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瘦素和脂联素补充剂可改变哺乳期大鼠肠系膜淋巴结淋巴细胞组成和功能。

Leptin and adiponectin supplementation modifies mesenteric lymph node lymphocyte composition and functionality in suckling rats.

机构信息

1Section of Physiology,Department of Biochemistry and Physiology, Faculty of Pharmacy and Food Science,University of Barcelona,08028 Barcelona,Spain.

出版信息

Br J Nutr. 2018 Mar;119(5):486-495. doi: 10.1017/S0007114517003786.

DOI:10.1017/S0007114517003786
PMID:29508690
Abstract

At birth, when immune responses are insufficient, there begins the development of the defence capability against pathogens. Leptin and adiponectin, adipokines that are present in breast milk, have been shown to play a role in the regulation of immune responses. We report here, for the first time, the influence of in vivo adipokine supplementation on the intestinal immune system in early life. Suckling Wistar rats were daily supplemented with leptin (0·7 μg/kg per d, n 36) or adiponectin (35 μg/kg per d, n 36) during the suckling period. The lymphocyte composition, proliferation and cytokine secretion from mesenteric lymph node lymphocytes (on days 14 and 21), as well as intestinal IgA and IgM concentration (day 21), were evaluated. At day 14, leptin supplementation significantly increased the TCRαβ + cell proportion in mesenteric lymph nodes, in particular owing to an increase in the TCRαβ + CD8+ cell population. Moreover, the leptin or adiponectin supplementation promoted the early development CD8+ cells, with adiponectin being the only adipokine capable of enhancing the lymphoproliferative ability at the end of the suckling period. Although leptin decreased intestinal IgA concentration, it had a trophic effect on the intestine in early life. Supplementation of both adipokines modulated the cytokine profile during (day 14) and at the end (day 21) of the suckling period. These results suggest that leptin and adiponectin during suckling play a role in the development of mucosal immunity in early life.

摘要

在生命早期,当免疫反应不足时,机体开始发展对抗病原体的防御能力。瘦素和脂联素是存在于母乳中的两种脂肪细胞因子,它们在调节免疫反应方面发挥作用。我们首次报道了体内脂肪细胞因子补充对生命早期肠道免疫系统的影响。哺乳期 Wistar 大鼠每天补充瘦素(0.7μg/kg/d,n=36)或脂联素(35μg/kg/d,n=36)。评估了肠系膜淋巴结淋巴细胞的淋巴细胞组成、增殖和细胞因子分泌(第 14 天和第 21 天)以及肠道 IgA 和 IgM 浓度(第 21 天)。第 14 天,瘦素补充显著增加了肠系膜淋巴结中 TCRαβ+细胞的比例,特别是由于 TCRαβ+CD8+细胞群的增加。此外,瘦素或脂联素补充促进了早期 CD8+细胞的发育,而脂联素是唯一能够增强哺乳期结束时淋巴增殖能力的脂肪细胞因子。尽管瘦素降低了肠道 IgA 浓度,但它对生命早期的肠道具有营养作用。两种脂肪细胞因子的补充均调节了哺乳期(第 14 天)和结束时(第 21 天)的细胞因子谱。这些结果表明,哺乳期的瘦素和脂联素在生命早期黏膜免疫的发育中发挥作用。

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