Bacteroides thetaiotaomicron and its inactivated bacteria ameliorate colitis by inhibiting macrophage activation.

bacteroides thetaiotaomicron colitis gut microbiota inflammatory bowel disease

Journal

Clinics and research in hepatology and gastroenterology
ISSN: 2210-741X
Titre abrégé: Clin Res Hepatol Gastroenterol
Pays: France
ID NLM: 101553659

Informations de publication

Date de publication:
27 Dec 2023
Historique:
received: 21 11 2023
revised: 16 12 2023
accepted: 27 12 2023
medline: 2 1 2024
pubmed: 2 1 2024
entrez: 29 12 2023
Statut: aheadofprint

Résumé

Studies have demonstrated that Bacteroides thetaiotaomicron (BT) has protective effect against colon inflammation in murine models. Macrophages play an important role in gut immunity. However, the specific mechanisms of BT on macrophage are still unelucidated. Thus, our study investigates the anti-inflammatory effect of BT and its heat-treated inactivated bacteria on experimental colitis and macrophages. A dextran sulfate sodium (DSS)-induced acute colitis model with male C57BL/6 mice, BT (ATCC29148) strain, THP1 cell lines were used in this study. Live and heat-treated inactivated BT (IBT) solution (1×10^ Both live and heat-treated inactivated BT decreased the DAIand histological scores as well as levels of inflammatory factors, particularly IL-6 while increasing IL-22 of DSS-induced colitis murine models. The cell experiments showed that inactivated BT downregulates IL-6 expression in THP1 via inhibiting p38 phosphorylation and affecting M1 polarization. Moreover, the 16S rRNA sequencing results showed that BT and IBT gavage could increase beta-diversity of gut flora in DSS-induced colitis mice. Furthermore, the significance test for differences between the groups showed that BT could increase Faecalebaculum, Lactobacillus and Bacteroides, while decreasing Akkermansia. In summary, our findings imply that BT and its heat-treated inactivated bacteria exert a protective effect by suppressing macrophage-induced IL-6 through the inhibition of p38 MAPK pathway and ameliorating intestinal gut dysbiosis in experimental colitis.

Sections du résumé

BACKGROUND BACKGROUND
Studies have demonstrated that Bacteroides thetaiotaomicron (BT) has protective effect against colon inflammation in murine models. Macrophages play an important role in gut immunity. However, the specific mechanisms of BT on macrophage are still unelucidated. Thus, our study investigates the anti-inflammatory effect of BT and its heat-treated inactivated bacteria on experimental colitis and macrophages.
METHODS METHODS
A dextran sulfate sodium (DSS)-induced acute colitis model with male C57BL/6 mice, BT (ATCC29148) strain, THP1 cell lines were used in this study. Live and heat-treated inactivated BT (IBT) solution (1×10^
RESULTS RESULTS
Both live and heat-treated inactivated BT decreased the DAIand histological scores as well as levels of inflammatory factors, particularly IL-6 while increasing IL-22 of DSS-induced colitis murine models. The cell experiments showed that inactivated BT downregulates IL-6 expression in THP1 via inhibiting p38 phosphorylation and affecting M1 polarization. Moreover, the 16S rRNA sequencing results showed that BT and IBT gavage could increase beta-diversity of gut flora in DSS-induced colitis mice. Furthermore, the significance test for differences between the groups showed that BT could increase Faecalebaculum, Lactobacillus and Bacteroides, while decreasing Akkermansia.
CONCLUSION CONCLUSIONS
In summary, our findings imply that BT and its heat-treated inactivated bacteria exert a protective effect by suppressing macrophage-induced IL-6 through the inhibition of p38 MAPK pathway and ameliorating intestinal gut dysbiosis in experimental colitis.

Identifiants

DOI: 10.1016/j.clinre.2023.102276 PMID: 38158154
pubmed: 38158154
pii: S2210-7401(23)00201-2
doi: 10.1016/j.clinre.2023.102276
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

102276

Informations de copyright

Copyright © 2023. Published by Elsevier Masson SAS.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no conflict of interests.

Auteurs

Sikong Yinhe (S)

Department of Gastroenterology, Qilu Hospital of Shandong University, Jinan, Shandong, China; Department of Gastroenterology, Qilu Hospital of Shandong University Qingdao, Qingdao, Shandong, China.

Li Lixiang (L)

Department of Gastroenterology, Qilu Hospital of Shandong University, Jinan, Shandong, China; Shandong Provincial Clinical Research Center for digestive disease, Shandong, China.

Li Yan (L)

Department of Gastroenterology, Qilu Hospital of Shandong University Qingdao, Qingdao, Shandong, China.

Gu Xiang (G)

Department of Gastroenterology, Qilu Hospital of Shandong University, Jinan, Shandong, China.

Li Yanqing (L)

Department of Gastroenterology, Qilu Hospital of Shandong University, Jinan, Shandong, China; Department of Gastroenterology, Qilu Hospital of Shandong University Qingdao, Qingdao, Shandong, China; Shandong Provincial Clinical Research Center for digestive disease, Shandong, China; Laboratory of Translational Gastroenterology, Qilu Hospital of Shandong University, Jinan, Shandong, China; Robot engineering laboratory for precise diagnosis and therapy of GI tumor, Qilu Hospital of Shandong University, Jinan, Shandong, China.

Zuo Xiuli (Z)

Department of Gastroenterology, Qilu Hospital of Shandong University, Jinan, Shandong, China; Department of Gastroenterology, Qilu Hospital of Shandong University Qingdao, Qingdao, Shandong, China; Shandong Provincial Clinical Research Center for digestive disease, Shandong, China; Laboratory of Translational Gastroenterology, Qilu Hospital of Shandong University, Jinan, Shandong, China; Robot engineering laboratory for precise diagnosis and therapy of GI tumor, Qilu Hospital of Shandong University, Jinan, Shandong, China. Electronic address: zuoxiuli@sdu.edu.cn.

Classifications MeSH