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番木瓜的成熟过程调节果胶与免疫受体的相互作用。

Pectin Interaction with Immune Receptors is Modulated by Ripening Process in Papayas.

机构信息

Department of Food Science and Experimental Nutrition, School of Pharmaceutical Sciences, University of São Paulo, São Paulo, SP, Brazil.

Food Research Center (FoRC), CEPID-FAPESP (Research, Innovation and Dissemination Centers, São Paulo Research Foundation), São Paulo, SP, Brazil.

出版信息

Sci Rep. 2020 Feb 3;10(1):1690. doi: 10.1038/s41598-020-58311-0.

Abstract

Dietary fibers have been shown to exert immune effects via interaction with pattern recognition receptors (PRR) such as toll-like receptors (TLR) and nucleotide-binding oligomerization domain (NOD)-like receptors. Pectin is a dietary fiber that interacts with PRR depending on its chemical structure. Papaya pectin retains different chemical structures at different ripening stages. How this influence PRR signaling is unknown. The aim of this work was to determine how ripening influences pectin structures and their ability to interact with TLR2, 3, 4, 5 and 9, and NOD1 and 2. It was evaluated the interaction of the water-soluble fractions rich in pectin extracted from unripe to ripe papayas. The pectin extracted from ripe papayas activated all the TLR and, to a lesser extent, the NOD receptors. The pectin extracted from unripe papayas also activated TLR2, 4 and 5 but inhibited the activation of TLR3 and 9. The differences in pectin structures are the higher methyl esterification and smaller galacturonan chains of pectin from ripe papayas. Our finding might lead to selection of ripening stages for tailored modulation of PRR to support or attenuate immunity.

摘要

膳食纤维已被证明通过与模式识别受体(PRR)相互作用发挥免疫作用,如 Toll 样受体(TLR)和核苷酸结合寡聚结构域(NOD)样受体。果胶是一种膳食纤维,其根据化学结构与 PRR 相互作用。木瓜果胶在不同成熟阶段保留不同的化学结构。这种影响 PRR 信号的方式尚不清楚。本工作旨在确定成熟度如何影响果胶结构及其与 TLR2、3、4、5 和 9 以及 NOD1 和 2 相互作用的能力。评估了从未成熟到成熟木瓜中提取的富含果胶的水溶性部分的相互作用。从成熟木瓜中提取的果胶激活了所有 TLR,并且在较小程度上激活了 NOD 受体。从未成熟木瓜中提取的果胶也激活了 TLR2、4 和 5,但抑制了 TLR3 和 9 的激活。果胶结构的差异在于成熟木瓜果胶的甲酯化程度较高和半乳糖醛酸链较小。我们的发现可能会导致选择成熟阶段,以针对 PRR 进行有针对性的调节,以支持或减弱免疫。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fae/6997392/1b0c52386795/41598_2020_58311_Fig1_HTML.jpg

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