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

Publication date

2020-06-18T10:11:54Z

2020-06-18T10:11:54Z

2018-03

2020-06-18T10:11:54Z

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.

Document Type

Article


Accepted version

Language

English

Publisher

Cambridge University Press

Related items

Versió postprint del document publicat a: https://doi.org/10.1017/S0007114517003786

British Journal of Nutrition, 2018, vol. 119, num. 5, p. 486-495

https://doi.org/10.1017/S0007114517003786

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(c) Cambridge University Press, 2018

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