Sulforaphane attenuates dextran sodium sulphate induced intestinal inflammation via IL-10/STAT3 signaling mediated macrophage phenotype switching

Innate immunity, particularly macrophages, is critical for intestinal homeostasis. Sulforaphane, a dietary isothiocyanate from cruciferous vegetables, has been reported to protect against intestinal inflammation. However, the role of macrophages in sulforaphane mediated intestinal inflammation and t...

Full description

Saved in:
Bibliographic Details
Main Authors: Yuyang Sun, Jiqing Tang, Cui Li, Jun Liu, Haijie Liu
Format: Article
Language:English
Published: Tsinghua University Press 2022-01-01
Series:Food Science and Human Wellness
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S221345302100080X
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1832568779906744320
author Yuyang Sun
Jiqing Tang
Cui Li
Jun Liu
Haijie Liu
author_facet Yuyang Sun
Jiqing Tang
Cui Li
Jun Liu
Haijie Liu
author_sort Yuyang Sun
collection DOAJ
description Innate immunity, particularly macrophages, is critical for intestinal homeostasis. Sulforaphane, a dietary isothiocyanate from cruciferous vegetables, has been reported to protect against intestinal inflammation. However, the role of macrophages in sulforaphane mediated intestinal inflammation and the underlying molecular mechanisms have not been studied yet. In this study, sulforaphane effectively attenuated dextran sodium sulphate (DSS) induced intestinal inflammation in murine model. Of note, sulforaphane skewed the switching from classically (M1) to alternatively (M2) activated phenotype both in intestinal and bone marrow-derived macrophages (BMDMs). The expression levels of M1 associated maker genes induced by DSS or lipopolysaccharide (LPS) plus interferon gamma-γ (IFN-γ) were suppressed by sulforaphane while M2 marker gene expression levels were improved. This resulted in alteration of inflammatory mediators, particularly interleukin-10 (IL-10), both in colon tissues and culture medium of BMDMs. Subsequently, IL-10 was found to mediate the sulforaphane induced M2 phenotype switching of BMDMs through the activation of STAT3 signaling. This was confirmed by immunofluorescence analysis with increased number of p-STAT3-positive cells in the colon sections. Moreover, anti-IL-10 neutralizing antibody significantly interfered M2 phenotyping of BMDMs induced by sulforaphane with reduced STAT3 phosphorylation. Findings here introduced a potential utilization of sulforaphane for intestinal inflammation treatment with macrophages as the therapeutic targets.
format Article
id doaj-art-6d530a0b58514bdd8902d1690250dc19
institution Kabale University
issn 2213-4530
language English
publishDate 2022-01-01
publisher Tsinghua University Press
record_format Article
series Food Science and Human Wellness
spelling doaj-art-6d530a0b58514bdd8902d1690250dc192025-02-03T00:27:31ZengTsinghua University PressFood Science and Human Wellness2213-45302022-01-01111129142Sulforaphane attenuates dextran sodium sulphate induced intestinal inflammation via IL-10/STAT3 signaling mediated macrophage phenotype switchingYuyang Sun0Jiqing Tang1Cui Li2Jun Liu3Haijie Liu4College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, ChinaCollege of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, ChinaCollege of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, ChinaCollege of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China; Beijing Advanced Innovation Center for Food Nutrition and Human Health, Beijing Technology and Business University, Beijing 100048, China; Corresponding authors at: College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China.College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China; Corresponding authors at: College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China.Innate immunity, particularly macrophages, is critical for intestinal homeostasis. Sulforaphane, a dietary isothiocyanate from cruciferous vegetables, has been reported to protect against intestinal inflammation. However, the role of macrophages in sulforaphane mediated intestinal inflammation and the underlying molecular mechanisms have not been studied yet. In this study, sulforaphane effectively attenuated dextran sodium sulphate (DSS) induced intestinal inflammation in murine model. Of note, sulforaphane skewed the switching from classically (M1) to alternatively (M2) activated phenotype both in intestinal and bone marrow-derived macrophages (BMDMs). The expression levels of M1 associated maker genes induced by DSS or lipopolysaccharide (LPS) plus interferon gamma-γ (IFN-γ) were suppressed by sulforaphane while M2 marker gene expression levels were improved. This resulted in alteration of inflammatory mediators, particularly interleukin-10 (IL-10), both in colon tissues and culture medium of BMDMs. Subsequently, IL-10 was found to mediate the sulforaphane induced M2 phenotype switching of BMDMs through the activation of STAT3 signaling. This was confirmed by immunofluorescence analysis with increased number of p-STAT3-positive cells in the colon sections. Moreover, anti-IL-10 neutralizing antibody significantly interfered M2 phenotyping of BMDMs induced by sulforaphane with reduced STAT3 phosphorylation. Findings here introduced a potential utilization of sulforaphane for intestinal inflammation treatment with macrophages as the therapeutic targets.http://www.sciencedirect.com/science/article/pii/S221345302100080XBMDMsIntestinal inflammationIL-10Macrophage phenotypeSTAT3Sulforaphane
spellingShingle Yuyang Sun
Jiqing Tang
Cui Li
Jun Liu
Haijie Liu
Sulforaphane attenuates dextran sodium sulphate induced intestinal inflammation via IL-10/STAT3 signaling mediated macrophage phenotype switching
Food Science and Human Wellness
BMDMs
Intestinal inflammation
IL-10
Macrophage phenotype
STAT3
Sulforaphane
title Sulforaphane attenuates dextran sodium sulphate induced intestinal inflammation via IL-10/STAT3 signaling mediated macrophage phenotype switching
title_full Sulforaphane attenuates dextran sodium sulphate induced intestinal inflammation via IL-10/STAT3 signaling mediated macrophage phenotype switching
title_fullStr Sulforaphane attenuates dextran sodium sulphate induced intestinal inflammation via IL-10/STAT3 signaling mediated macrophage phenotype switching
title_full_unstemmed Sulforaphane attenuates dextran sodium sulphate induced intestinal inflammation via IL-10/STAT3 signaling mediated macrophage phenotype switching
title_short Sulforaphane attenuates dextran sodium sulphate induced intestinal inflammation via IL-10/STAT3 signaling mediated macrophage phenotype switching
title_sort sulforaphane attenuates dextran sodium sulphate induced intestinal inflammation via il 10 stat3 signaling mediated macrophage phenotype switching
topic BMDMs
Intestinal inflammation
IL-10
Macrophage phenotype
STAT3
Sulforaphane
url http://www.sciencedirect.com/science/article/pii/S221345302100080X
work_keys_str_mv AT yuyangsun sulforaphaneattenuatesdextransodiumsulphateinducedintestinalinflammationviail10stat3signalingmediatedmacrophagephenotypeswitching
AT jiqingtang sulforaphaneattenuatesdextransodiumsulphateinducedintestinalinflammationviail10stat3signalingmediatedmacrophagephenotypeswitching
AT cuili sulforaphaneattenuatesdextransodiumsulphateinducedintestinalinflammationviail10stat3signalingmediatedmacrophagephenotypeswitching
AT junliu sulforaphaneattenuatesdextransodiumsulphateinducedintestinalinflammationviail10stat3signalingmediatedmacrophagephenotypeswitching
AT haijieliu sulforaphaneattenuatesdextransodiumsulphateinducedintestinalinflammationviail10stat3signalingmediatedmacrophagephenotypeswitching