Lactobacillus acidophilus and Clostridium butyricum ameliorate colitis in murine by strengthening the gut barrier function and decreasing inflammatory factors

2018 ◽  
Vol 9 (5) ◽  
pp. 775-787 ◽  
Author(s):  
Y. Wang ◽  
Y. Gu ◽  
K. Fang ◽  
K. Mao ◽  
J. Dou ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Lactobacillus Acidophilus ◽  
Barrier Function ◽  
Clostridium Butyricum ◽  
In Vivo Studies ◽  
Inflammatory Factors ◽  
Sprague Dawley ◽  
Trinitrobenzenesulfonic Acid ◽  
Gut Barrier Function ◽  
Anti Inflammatory

Ulcerative colitis is a type of chronic inflammation present in the intestines for which the aetiology is not yet clear. The current therapies for ulcerative colitis cannot be considered to be long-term management strategies due to their significant side effects. Therefore, it is essential to identify an alternative therapeutic strategy for ulcerative colitis. The present study focused on the evaluation of the anti-inflammatory activities of Lactobacillus acidophilus CGMCC 7282 and Clostridium butyricum CGMCC 7281. The roles of both single and combination of L. acidophilus CGMCC 7282 and C. butyricum CGMCC 7281 in ulcerative colitis were investigated in 2,4,6-trinitrobenzenesulfonic acid-induced acute colitis (Th1-type colitis) in Sprague-Dawley rats and oxazolone-induced chronic colitis (Th2-type colitis) in BALB/c mice. The in vivo studies showed that the administration of L. acidophilus CGMCC 7282, C. butyricum CGMCC 7281 and L. acidophilus CGMCC 7282 plus C. butyricum CGMCC 7281 could reduce the Th1-type colitis as well as the Th2-type colitis, and the combination of the two strains exhibited the most notable effects, as indicated by the reduced mortality rates, the suppressed disease activity indices, the improved body weights, the reduced colon weight/colon length and colon weight/body weight ratios, and the improved gross anatomic characteristics and histological features (ameliorations of neutrophil infiltration and ulceration in the colon). It was found that the alterations of the gut microbiome, the barrier function changing and the selected inflammation-related cytokines are observed in the ulcerative colitis rats/mice treated with L. acidophilus CGMCC 7282 and C. butyricum CGMCC 7281. The combination of L. acidophilus CGMCC 7282 plus C. butyricum CGMCC 7281 also exerted a stronger anti-inflammatory effect than either of the single strains alone in vitro. These findings provide evidence that the administration of L. acidophilus CGMCC 7282 plus C. butyricum CGMCC 7281 may be a promising therapy for ulcerative colitis.

Abstract 131: Anti-inflammatory and Mitochondrial Effects of Butyrate in Shr Astrocytes in vitro

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Tao Yang ◽  
Ty Redler ◽  
Carla G Bueno Silva ◽  
Rebeca Arocha ◽  
Jordan Schmidt ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Rna Isolation ◽  
Inflammatory Factors ◽  
Pcr Analysis ◽  
Sprague Dawley ◽  
Beneficial Effects ◽  
Sd Rats ◽  
Anti Inflammatory

Emerging evidence demonstrates a significant link between gut dysbiosis and hypertension (HTN). Butyrate is one of the major fermented end-products of gut microbiota that reportedly produces beneficial effects on the immune system and metabolism. A contraction in butyrate-producing bacteria in the gut of spontaneously hypertensive rats (SHR) suggests that reduced butyrate may be associated with HTN. Considering its role in mitochondrial metabolism, we proposed that the positive anti-inflammatory effects of butyrate may be mediated via improvement in mitochondrial function in astrocytes. Methods: Sprague Dawley (SD) and SHR primary astrocytes from two-day old pups were cultured in DMEM, supplemented with 10% FBS and 1% pen/strep, for 14 days, prior to treatment with butyrate (0-1mM) for 4 hours. Cells were then subjected to the Seahorse XFe24 Extracellular Flux Analyzer to evaluate mitochondrial function following butyrate treatment. Additional samples were collected for total RNA isolation for real time PCR analysis of inflammatory factors and transcripts related to mitochondrial function and stress. Results: Butyrate significantly increased both basal and maximal mitochondrial respiration (by 3-4 fold, P<0.001) and elevated proton leak (by 4 fold, P<0.01) in astrocytes from SD rats but not SHR. Furthermore, we observed a trend for an increase in both ATP-linked and non-mitochondrial respiration in SD astrocytes compared to SHR (by 2-3 fold, P=0.07). This was associated with a significant reduction in relative expression levels in catalase (by 50%, P<0.05) and a trend in reduction in Sod1 and Sod2 (by 25%-50%, P=0.1) in astrocytes harvested from SD rats but not the SHR. Conversely, butyrate significantly lowered expression of pro-inflammatory Ccl2 (by 33%, P<0.05) and Tlr4 (by 48%, P <0.05) in astrocytes of SHR, but not SD rats. Conclusion: Butyrate modulated mitochondrial bioenergetics in SD but not the SHR, suggesting that the mitochondria of astrocytes may be less sensitive to the effects of butyrate in HTN. In addition, butyrate reduced inflammatory mediators in the SHR, but had no effect in the SD rat astrocytes. Thus, central anti-inflammatory effects of butyrate may be mediated via a mitochondria-independent mechanism.

scholarly journals Lentivirus-mediated downregulation of α-synuclein reduces neuroinflammation and promotes functional recovery in rats with spinal cord injury

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Hong Zeng ◽  
Nan Liu ◽  
Yan-yan Yang ◽  
Hua-yi Xing ◽  
Xiao-xie Liu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Functional Recovery ◽  
Barrier Function ◽  
Central Canal ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Sprague Dawley ◽  
Inflammatory Infiltration ◽  
Cord Injury

Abstract Background The prognosis of spinal cord injury (SCI) is closely related to secondary injury, which is dominated by neuroinflammation. There is evidence that α-synuclein aggregates after SCI and that inhibition of α-synuclein aggregation can improve the survival of neurons after SCI, but the mechanism is still unclear. This study was designed to investigate the effects of α-synuclein on neuroinflammation after SCI and to determine the underlying mechanisms. Method A T3 spinal cord contusion model was established in adult male Sprague-Dawley rats. An SNCA-shRNA-carrying lentivirus (LV-SNCA-shRNA) was injected into the injury site to block the expression of α-synuclein (forming the SCI+KD group), and the SCI and sham groups were injected with an empty vector. Basso-Beattie-Bresnahan (BBB) behavioural scores and footprint analysis were used to detect motor function. Inflammatory infiltration and myelin loss were measured in the spinal cord tissues of each group by haematoxylin-eosin (HE) and Luxol Fast Blue (LFB) staining, respectively. Immunohistochemistry, Western blot analysis, and RT-qPCR were used to analyse protein expression and transcription levels in the tissues. Immunofluorescence was used to determine the morphology and function of glial cells and the expression of matrix metalloproteinase-9 in the central canal of the spinal cord. Finally, peripheral serum cytokine levels were determined by enzyme-linked immunosorbent assay. Results Compared with the SCI group, the SCI+KD group exhibited reduced inflammatory infiltration, preserved myelin, and functional recovery. Specifically, the early arrest of α-synuclein inhibited the pro-inflammatory factors IL-1β, TNF-α, and IL-2 and increased the expression of the anti-inflammatory factors IL-10, TGF-β, and IL-4. The neuroinflammatory response was regulated by reduced proliferation of Iba1+ microglia/macrophages and promotion of the shift of M1-polarized Iba1+/iNOS+ microglia/macrophages to M2-polarized Iba1+/Arg1+ microglia/macrophages after injury. In addition, compared with the SCI group, the SCI+KD group also exhibited a smaller microglia/astrocyte (Iba1/GFAP) immunostaining area in the central canal, lower MMP-9 expression, and improved cerebrospinal barrier function. Conclusion Lentivirus-mediated downregulation of α-synuclein reduces neuroinflammation, improves blood-cerebrospinal barrier function, promotes functional recovery, reduces microglial activation, and promotes the polarization of M1 microglia/macrophages to an M2 phenotype to confer a neuroprotective immune microenvironment in rats with SCI.

scholarly journals Inflammatory Disease Processes and Interactions with Nutrition

2009 ◽  
Vol 101 (S1) ◽  
pp. 1-45 ◽  
Author(s):  
P. C. Calder ◽  
R. Albers ◽  
J.-M. Antoine ◽  
S. Blum ◽  
R. Bourdet-Sicard ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Vitamin E ◽  
Barrier Function ◽  
Inflammatory Responses ◽  
Clinical Symptoms ◽  
Tissue Injury ◽  
Inflammatory Reactions ◽  
Gut Barrier Function ◽  
Dietary Components ◽  
Anti Inflammatory

Inflammation is a stereotypical physiological response to infections and tissue injury; it initiates pathogen killing as well as tissue repair processes and helps to restore homeostasis at infected or damaged sites. Acute inflammatory reactions are usually self-limiting and resolve rapidly, due to the involvement of negative feedback mechanisms. Thus, regulated inflammatory responses are essential to remain healthy and maintain homeostasis. However, inflammatory responses that fail to regulate themselves can become chronic and contribute to the perpetuation and progression of disease. Characteristics typical of chronic inflammatory responses underlying the pathophysiology of several disorders include loss of barrier function, responsiveness to a normally benign stimulus, infiltration of inflammatory cells into compartments where they are not normally found in such high numbers, and overproduction of oxidants, cytokines, chemokines, eicosanoids and matrix metalloproteinases. The levels of these mediators amplify the inflammatory response, are destructive and contribute to the clinical symptoms. Various dietary components including long chain ω-3 fatty acids, antioxidant vitamins, plant flavonoids, prebiotics and probiotics have the potential to modulate predisposition to chronic inflammatory conditions and may have a role in their therapy. These components act through a variety of mechanisms including decreasing inflammatory mediator production through effects on cell signaling and gene expression (ω-3 fatty acids, vitamin E, plant flavonoids), reducing the production of damaging oxidants (vitamin E and other antioxidants), and promoting gut barrier function and anti-inflammatory responses (prebiotics and probiotics). However, in general really strong evidence of benefit to human health through anti-inflammatory actions is lacking for most of these dietary components. Thus, further studies addressing efficacy in humans linked to studies providing greater understanding of the mechanisms of action involved are required.

scholarly journals Rottlerin ameliorates DSS-induced colitis by improving intestinal barrier function via activation of the Epac-2/Rap-1 signaling pathway

2020 ◽  
Author(s):  
Xue Song ◽  
Lugen Zuo ◽  
Luyao Wang ◽  
Zihan Zhu ◽  
Jing Tao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Inflammatory Factors ◽  
Intestinal Barrier Function ◽  
Control Group ◽  
Treatment Groups ◽  
Normal Feeding ◽  
Anti Inflammatory

ABSTRACTOBJECTIVESRottlerin, a pan PDE inhibitor, has a variety of pharmacological activities, including enhancing barrier function and mediating anti-inflammatory activity by changing the distribution of occludin and ZO-1. Nevertheless, the function of rottlerin on Crohn disease (CD) keep unknown. Our aim of the study is to investigate the role of rottlerin on CD-like colitis and its mechanism.METHODSWild-type mice which were 8-10 weeks old were randomly divided into three treatment groups: (i) the normal feeding, no administration (control) group, (ii) the group administered 3% dextran sodium sulfate (DSS) alone, and (iii) the group administered rottlerin (100 mg/kg) and 3% DSS. In this study, the effect of rottlerin on the function and structure of the intestinal barrier was investigated, and the possible mechanism was discussed. We performed signaling pathway analysis and flow cytometry to identify the detailed mechanisms by which rottlerin (10 μg/mL) treatment inhibits cell growth arrest and the attenuation of TJ proteins in LPS-treated FHs 74 int cells.RESULTSRottlerin treatment significantly ameliorated colitis induced by DSS in WT mice, which was manifested by a decrease in inflammation score, the attenuation of inflammatory factors and the inhibition of destruction on intestinal barrier structure. Rottlerin enhanced the levels of occludin and ZO-1, and improved the function of intestinal barrier, which may have been why rottlerin ameliorated colitis in WT mice. The anti-inflammatory effect of rottlerin may be partly due to the activation of Epac-2/Rap-1 signaling.CONCLUSIONSRottlerin may treat CD in humans via enhancing TJ proteins expression and improving the function of intestinal barrier.

scholarly journals The Anti-Inflammatory Effect and Mucosal Barrier Protection of Clostridium butyricum RH2 in Ceftriaxone-Induced Intestinal Dysbacteriosis

2021 ◽  
Vol 11 ◽  
Author(s):  
Yuyuan Li ◽  
Man Liu ◽  
He Liu ◽  
Xue Sui ◽  
Yinhui Liu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Intestinal Inflammation ◽  
Clostridium Butyricum ◽  
Mucosal Barrier ◽  
Inflammatory Factors ◽  
High Dose ◽  
Intestinal Integrity ◽  
Tnf Α ◽  
Anti Inflammatory

This study aimed at determining the beneficial effect of Clostridium butyricum (CB) RH2 on ceftriaxone-induced dysbacteriosis. To this purpose, BALB/c mice were exposed to ceftriaxone (400 mg/ml) or not (control) for 7 days, and administered a daily oral gavage of low-, and high-dose CB RH2 (108 and 1010 CFU/ml, respectively) for 2 weeks. CB RH2 altered the diversity of gut microbiota, changed the composition of gut microbiota in phylum and genus level, decreased the F/B ratio, and decreased the pro-inflammatory bacteria (Deferribacteres, Oscillibacter, Desulfovibrio, Mucispirillum and Parabacteroides) in ceftriaxone-treated mice. Additionally, CB RH2 improved colonic architecture and intestinal integrity by improving the mucous layer and the tight junction barrier. Furthermore, CB RH2 also mitigated intestinal inflammation through decreasing proinflammatory factors (TNF-α and COX-2) and increasing anti-inflammatory factors (IL-10). CB RH2 had direct effects on the expansion of CD4+ T cells in Peyer’s patches (PPs) in vitro, which in turn affected their immune response upon challenge with ceftriaxone. All these data suggested that CB RH2 possessed the ability to modulate the intestinal mucosal and systemic immune system in limiting intestinal alterations to relieve ceftriaxone-induced dysbacteriosis.

Hypothesis about mechanisms through which nicotine might exert its effect on the interdependence of inflammation and gut barrier function in ulcerative colitis

2007 ◽  
Vol 13 (1) ◽  
pp. 108-115 ◽  
Author(s):  
Victoria E. McGilligan ◽  
Julie M. W. Wallace ◽  
Patricia M. Heavey ◽  
Diana L. Ridley ◽  
Ian R. Rowland
Keyword(s):  
Ulcerative Colitis ◽  
Barrier Function ◽  
Gut Barrier ◽  
Gut Barrier Function

scholarly journals Pingkui Enema Alleviates TNBS-Induced Ulcerative Colitis by Regulation of Inflammatory Factors, Gut Bifidobacterium, and Intestinal Mucosal Barrier in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Hai-Feng Yun ◽  
Rui Liu ◽  
Dan Han ◽  
Xin Zhao ◽  
Jin-Wei Guo ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Survival Rate ◽  
Serum Concentration ◽  
Mucosal Barrier ◽  
Inflammatory Factors ◽  
High Dose ◽  
Trinitrobenzene Sulfonic Acid ◽  
Sprague Dawley ◽  
Intestinal Mucosal Barrier ◽  
Intestinal Mucus

Background. Ulcerative colitis (UC) is a chronic recurrent inflammation of the colon, and clinical outcome of UC is still unsatisfied. Pingkui enema, a traditional Chinese medicine prescription, has been safely applied for the treatment of diarrhea and dysentery in clinic for many years. However, its mechanism is still elusive. The present study is designed to investigate the effect of Pingkui enema on trinitrobenzene sulfonic acid- (TNBS-) induced ulcerative colitis (UC) and possible mechanism in rats. Methods. UC was induced by intracolonic instillation of TNBS in male Sprague-Dawley rats, which were treated with different dosages of Pingkui enema (low, medium, and high) or sulfasalazine for ten days. Survival rate was calculated. A clinical disease activity score was evaluated. Histological colitis severity was analyzed by hematoxylin-eosin (HE) staining. Content of Bifidobacterium in intestinal tissue was analyzed by RT-PCR. Concentration of IL-8, IL-13, TNF-α, D-lactic acid (D-LA), and diamine oxidase (DAO) in serum and contents of adhesin and receptor of Bifidobacterium adhesion in rat intestinal mucus were measured by ELISA. Results. The results showed that Pingkui enema treatment with high dosage markedly improved the survival rate compared with untreated and sulfasalazine treated groups. All dosages of Pingkui enema reduced pathological score. High dosage of Pingkui enema and sulfasalazine treatments significantly reduced the serum concentration of IL-8, TNF-α, D-LA, and DAO and markedly increased the serum concentration of IL-13. In addition, high-dose Pingkui enema and sulfasalazine treatments increased gut content of Bifidobacterium, gut mucus expressions of adhesin, and adhesin receptor of Bifidobacterium. Conclusions. Pingkui enema has therapeutic effect on TNBS-induced UC, and possible mechanism may be via regulation of gut probiotics (Bifidobacterium) and inflammatory factors and protection of intestinal mucosal barrier.

Protective effect of dexmedetomidine on intestinal mucosal barrier function in rats after cardiopulmonary bypass

2021 ◽  
pp. 153537022110625
Author(s):  
Tong Jia ◽  
Zhen Xing ◽  
Huijuan Wang and ◽  
Guoli Li
Keyword(s):  
Cardiopulmonary Bypass ◽  
Inflammatory Response ◽  
Barrier Function ◽  
Mucosal Damage ◽  
Mucosal Barrier ◽  
Inflammatory Factors ◽  
Intestinal Damage ◽  
Intestinal Mucosal Barrier ◽  
Mucosal Barrier Function ◽  
Anti Inflammatory

Cardiopulmonary bypass can result in damage to the intestines, leading to the occurrence of systemic inflammatory response syndrome. Dexmedetomidine is reported to confer anti-inflammatory properties. Here, the purpose of this study is to investigate the effect of dexmedetomidine on the intestinal mucosa barrier damage in a rat model of cardiopulmonary bypass. It was observed that cardiopulmonary bypass greatly decreased the levels of hemodynamic parameters than SHAM group, whereas dexmedetomidine pretreatment in a cardiopulmonary bypass model rat prevented this reduction. Also, it showed that compared with control animals, cardiopulmonary bypass caused obvious mucosal damage, which was attenuated in dexmedetomidine + cardiopulmonary bypass group. The above findings were in line with that of dexmedetomidine pretreatment, which increased the expression of tight junction proteins, but it decreased the levels of DAO, D-LA, FABP2, and endotoxin. Moreover, the results demonstrated that due to pre-administration of dexmedetomidine, the level of pro-inflammatory factors was decreased, while the level of anti-inflammatory cytokine was increased. Also, it showed that dexmedetomidine suppressed TLR4/JAK2/STAT3 pathway that was activated by cardiopulmonary bypass. Together, these results revealed that dexmedetomidine pretreatment relieves intestinal microcirculation, attenuates intestinal damage, and inhibits the inflammatory response of cardiopulmonary bypass model rats, demonstrating that in CPB-induced damage of intestinal mucosal barrier function, dexmedetomidine pretreatment plays a protective role by inactivating TLR4/JAK2/STAT3-mediated inflammatory pathway.

scholarly journals Anti-Acetylcholinesterase, Anti-Inflammatory and Anti-Oxidant Activities of Raw-Extract Centella Asiatica (RECA) on Lipopolysaccharide (LPS)-Induced Neuroinflammation Sprague Dawley Rats

2019 ◽  
Vol 7 (4.14) ◽  
pp. 96
Author(s):  
Z Hafiz ◽  
N Shamsuddin ◽  
S M Mukhtar ◽  
R J James ◽  
M I Adenan
Keyword(s):  
Oxidative Stress ◽  
Centella Asiatica ◽  
In Vivo Studies ◽  
Ache Inhibitor ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Anti Oxidant ◽  
Anti Inflammatory ◽  
And Oxidative Stress

The present study was designed to investigate the potential of raw-extract of Centella asiatica (RECA) in suppressing acetylcholinesterase (AChE), inflammations and oxidative stress via induction of lipopolysaccharide (LPS) on animal model of Sprague Dawley rats. Centella asiatica is a plant that has been used as a traditional herbal remedy for the management of several diseases, including memory improvement, treatment of mental fatigue and wound healing. Pre-treatment with RECA in vitro significantly reduced the AChE activity in a concentration-dependent manner with IC50 value of 57.47 ± 13.55 µg/ml. Interestingly, this result was parallel with in vivo studies. Moreover, the level of pro-inflammatory cytokines and oxidative stress were significantly reduced by RECA in dose-dependent manner. Overall, our findings clearly dictate the potential of RECA as AChE inhibitor as well anti-inflammatory and anti-oxidant agents. 

Bofutsushosan Improves Gut Barrier Function with a Bloom of Akkermansia Muciniphila and Improves Glucose Metabolism in Diet-Induced Obese Mice

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1990-P ◽  
Author(s):  
SHIHO FUJISAKA ◽  
ISAO USUI ◽  
ALLAH NAWAZ ◽  
YOSHIKO IGARASHI ◽  
TOMONOBU KADO ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Barrier Function ◽  
Obese Mice ◽  
Gut Barrier ◽  
Akkermansia Muciniphila ◽  
Gut Barrier Function
Sign in / Sign up

Export Citation Format

Share Document