Dietary palmitoleic acid reprograms gut microbiota and improves biological therapy against colitis
Magnitude and diversity of gut microbiota and metabolic systems are critical in shaping human health and diseases, but it remains largely unclear how complex metabolites may selectively regulate gut microbiota and determine health and diseases. Here, we show that failures or compromised effects of anti-TNF-α therapy in inflammatory bowel diseases (IBD) patients were correlated with intestinal dysbacteriosis with more pro-inflammatory bacteria, extensive unresolved inflammation, failed mucosal repairment, and aberrant lipid metabolism, particularly lower levels of palmitoleic acid (POA). Dietary POA repaired gut mucosal barriers, reduced inflammatory cell infiltrations and expressions of TNF-α and IL-6, and improved efficacy of anti-TNF-α therapy in both acute and chronic IBD mouse models. Ex vivo treatment with POA in cultured inflamed colon tissues derived from Crohn's disease (CD) patients reduced pro-inflammatory signaling/cytokines and conferred appreciable tissue repairment. Mechanistically, POA significantly upregulated the transcriptional signatures of cell division and biosynthetic process of Akkermansia muciniphila, selectively increased the growth and abundance of Akkermansia muciniphila in gut microbiota, and further reprogrammed the composition and structures of gut microbiota. Oral transfer of such POA-reprogrammed, but not control, gut microbiota induced better protection against colitis in anti-TNF-α mAb-treated recipient mice, and co-administration of POA with Akkermansia muciniphila showed significant synergistic protections against colitis in mice. Collectively, this work not only reveals the critical importance of POA as a polyfunctional molecular force to shape the magnitude and diversity of gut microbiota and therefore promote the intestinal homeostasis, but also implicates a new potential therapeutic strategy against intestinal or abenteric inflammatory diseases.
Medienart: |
E-Artikel |
---|
Erscheinungsjahr: |
2023 |
---|---|
Erschienen: |
2023 |
Enthalten in: |
Zur Gesamtaufnahme - volume:15 |
---|---|
Enthalten in: |
Gut microbes - 15(2023), 1 vom: 18. Jan., Seite 2211501 |
Sprache: |
Englisch |
---|
Beteiligte Personen: |
Chen, Yiwei [VerfasserIn] |
---|
Links: |
---|
Anmerkungen: |
Date Completed 22.05.2023 Date Revised 09.06.2023 published: Print Citation Status MEDLINE |
---|
doi: |
10.1080/19490976.2023.2211501 |
---|
funding: |
|
---|---|
Förderinstitution / Projekttitel: |
|
PPN (Katalog-ID): |
NLM357057570 |
---|
LEADER | 01000naa a22002652 4500 | ||
---|---|---|---|
001 | NLM357057570 | ||
003 | DE-627 | ||
005 | 20231226071755.0 | ||
007 | cr uuu---uuuuu | ||
008 | 231226s2023 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.1080/19490976.2023.2211501 |2 doi | |
028 | 5 | 2 | |a pubmed24n1190.xml |
035 | |a (DE-627)NLM357057570 | ||
035 | |a (NLM)37203220 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
100 | 1 | |a Chen, Yiwei |e verfasserin |4 aut | |
245 | 1 | 0 | |a Dietary palmitoleic acid reprograms gut microbiota and improves biological therapy against colitis |
264 | 1 | |c 2023 | |
336 | |a Text |b txt |2 rdacontent | ||
337 | |a ƒaComputermedien |b c |2 rdamedia | ||
338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
500 | |a Date Completed 22.05.2023 | ||
500 | |a Date Revised 09.06.2023 | ||
500 | |a published: Print | ||
500 | |a Citation Status MEDLINE | ||
520 | |a Magnitude and diversity of gut microbiota and metabolic systems are critical in shaping human health and diseases, but it remains largely unclear how complex metabolites may selectively regulate gut microbiota and determine health and diseases. Here, we show that failures or compromised effects of anti-TNF-α therapy in inflammatory bowel diseases (IBD) patients were correlated with intestinal dysbacteriosis with more pro-inflammatory bacteria, extensive unresolved inflammation, failed mucosal repairment, and aberrant lipid metabolism, particularly lower levels of palmitoleic acid (POA). Dietary POA repaired gut mucosal barriers, reduced inflammatory cell infiltrations and expressions of TNF-α and IL-6, and improved efficacy of anti-TNF-α therapy in both acute and chronic IBD mouse models. Ex vivo treatment with POA in cultured inflamed colon tissues derived from Crohn's disease (CD) patients reduced pro-inflammatory signaling/cytokines and conferred appreciable tissue repairment. Mechanistically, POA significantly upregulated the transcriptional signatures of cell division and biosynthetic process of Akkermansia muciniphila, selectively increased the growth and abundance of Akkermansia muciniphila in gut microbiota, and further reprogrammed the composition and structures of gut microbiota. Oral transfer of such POA-reprogrammed, but not control, gut microbiota induced better protection against colitis in anti-TNF-α mAb-treated recipient mice, and co-administration of POA with Akkermansia muciniphila showed significant synergistic protections against colitis in mice. Collectively, this work not only reveals the critical importance of POA as a polyfunctional molecular force to shape the magnitude and diversity of gut microbiota and therefore promote the intestinal homeostasis, but also implicates a new potential therapeutic strategy against intestinal or abenteric inflammatory diseases | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Research Support, Non-U.S. Gov't | |
650 | 4 | |a Akkermansia muciniphila | |
650 | 4 | |a Biological therapy | |
650 | 4 | |a Gut microbiota | |
650 | 4 | |a Inflammatory bowel diseases | |
650 | 4 | |a TNF-α | |
650 | 7 | |a palmitoleic acid |2 NLM | |
650 | 7 | |a 209B6YPZ4I |2 NLM | |
650 | 7 | |a Tumor Necrosis Factor Inhibitors |2 NLM | |
650 | 7 | |a Tumor Necrosis Factor-alpha |2 NLM | |
650 | 7 | |a Dextran Sulfate |2 NLM | |
650 | 7 | |a 9042-14-2 |2 NLM | |
700 | 1 | |a Mai, Qiongdan |e verfasserin |4 aut | |
700 | 1 | |a Chen, Zixu |e verfasserin |4 aut | |
700 | 1 | |a Lin, Tao |e verfasserin |4 aut | |
700 | 1 | |a Cai, Yongjie |e verfasserin |4 aut | |
700 | 1 | |a Han, Jing |e verfasserin |4 aut | |
700 | 1 | |a Wang, Ying |e verfasserin |4 aut | |
700 | 1 | |a Zhang, Mudan |e verfasserin |4 aut | |
700 | 1 | |a Tan, Shimin |e verfasserin |4 aut | |
700 | 1 | |a Wu, Zhiying |e verfasserin |4 aut | |
700 | 1 | |a Chen, Lingming |e verfasserin |4 aut | |
700 | 1 | |a Zhang, Zhiyi |e verfasserin |4 aut | |
700 | 1 | |a Yang, Yi |e verfasserin |4 aut | |
700 | 1 | |a Cui, Taimei |e verfasserin |4 aut | |
700 | 1 | |a Ouyang, Beiyin |e verfasserin |4 aut | |
700 | 1 | |a Sun, Yue |e verfasserin |4 aut | |
700 | 1 | |a Yang, Lijia |e verfasserin |4 aut | |
700 | 1 | |a Xu, Lin |e verfasserin |4 aut | |
700 | 1 | |a Zhang, Sien |e verfasserin |4 aut | |
700 | 1 | |a Li, Jian |e verfasserin |4 aut | |
700 | 1 | |a Shen, Hongbo |e verfasserin |4 aut | |
700 | 1 | |a Liu, Linna |e verfasserin |4 aut | |
700 | 1 | |a Zeng, Lingchan |e verfasserin |4 aut | |
700 | 1 | |a Zhang, Shenghong |e verfasserin |4 aut | |
700 | 1 | |a Zeng, Gucheng |e verfasserin |4 aut | |
773 | 0 | 8 | |i Enthalten in |t Gut microbes |d 2010 |g 15(2023), 1 vom: 18. Jan., Seite 2211501 |w (DE-627)NLM199892369 |x 1949-0984 |7 nnns |
773 | 1 | 8 | |g volume:15 |g year:2023 |g number:1 |g day:18 |g month:01 |g pages:2211501 |
856 | 4 | 0 | |u http://dx.doi.org/10.1080/19490976.2023.2211501 |3 Volltext |
912 | |a GBV_USEFLAG_A | ||
912 | |a GBV_NLM | ||
951 | |a AR | ||
952 | |d 15 |j 2023 |e 1 |b 18 |c 01 |h 2211501 |