higher levels of IL-2 (P = .002) and tended to produce higher levels of IL-4 (P = .053) than those from the normal-weight group. No significant differences in the production of inflammatory cytokines by either whole-blood lymphocytes or peripheral blood mononuclear cells stimulated with lipopolysaccharide were observed between the obese and normal-weight subjects. These results suggest that obesity with a BMI less than 30 does not significantly impair immune function in young adults. However, further research is needed to investigate the clinical significance of a lower CD8+ T-cell population associated with obesity.
肥胖伴随着各种代谢和免疫变化。来自流行病学、动物和人体研究的证据将肥胖与免疫功能受损联系起来。然而，研究肥胖人群免疫能力的人体研究仍然有限。我们研究了肥胖（体重指数 [BMI]，28.3 ± 0.5 kg/m²；n = 30）和正常体重（BMI，21.2 ± 0.3 kg/m²；n = 15）年轻成年人的免疫和炎症反应，以检验肥胖与免疫功能受损和炎症反应失调相关的假设。检测了血清脂肪因子和免疫细胞亚群的水平。测定了全血淋巴细胞的体外增殖反应、炎症细胞因子（白细胞介素 [IL] 1β、IL-6 和肿瘤坏死因子 α）和 T 辅助 1/T 辅助 2 细胞因子（IL-2、干扰素 γ、IL-4 和 IL-10）的产生。肥胖组血清瘦素水平明显高于正常体重组（P <.001），CD8+ T 细胞亚群明显低于正常体重组（P =.044）。两组全血淋巴细胞对 T 细胞有丝分裂原的增殖反应无差异。与正常体重组相比，肥胖组植物血凝素刺激的外周血单个核细胞产生的 IL-2 水平显著升高（P =.002），且有更高产生 IL-4 的趋势（P =.053）。肥胖组和正常体重组经脂多糖刺激的全血淋巴细胞和外周血单个核细胞产生的炎症细胞因子无显著差异。这些结果表明，BMI 低于 30 的肥胖并未显著损害年轻成年人的免疫功能。然而，需要进一步研究与肥胖相关的 CD8+ T 细胞群体减少的临床意义。
