Novel mechanism of Clostridium butyricum alleviated coprophagy prevention-induced intestinal inflammation in rabbit
Copyright © 2024 Elsevier B.V. All rights reserved..
As bacteria synthesize nutrients primarily in the cecum, coprophagy is indispensable for supplying rabbits with essential nutrients. Recent research has demonstrated its pivotal role in maintaining intestinal microbiota homeostasis and immune regulation in rabbits, although the specific mechanism remains unknown. Here, we used coprophagy prevention (CP) to investigate the effects of coprophagy on the cecum homeostasis and microbiota in New Zealand white rabbits. Furthermore, whether supplementation of Clostridium butyricum (C. butyricum) may alleviate the cecum inflammation and apoptosis caused by CP was also explored. Four groups were randomly assigned: control (Con), sham-coprophagy prevention (SCP), coprophagy prevention (CP), and CP and C. butyricum addition (CPCB). Compared to Con and SCP, CP augmented cecum inflammation and apoptosis, as well as bacterial adhesion to the cecal epithelial mucosa, while decreasing the expression of tight junction proteins (ZO-1, occluding, and claudin-1). The relative abundance of short-chain fatty acids (SCFAs)-producing bacteria was significantly decreased in the CP group. Inversely, there was an increase in the Firmicutes/Bacteroidetes ratio and the relative abundance of Christensenellaceae_R-7_group. Additionally, CP increased the levels of Flagellin, IFN-γ, TNF-a, and IL-1β in cecum contents and promoted the expression of TLR5/MyD88/NF-κB pathway in cecum tissues. However, the CPCB group showed significant improvements in all parameters compared to the CP group. Dietary C. butyricum supplementation significantly increased the production of SCFAs, particularly butyric acid, triggering anti-inflammatory, tissue repairing, and barrier-protective responses. Notably, CPCB effectively mitigated CP-induced apoptosis and inflammation. In summary, CP disrupts the cecum epithelial barrier and induces inflammation in New Zealand white rabbits, but these effects can be alleviated by C. butyricum supplementation. This process appears to be largely associated with the TLR5/MyD88/NF-κB signaling pathway.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2024 |
|---|---|
| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:130 |
|---|---|
| Enthalten in: |
International immunopharmacology - 130(2024) vom: 30. März, Seite 111773 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Li, Zhichao [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Clostridium butyricum |
|---|
| Anmerkungen: |
Date Completed 25.03.2024 Date Revised 25.03.2024 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1016/j.intimp.2024.111773 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM369206851 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM369206851 | ||
| 003 | DE-627 | ||
| 005 | 20240325235033.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 240304s2024 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.intimp.2024.111773 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1346.xml |
| 035 | |a (DE-627)NLM369206851 | ||
| 035 | |a (NLM)38430808 | ||
| 035 | |a (PII)S1567-5769(24)00291-1 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Li, Zhichao |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Novel mechanism of Clostridium butyricum alleviated coprophagy prevention-induced intestinal inflammation in rabbit |
| 264 | 1 | |c 2024 | |
| 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 25.03.2024 | ||
| 500 | |a Date Revised 25.03.2024 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2024 Elsevier B.V. All rights reserved. | ||
| 520 | |a As bacteria synthesize nutrients primarily in the cecum, coprophagy is indispensable for supplying rabbits with essential nutrients. Recent research has demonstrated its pivotal role in maintaining intestinal microbiota homeostasis and immune regulation in rabbits, although the specific mechanism remains unknown. Here, we used coprophagy prevention (CP) to investigate the effects of coprophagy on the cecum homeostasis and microbiota in New Zealand white rabbits. Furthermore, whether supplementation of Clostridium butyricum (C. butyricum) may alleviate the cecum inflammation and apoptosis caused by CP was also explored. Four groups were randomly assigned: control (Con), sham-coprophagy prevention (SCP), coprophagy prevention (CP), and CP and C. butyricum addition (CPCB). Compared to Con and SCP, CP augmented cecum inflammation and apoptosis, as well as bacterial adhesion to the cecal epithelial mucosa, while decreasing the expression of tight junction proteins (ZO-1, occluding, and claudin-1). The relative abundance of short-chain fatty acids (SCFAs)-producing bacteria was significantly decreased in the CP group. Inversely, there was an increase in the Firmicutes/Bacteroidetes ratio and the relative abundance of Christensenellaceae_R-7_group. Additionally, CP increased the levels of Flagellin, IFN-γ, TNF-a, and IL-1β in cecum contents and promoted the expression of TLR5/MyD88/NF-κB pathway in cecum tissues. However, the CPCB group showed significant improvements in all parameters compared to the CP group. Dietary C. butyricum supplementation significantly increased the production of SCFAs, particularly butyric acid, triggering anti-inflammatory, tissue repairing, and barrier-protective responses. Notably, CPCB effectively mitigated CP-induced apoptosis and inflammation. In summary, CP disrupts the cecum epithelial barrier and induces inflammation in New Zealand white rabbits, but these effects can be alleviated by C. butyricum supplementation. This process appears to be largely associated with the TLR5/MyD88/NF-κB signaling pathway | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Clostridium butyricum | |
| 650 | 4 | |a Coprophagy prevention | |
| 650 | 4 | |a Inflammation | |
| 650 | 4 | |a Microbiome | |
| 650 | 4 | |a Rabbits | |
| 650 | 4 | |a TLR5 | |
| 650 | 7 | |a NF-kappa B |2 NLM | |
| 650 | 7 | |a Myeloid Differentiation Factor 88 |2 NLM | |
| 650 | 7 | |a Toll-Like Receptor 5 |2 NLM | |
| 650 | 7 | |a Fatty Acids, Volatile |2 NLM | |
| 700 | 1 | |a He, Hui |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Mengjuan |e verfasserin |4 aut | |
| 700 | 1 | |a Ni, Mengke |e verfasserin |4 aut | |
| 700 | 1 | |a Guo, Chaohui |e verfasserin |4 aut | |
| 700 | 1 | |a Wan, Zhiyi |e verfasserin |4 aut | |
| 700 | 1 | |a Zhou, Jianshe |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Zhitong |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Yaling |e verfasserin |4 aut | |
| 700 | 1 | |a Cai, Hanfang |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Ming |e verfasserin |4 aut | |
| 700 | 1 | |a Sun, HuiZeng |e verfasserin |4 aut | |
| 700 | 1 | |a Xu, Huifen |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t International immunopharmacology |d 2001 |g 130(2024) vom: 30. März, Seite 111773 |w (DE-627)NLM112639542 |x 1878-1705 |7 nnns |
| 773 | 1 | 8 | |g volume:130 |g year:2024 |g day:30 |g month:03 |g pages:111773 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1016/j.intimp.2024.111773 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 130 |j 2024 |b 30 |c 03 |h 111773 | ||