scholarly journals Effects of probiotic BaSC06 on intestinal digestion and absorption function, antioxidant capacity and macrophage polarization and microbiota composition in fattening pigs

2020 ◽  
Author(s):  
Xuefang Cao ◽  
Li Tang ◽  
Zihan Zeng ◽  
Baikui Wang ◽  
Yuanhao Zhou ◽  
...  
Keyword(s):  
Antioxidant Capacity ◽  
Growth Performance ◽  
Intestinal Microbiota ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Microbiota Composition ◽  
Absorption Function ◽  
M2 Polarization ◽  
Intestinal Digestion ◽  
Fattening Pigs

Abstract Background: The previous study in our team found that supplementation of probiotic Bacillus amyloliquefaciens SC06 (BaSC06) as an alternative to antibiotics (Kitasamycin) can effectively reduce the diarrhea rate and promote the growth performance of weaned piglets. We speculate that BaSC06 may become a better substitute for antibiotics for fattening pigs. Hence, the objective of the present study is to evaluate the effects of BaSC06 substitute antibiotics on growth performance, digestive functions, antioxidant capacity, macrophage polarization and intestinal microbiota of fattening pigs. Methods: A total of 117 fattening pigs with similar weight and genetic basis were selected and divided into three groups: Anti group, fed with basal diet supplemented with 40 g/t Kitasamycin; Anti + Ba group, fed with 1 × 108 CFU/kg BaSC06 and 20 g/t Kitasamycin; Ba group, fed with 1 × 108 CFU/kg BaSC06 replaced Kitasamycin. Each treatment had three replications of 13 pigs per pen. Results: It indicated that BaSC06 replacement significantly improved ADFI and ADG in fattening pigs. It also improved intestinal digestion and absorption function with the increased activities of intestinal digestive enzymes and higher expression of glucose transporters SGLT1 and small peptide transporters PEPT1, maintained intestinal integrity significantly. Besides, supplementation with BaSC06 enhanced intestinal and body antioxidant capacity by activating Nrf2/ Keap1 antioxidant signaling pathway. In addition, BaSC06 as a substitute could alleviate intestinal inflammation by inhibiting the production of pro-inflammatory cytokines and chemokine and simultaneously increase the expression of M1 and M2 macrophage marker proteins in the intestinal mucosa. The transcription factor STAT3 regulated M2 polarization, which maintained immune homeostasis and reduced inflammation. What’s more, BaSC06 could improve the composition of the microbiota as well by increasing the proportion of Firmicutes, and reducing the proportion of Bacteroidetes and Proteobacteria. Conclusions: Taken together, our findings indicated that diet supplementation with BaSC06 instead of antibiotics increased the growth performance of piglets by improving the digestion and absorption of nutrients, intestinal microbiota composition and mucosal structure, antioxidative capacity and immune functions (including increasing M1and M2 polarization of macrophage).

scholarly journals Blockade of the Notch Signaling Pathway Promotes M2 Macrophage Polarization to Suppress Cardiac Fibrosis Remodeling in Mice With Myocardial Infarction

2022 ◽  
Vol 8 ◽  
Author(s):  
Zhi Li ◽  
Miao Nie ◽  
Liming Yu ◽  
Dengshun Tao ◽  
Qiang Wang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Cardiac Fibrosis ◽  
Macrophage Polarization ◽  
Notch Signaling Pathway ◽  
Inflammatory Factors ◽  
M2 Macrophage ◽  
M2 Polarization

Myocardial infarction (MI) is regarded as a serious ischemic heart disease on a global level. The current study set out to explore the mechanism of the Notch signaling pathway in the regulation of fibrosis remodeling after the occurrence of MI. First, experimental mice were infected with recombination signal binding protein J (RBP-J) shRNA and empty adenovirus vector, followed by the establishment of MI mouse models and detection of cardiac function. After 4 weeks of MI, mice in the sh-RBP-J group were found to exhibit significantly improved cardiac function relative to the sh-NC group. Moreover, knockdown of RBP-J brought about decreased infarct area, promoted cardiac macrophages M2 polarization, reduced cardiac fibrosis, and further decreased transcription and protein expressions of inflammatory factors and fibrosis-related factors. Furthermore, downregulation of cylindromatosis (CYLD) using si-CYLD reversed the results that knockdown of RBP-J inhibited fibrogenesis and the release of inflammatory factors. Altogether, our findings indicated that the blockade of Notch signaling promotes M2 polarization of cardiac macrophages and improves cardiac function by inhibiting the imbalance of fibrotic remodeling after MI.

A core–shell structure QRu-PLGA-RES-DS NP nanocomposite with photothermal response-induced M2 macrophage polarization for rheumatoid arthritis therapy

Nanoscale ◽  
2019 ◽  
Vol 11 (39) ◽  
pp. 18209-18223 ◽  
Author(s):  
Xu Chen ◽  
Xufeng Zhu ◽  
Litao Ma ◽  
Ange Lin ◽  
Youcong Gong ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Shell Structure ◽  
Therapeutic Strategy ◽  
Macrophage Polarization ◽  
Core Shell ◽  
M2 Macrophage ◽  
M2 Polarization ◽  
M2 Macrophage Polarization ◽  
Core Shell Structure ◽  
Novel Therapeutic

A novel therapeutic strategy for inducing macrophage M2 polarization by a core–shell QRu-PLGA-RES-DS NPs nanocomposite with photothermal response for RA therapy.

Effect of dietary soybean meal associated with feeding time on the growth performance and intestinal microbiota composition of northern snakehead

2019 ◽  
Vol 50 (10) ◽  
pp. 2751-2759
Author(s):  
Shuyan Miao ◽  
Jinyu Zhu ◽  
Chenze Zhao ◽  
Longsheng Sun ◽  
Xiaojing Dong ◽  
...  
Keyword(s):  
Growth Performance ◽  
Intestinal Microbiota ◽  
Soybean Meal ◽  
Feeding Time ◽  
Microbiota Composition

scholarly journals MicroRNA-720 suppresses M2 macrophage polarization by targeting GATA3

2016 ◽  
Vol 36 (4) ◽  
Author(s):  
Yan Zhong ◽  
Chun Yi
Keyword(s):  
Macrophage Polarization ◽  
Ectopic Expression ◽  
Tumour Microenvironment ◽  
M2 Macrophage ◽  
Breast Carcinomas ◽  
Downstream Target ◽  
M2 Polarization ◽  
M2 Macrophage Polarization ◽  
And Function ◽  
M2 Phenotype

Macrophages are highly plastic cells with the ability to differentiate into both M1- and M2-polarized phenotypes. As a distinct M2-polarized population, tumour-associated macrophages (TAMs) promote tumorigenesis owing to their pro-angiogenic and immune-suppressive functions in tumour microenvironment. In the present study, we found that the microRNA-720 (miR-720) was down-regulated in TAMs isolated from breast carcinomas and M2-polarization macrophages. Overexpression of miR-720 attenuated M2 phenotype expression and thus inhibited M2 polarization. We further identified GATA binding protein 3 (GATA3), a transcriptional factor that plays an important role in M2 macrophage polarization, was the downstream target of miR-720. Ectopic expression of GATA3 restored the M2 phenotype in miR-720 overexpressed macrophages. Importantly, overexpression of miR-720 inhibited pro-migration behaviour and phagocytic ability of M2-polarized macrophages. Thus, our data suggest that miR-720 plays an important role in regulating M2 macrophage polarization and function.

scholarly journals CXCL16/CXCR6 Axis in Adipocytes Differentiated from Human Adipose Derived Mesenchymal Stem Cells Regulates Macrophage Polarization

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3410
Author(s):  
Seung-Cheol Lee ◽  
Yoo-Jung Lee ◽  
Inho Choi ◽  
Min Kim ◽  
Jung-Suk Sung
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Adipose Tissue ◽  
Macrophage Polarization ◽  
Inflammatory Factors ◽  
M2 Macrophage ◽  
M2 Polarization ◽  
Chemokine Ligand ◽  
Anti Inflammatory ◽  
Underlying Mechanisms

Adipocytes interact with adipose tissue macrophages (ATMs) that exist as a form of M2 macrophage in healthy adipose tissue and are polarized into M1 macrophages upon cellular stress. ATMs regulate adipose tissue inflammation by secreting cytokines, adipokines, and chemokines. CXC-motif receptor 6 (CXCR6) is the chemokine receptor and interactions with its specific ligand CXC-motif chemokine ligand 16 (CXCL16) modulate the migratory capacities of human adipose-derived mesenchymal stem cells (hADMSCs). CXCR6 is highly expressed on differentiated adipocytes that are non-migratory cells. To evaluate the underlying mechanisms of CXCR6 in adipocytes, THP-1 human monocytes that can be polarized into M1 or M2 macrophages were co-cultured with adipocytes. As results, expression levels of the M1 polarization-inducing factor were decreased, while those of the M2 polarization-inducing factor were significantly increased in differentiated adipocytes in a co-cultured environment with additional CXCL16 treatment. After CXCL16 treatment, the anti-inflammatory factors, including p38 MAPK ad ERK1/2, were upregulated, while the pro-inflammatory pathway mediated by Akt and NF-κB was downregulated in adipocytes in a co-cultured environment. These results revealed that the CXCL16/CXCR6 axis in adipocytes regulates M1 or M2 polarization and displays an immunosuppressive effect by modulating pro-inflammatory or anti-inflammatory pathways. Our results may provide an insight into a potential target as a regulator of the immune response via the CXCL16/CXCR6 axis in adipocytes.

scholarly journals Modulation of M2 macrophage polarization by the crosstalk between Stat6 and Trim24

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Tao Yu ◽  
Shucheng Gan ◽  
Qingchen Zhu ◽  
Dongfang Dai ◽  
Ni Li ◽  
...  
Keyword(s):  
Immune Responses ◽  
Macrophage Activation ◽  
Regulatory Mechanism ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Creb Binding Protein ◽  
Human Macrophages ◽  
M2 Polarization ◽  
M2 Macrophage Polarization ◽  
Negative Regulatory Mechanism

Abstract Stat6 is known to drive macrophage M2 polarization. However, how macrophage polarization is fine-tuned by Stat6 is poorly understood. Here, we find that Lys383 of Stat6 is acetylated by the acetyltransferase CREB-binding protein (CBP) during macrophage activation to suppress macrophage M2 polarization. Mechanistically, Trim24, a CBP-associated E3 ligase, promotes Stat6 acetylation by catalyzing CBP ubiquitination at Lys119 to facilitate the recruitment of CBP to Stat6. Loss of Trim24 inhibits Stat6 acetylation and thus promotes M2 polarization in both mouse and human macrophages, potentially compromising antitumor immune responses. By contrast, Stat6 mediates the suppression of TRIM24 expression in M2 macrophages to contribute to the induction of an immunosuppressive tumor niche. Taken together, our findings establish Stat6 acetylation as an essential negative regulatory mechanism that curtails macrophage M2 polarization.

scholarly journals Urolithin A, a Gut Metabolite, Induces Metabolic Reprogramming of Adipose Tissue by Promoting M2 Macrophage Polarization and Mitochondrial Function (OR12-02-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Ashley Toney ◽  
Soonkyu Chung
Keyword(s):  
Adipose Tissue ◽  
Mitochondrial Function ◽  
Macrophage Polarization ◽  
Peritoneal Macrophages ◽  
M2 Macrophage ◽  
M2 Polarization ◽  
M1 Polarization ◽  
Urolithin A ◽  
M2 Macrophage Polarization

Abstract Objectives Macrophage polarization into pro-inflammatory M1 status is associated with the pathologic progression of adipose remodeling, while M2 polarization is linked with the resolution of inflammation. Urolithin A (UroA) is a gut metabolite derived from ellagic acid found in berries and nuts. Emerging evidence suggests UroA exerts anti-inflammatory function, but the underlying mechanism remains unknown. This study aims to test the hypothesis that UroA attenuates adipose inflammation by promoting M2 macrophage polarization. Methods To investigate the direct role of UroA in vitro, primary bone marrow-derived macrophages (BMDM) were stimulated with LPS for M1 polarization or IL-4/IL-13 for M2 polarization. Oxygen consumption rate was determined in BMDM by Seahorse extracellular flux analyzer. The anti-inflammatory role of UroA is validated by pro-IL-1β Gaussia luciferase (iGLuc) reporter assay and IL-1β secretion in J774 macrophages. Additionally, C57BL/6 mice were fed with a HF diet for 12 weeks along with UroA administration. The M1/M2 polarization status were examined in adipose tissue macrophages (ATM) and peritoneal macrophages by qPCR and protein markers. Results UroA treatment in BMDM in vitro significantly decreased Il-1β (P < 0.001), while increasing M2 markers of Arg1, Ch313 and Mgl2 (P < 0.01). UroA treatment suppressed NLRP3 inflammasome activation in J774 macrophages by decreasing iGLuc activity and IL-1β secretion in a dose-dependent manner. In vivo, UroA administration reduced HF-induced adipocyte hypertrophy, inflammatory markers, and ATM recruitment (P < 0.01) in the adipose tissue. Consistently, UroA suppressed M1 polarization but switched to M2 polarization in peritoneal macrophages, evidenced by decreased M1 signature genes of Cd11c, Tnf-α, Il-6, and Il-1β (P < 0.01), while elevated M2 markers of Ch313 and Mgl2 (P < 0.05). Lastly, UroA not only inhibits HF-driven pathogenic remodeling of adipose tissue, but also promote mitochondrial function and biogenesis. Conclusions UroA attenuates HF-driven pathologic remodeling of adipose tissue by favoring M2 macrophage polarization and augmenting mitochondrial function. Intake of UroA-producing foods may be a promising intervention strategy to mitigate obesity-mediated chronic inflammation and metabolic dysfunction. Funding Sources United States Department of Agriculture National Institute for Food and Agriculture.

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