scholarly journals Probiotic Bifidobacterium bifidum G9-1 Has a Preventive Effect on the Acceleration of Colonic Permeability and M1 Macrophage Population in Maternally Separated Rats

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 641
Author(s):  
Xuan Wang ◽  
Hirokazu Fukui ◽  
Ying Ran ◽  
Xin Xu ◽  
Nobuhiko Ebisutani ◽  
...  
Keyword(s):  
Maternal Separation ◽  
Ussing Chamber ◽  
Bifidobacterium Bifidum ◽  
Preventive Effect ◽  
Mucosal Permeability ◽  
Macrophage Population ◽  
Mucosal Integrity ◽  
Caco2 Cells ◽  
M1 Macrophage ◽  
Ifn Γ

Although probiotics may be useful for the treatment of irritable bowel syndrome (IBS), it is unclear how probiotics play a role in colonic mucosal integrity and immunity. Here, we aimed to investigate the effect of Bifidobacterium bifidum G9-1 (BBG9-1) on colonic mucosal integrity and macrophage behavior in rats subjected to maternal separation (MS) as a model of IBS. MS pups were individually separated from their mother rats, and a proportion of the MS rats were orally administered BBG9-1. The colonic mucosal permeability was evaluated by Ussing chamber assay. The expression of tight junction proteins and cytokines and the population of CD80-positive cells was examined in the colonic tissues by real-time reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry. Caco2 cells were stimulated with cytokines and the transepithelial electric resistance (TEER) was measured. MS rats showed significantly higher colonic permeability and lower claudin 4 expression in the colonic epithelium relative to controls. The number of CD80-positive macrophages was significantly increased in the colonic mucosa of MS rats, accompanied by the increase of IL-6 and IFN-γ expression. BBG9-1 treatment ameliorated the increase of M1 macrophage and IL-6/IFN-γ expression in the colonic tissue of MS rats. Simultaneously, BBG9-1 treatment improved the enhanced mucosal permeability and the decreased claudin 4 expression in the colon of MS rats. IL-6 and IFN-γ, whose expression is enhanced in the colon of MS rats, significantly decreased TEER in Caco2 cells in vitro. Probiotic BBG9-1 has a preventive effect on the acceleration of colonic permeability and M1 macrophage population in maternally separated rats.

scholarly journals Alteration of Colonic Mucosal Permeability during Antibiotic-Induced Dysbiosis

2020 ◽  
Vol 21 (17) ◽  
pp. 6108
Author(s):  
Ying Ran ◽  
Hirokazu Fukui ◽  
Xin Xu ◽  
Xuan Wang ◽  
Nobuhiko Ebisutani ◽  
...  
Keyword(s):  
Colonic Mucosa ◽  
Polymyxin B ◽  
Mucosal Barrier ◽  
Rt Pcr ◽  
Mucosal Permeability ◽  
16S Rrna Analysis ◽  
Caco2 Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Microbiota Diversity

Although dysbiosis is likely to disturb the mucosal barrier system, the mechanism involved has remained unclear. Here, we investigated alterations of colonic mucosal permeability and tight junction (TJ) molecules in mice with antibiotic-induced dysbiosis. Mice were orally administered vancomycin or polymyxin B for 7 days, and then fecal samples were subjected to microbial 16S rRNA analysis. The colonic mucosal permeability was evaluated by chamber assay. The colonic expression of TJ molecules and cytokines was examined by real-time RT-PCR, Western blotting, and immunohistochemistry. Caco2 cells were stimulated with cytokines and their transepithelial electric resistance (TEER) was measured. Vancomycin-treated mice showed significantly lower gut microbiota diversity than controls, and the same tendency was evident in polymyxin B-treated mice. The colonic mucosal permeability was significantly elevated in both vancomycin- and polymyxin B-treated mice. The expression of claudin 4 in the colonic mucosa was decreased in both vancomycin- and polymyxin B-treated mice. Colonic expression of TNF-α and/or IFN-γ was significantly increased in mice that had been administered antibiotics. TNF-α and IFN-γ stimulation dose-dependently decreased TEER in Caco2 cells. Antibiotic-induced dysbiosis is correlated with the enhancement in colonic tissue permeability, accompanied by a reduction in claudin 4 expression and enhancement in TNF-α and/or IFN-γ expression in mice.

scholarly journals Role of interplay between IL-4 and IFN-γ in the in regulating M1 macrophage polarization induced by Nattectin

2012 ◽  
Vol 14 (4) ◽  
pp. 513-522 ◽  
Author(s):  
Edson Kiyotaka Ishizuka ◽  
Marcio José Ferreira ◽  
Lidiane Zito Grund ◽  
Erica Maria Martins Coutinho ◽  
Evilin Naname Komegae ◽  
...  
Keyword(s):  
Macrophage Polarization ◽  
M1 Macrophage ◽  
Ifn Γ

scholarly journals Chronic Hepatitis C Virus Infection Impairs M1 Macrophage Differentiation and Contributes to CD8+ T-Cell Dysfunction

Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 374 ◽  
Author(s):  
Faria Ahmed ◽  
Andrea Ibrahim ◽  
Curtis L. Cooper ◽  
Ashok Kumar ◽  
Angela M. Crawley
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cells ◽  
Cd8 T Cell ◽  
Hcv Infection ◽  
M1 Macrophage ◽  
T Cell Dysfunction ◽  
Chronic Hcv Infection ◽  
Ifn Γ ◽  
Chronic Hcv

Chronic hepatitis C virus (HCV) infection causes generalized CD8+ T cell impairment, not limited to HCV-specific CD8+ T-cells. Liver-infiltrating monocyte-derived macrophages (MDMs) contribute to the local micro-environment and can interact with and influence cells routinely trafficking through the liver, including CD8+ T-cells. MDMs can be polarized into M1 (classically activated) and M2a, M2b, and M2c (alternatively activated) phenotypes that perform pro- and anti-inflammatory functions, respectively. The impact of chronic HCV infection on MDM subset functions is not known. Our results show that M1 cells generated from chronic HCV patients acquire M2 characteristics, such as increased CD86 expression and IL-10 secretion, compared to uninfected controls. In contrast, M2 subsets from HCV-infected individuals acquired M1-like features by secreting more IL-12 and IFN-γ. The severity of liver disease was also associated with altered macrophage subset differentiation. In co-cultures with autologous CD8+ T-cells from controls, M1 macrophages alone significantly increased CD8+ T cell IFN-γ expression in a cytokine-independent and cell-contact-dependent manner. However, M1 macrophages from HCV-infected individuals significantly decreased IFN-γ expression in CD8+ T-cells. Therefore, altered M1 macrophage differentiation in chronic HCV infection may contribute to observed CD8+ T-cell dysfunction. Understanding the immunological perturbations in chronic HCV infection will lead to the identification of therapeutic targets to restore immune function in HCV+ individuals, and aid in the mitigation of associated negative clinical outcomes.

Effect of curcumin on the non-alcoholic steatohepatitis via inhibiting the M1 polarization of macrophages

2021 ◽  
pp. 096032712110387
Author(s):  
Cong Tong ◽  
Hongfei Wu ◽  
Da Gu ◽  
Yanian Li ◽  
Yuhan Fan ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Mrna Expression ◽  
Tunel Staining ◽  
Rt Pcr ◽  
Alcoholic Steatohepatitis ◽  
M1 Polarization ◽  
M1 Macrophage ◽  
Tnf Α ◽  
Hematoxylin And Eosin ◽  
Ifn Γ

Background Non-alcoholic steatohepatitis (NASH) is a global medical problem and macrophages’ activation is closely related to the pathogenesis of NASH. Curcumin is a polyphenol from turmeric with significant anti-inflammatory activity. Objective The objective of present study was to observe the effect of curcumin on macrophages’ activation and secretion of pro-inflammatory cytokines in NASH. Methods Hematoxylin and eosin and TUNEL staining were used to observe the hepatic function. RT-PCR was conducted to evaluate the hepatic mRNA expression of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). Flow cytometry was adopted to detect the M1 polarization of macrophages. The RAW264.7 macrophage was pretreated with different doses of curcumin, and then lipopolysaccharide (LPS) and interferon-γ (IFN-γ) were given to activate the M1 macrophage. The activation ratio of M1 macrophage was observed by flow cytometry, and IL-1β and TNF-α expression was detected by RT-PCR and ELISA. Results After treatment with curcumin, the activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), the mRNA expression of TNF-α and IL-1β, and M1 polarization of macrophages were significantly decreased. Hematoxylin and eosin and TUNEL staining showed that inflammation and apoptosis in the liver were improved. What is more, curcumin can effectively inhibit M1 macrophage activation induced by lipopolysaccharide and IFN-γ and reduce the secretion of IL-1β and TNF-α. Conclusion Curcumin can effectively improve NASH and reduce hepatic cell necrosis by inhibiting the M1 polarization of macrophages and the secretion of inflammatory factors.

scholarly journals Mucosal integrity and sensitivity to acid in the proximal esophagus in patients with gastroesophageal reflux disease

2016 ◽  
Vol 311 (1) ◽  
pp. G117-G122 ◽  
Author(s):  
Froukje B. van Hoeij ◽  
Pim W. Weijenborg ◽  
Marius A. van den Bergh Weerman ◽  
René M. J. G. J. van den Wijngaard ◽  
J. Verheij ◽  
...  
Keyword(s):  
Gastroesophageal Reflux Disease ◽  
Gastroesophageal Reflux ◽  
Reflux Disease ◽  
Distal Esophagus ◽  
Mucosal Permeability ◽  
Tissue Impedance ◽  
Mucosal Integrity ◽  
Proximal Esophagus ◽  
Acid Perfusion

Acid reflux episodes that extend to the proximal esophagus are more likely to be perceived. This suggests that the proximal esophagus is more sensitive to acid than the distal esophagus, which could be caused by impaired mucosal integrity in the proximal esophagus. Our aim was to explore sensitivity to acid and mucosal integrity in different segments of the esophagus. We used a prospective observational study, including 12 patients with gastroesophageal reflux disease (GERD). After stopping acid secretion-inhibiting medication, two procedures were performed: an acid perfusion test and an upper endoscopy with electrical tissue impedance spectroscopy and esophageal biopsies. Proximal and distal sensitivity to acid and tissue impedance were measured in vivo, and mucosal permeability and epithelial intercellular spaces at different esophageal levels were measured in vitro. Mean lag time to heartburn perception was much shorter after proximal acid perfusion (0.8 min) than after distal acid perfusion (3.9 min) ( P = 0.02). Median in vivo tissue impedance was significantly lower in the distal esophagus (4,563 Ω·m) compared with the proximal esophagus (8,170 Ω·m) ( P = 0.002). Transepithelial permeability, as measured by the median fluorescein flux was significantly higher in the distal (2,051 nmol·cm−2·h−1) than in the proximal segment (368 nmol·cm−2·h−1) ( P = 0.033). Intercellular space ratio and maximum heartburn intensity were not significantly different between the proximal and distal esophagus. In GERD patients off acid secretion-inhibiting medication, acid exposure in the proximal segment of the esophagus provokes symptoms earlier than acid exposure in the distal esophagus, whereas mucosal integrity is impaired more in the distal esophagus. These findings indicate that the enhanced sensitivity to proximal reflux episodes is not explained by increased mucosal permeability.

scholarly journals Preventive Effect of Blueberry Extract on Liver Injury Induced by Carbon Tetrachloride in Mice

Foods ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 48 ◽  
Author(s):  
Bihui Liu ◽  
Yuan Fang ◽  
Ruokun Yi ◽  
Xin Zhao
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Messenger Rna ◽  
Tbars Level ◽  
Preventive Effect ◽  
Polyphenol Content ◽  
Sod Activity ◽  
Standard Drug ◽  
Tnf Α ◽  
Ifn Γ

The blueberry is a common fruit that is rich in nutritional value and polyphenol substances. In this study, the blueberry polyphenol content in extract was analysed by spectrophotometry. The results showed that the blueberry polyphenol content in the extract reached 52.7%. A mouse model of liver injury induced by carbon tetrachloride (CCl4) was established to study the preventive effect of blueberry extract (BE) on liver injury in mice and the experimental animals were examined using biochemical and molecular biological methods. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are important clinical liver function indicators; the changes of triglyceride (TG) and total cholesterol (TC) are observed after liver injury; interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) are important inflammatory indexes; superoxide dismutase (SOD) activity and thiobarbituric acid reactive substances (TBARS) are important changes of oxidative stress indexes. The in vivo animal experiment results showed that BE decreased the liver index of mice with liver injury, BE could reduce the AST, ALT, TG and TC levels and also could reduce the serum cytokine IL-6, TNF-α and IFN-γ levels in mice with liver injury. Moreover, BE increased the SOD activity and decreased the TBARS level in the gastric tissues of mice with liver injury. After treatment with the highest concentration of BP in liver injury mice, these levels returned close to those obtained after treatment with the standard drug of silymarin. Detection of messenger RNA (mRNA) in liver tissue showed that BE upregulated the Cu/Zn-SOD, Mn-SOD and chloramphenicol acetyltransferase (CAT) expression levels and downregulated cyclooxygenase (COX)-2 expression. The effect of BE on mice with liver injury was positively correlated with the BE concentration and was similar to that of silymarin, which is a drug for liver injury, suggesting that BE had a good preventive effect on liver injury. Thus, BE rich in polyphenols is a bioactive substance with value for development and utilization.

scholarly journals TET1 Knockdown Inhibits Porphyromonas gingivalis LPS/IFN-γ-Induced M1 Macrophage Polarization through the NF-κB Pathway in THP-1 Cells

2019 ◽  
Vol 20 (8) ◽  
pp. 2023 ◽  
Author(s):  
Huang ◽  
Tian ◽  
Li ◽  
Xu
Keyword(s):  
Porphyromonas Gingivalis ◽  
Periodontal Diseases ◽  
Macrophage Polarization ◽  
Control Group ◽  
M1 Macrophages ◽  
Expression Levels ◽  
Hla Dr ◽  
M1 Macrophage ◽  
Significant Difference ◽  
Ifn Γ

Tet-eleven translocation 1 (TET1) is a dioxygenase that plays an important role in decreasing the abundance of DNA methylation and changing the expression levels of specific genes related to inflammation. Porphyromonas gingivalis (Pg.) lipopolysaccharide (LPS) can induce periodontal diseases that present with severe bone loss and collagen fiber destruction accompanied by a high number of M1 macrophages. M1-polarized macrophages are pivotal immune cells that promote the progression of the periodontal inflammatory response, but the function of TET1 during M1 macrophage activation is still unknown. Our results showed that the mRNA and protein expression levels of TET1 decreased in THP-1 cells during M1 macrophage differentiation. TET1 knockdown resulted in a significant decrease in the production of proinflammatory markers such as IL-6, TNF-α, CCL2, and HLA-DR in Pg. LPS/IFN-γ- and Escherichia coli (E. coli) LPS/IFN-γ-induced M1 macrophages. Mechanistically, TET1 knockdown downregulated the activity of the NF-κB signaling pathway. After treatment with the NF-κB inhibitor BAY 11-7082, M1 marker expression showed no significant difference between the TET1 knockdown group and the control group. Taken together, these results suggest that TET1 depletion inhibited Pg. LPS/IFN-γ-induced M1 macrophage polarization through the NF-κB pathway in THP-1 cells.

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