Bifidobacterium pseudocatenulatum CECT7765 induces an M2 anti-inflammatory transition in macrophages from patients with cirrhosis

Moratalla, Alba; Caparrós, Esther; Juanola, Oriol; Portune, Kevin J.; Puig‐Kröger, Amaya; Estrada-Capetillo, Lizbeth; Bellot, Pablo; Gómez‐Hurtado, Isabel; Piñero, Paula; Zapater, Pedro; González‐Navajas, José M.; Such, José; Sanz, Yolanda; Francés, Rubén

doi:10.1016/j.jhep.2015.08.020

Cited by 34 publications

(30 citation statements)

References 37 publications

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“…Studies have reported that gut microbiota play an important role in shaping the Treg/Th17 axis in adaptive immune response ( 69 ). Alba et al demonstrated the efficacy of Bifidobacterium for the treatment of patients with cirrhosis through inducing a morphologic, phenotypic and functional transition towards an anti-inflammatory profile ( 70 ). Rui Yu et al investigated two Bifidobacterium.…”

Section: Discussionmentioning

confidence: 99%

Bifidobacterium animalis ssp. Lactis 420 Mitigates Autoimmune Hepatitis Through Regulating Intestinal Barrier and Liver Immune Cells

Zhang

Liu

et al. 2020

Front. Immunol.

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Autoimmune hepatitis (AIH) is an immune-mediated inflammatory liver disease of uncertain cause. Accumulating evidence shows that gut microbiota and intestinal barrier play significant roles in AIH thus the gut–liver axis has important clinical significance as a potential therapeutic target. In the present study, we found that Bifidobacterium animalis ssp. lactis 420 (B420) significantly alleviated S100-induced experimental autoimmune hepatitis (EAH) and modulated the gut microbiota composition. While the analysis of clinical specimens revealed that the fecal SCFA quantities were decreased in AIH patients, and B420 increased the cecal SCFA quantities in EAH mice. Remarkably, B420 application improved intestinal barrier function through upregulation of tight junction proteins in both vitro and vivo experiments. Moreover, B420 decreased the serum endotoxin level and suppressed the RIP3 signaling pathway of liver macrophages in EAH mice thus regulated the proliferation of Th17 cells. Nevertheless, the inhibition effect of B420 on RIP3 signaling pathway was blunted in vitro studies. Together, our results showed that early intervention with B420 contributed to improve the liver immune homeostasis and liver injury in EAH mice, which might be partly due to the protection of intestinal barrier. Our study suggested the potential efficacy of probiotics application against AIH and the promising therapeutic strategies targeting gut–liver axis for AIH.

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Section: Discussionmentioning

confidence: 99%

Bifidobacterium animalis ssp. Lactis 420 Mitigates Autoimmune Hepatitis Through Regulating Intestinal Barrier and Liver Immune Cells

Zhang

Liu

et al. 2020

Front. Immunol.

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“…In addition, it has been suggested that probiotics can potentially influence equilibrium of commensal and pathogenic bacteria, and thereby destroy homeostasis in inflammatory conditions[13]. Moreover, probiotics modulate intestinal mucosal immune function, which plays a protective role in maintaining the intestinal barrier function[20].…”

Section: Discussionmentioning

confidence: 99%

“…Bifidobacterium is an anaerobic Gram-positive bacteria, with 32 subspecies, of which 28 subspecies have been detected in the human gut[13]. Intestinal bifidobacteria appear within 3 to 4 d postnatally, and bifidobacteria comprise approximately 25% of total intestinal bacteria[20].…”

Section: Discussionmentioning

confidence: 99%

“…Bifidobacterium, a bacterial commensal, reduces release of endotoxins through reduction of superfluous Gram-negative bacilli to normal levels, thereby functioning as a detoxifying agent[13]. Acidic products produced by protective bifidobacterium are essential to maintain normal intestinal conditions and improve mediation of intestinal defense by epithelial cells[14].…”

Section: Introductionmentioning

confidence: 99%

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Effect of EPEC endotoxin and bifidobacteria on intestinal barrier function through modulation of toll-like receptor 2 and toll-like receptor 4 expression in intestinal epithelial cell-18

Xia

Gao

et al. 2017

WJG

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AIMTo investigate toll-like receptor 2 (TLR2) and TLR4 expression, following bifidobacteria and low-dose EPEC endotoxin treatment, and intestinal barrier function in rat intestinal epithelial cell18 (IEC18).METHODSSix experimental groups were established - normal control, EPEC, Bifidobacteria infantis (B. infantis), B. longum, B. bifidum, and B. youth groups. Optimal EPEC endotoxin concentration, bifidobacteria fold dilution, and treatment duration were determined. Quantitative real-time polymerase chain reaction and western blot, respectively, were conducted to detect TLR2 and TLR4 mRNA and protein expression in IEC-18 cells. Transepithelial electrical resistance (TEER) was measured by the EVOM chopstick voltohmmeter in each group. All experiments were conducted in triplicate and data were analyzed on SPSS 16.RESULTSTLR2 and TLR4 mRNA and protein expression in the EPEC group were significantly higher than in the control group (P < 0.05). TLR2 mRNA and protein expression in the B. infantis, B. longum and B. youth groups were significantly lower than in the normal control group (P < 0.05). TLR4 mRNA and protein expression in the B. bifidum and B. youth groups were significantly lower than in normal controls (P < 0.05). In addition, the TEER in B. infantis, B. longum, B. bifidum, and B. youth groups were decreased by 19%, 18%, 23% and 23%, respectively, after 120 min of intervention, as compared to the control group. However, the TEER in the EPEC group was significantly decreased by 67% in comparison to the normal control group (P < 0.05).CONCLUSIONBifidobacteria protect IEC-18 cells against injury by down-regulating TLR2 and TLR4 expression and enhance intestinal barrier function to protect the intestinal epithelial cells from pathogenic invasion.

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“…LPS induces the production of inflammatory cytokines, resulting in subsequent liver tissue injury (5). Furthermore, LPS induces Kupffer cell activation via the Toll-like receptor 4 signaling pathway, and subsequently activates nuclear factor (NF)-κB and initiates the release of inflammatory cytokines, including interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α (6,7).…”

Section: Introductionmentioning

confidence: 99%

Nobiletin attenuates lipopolysaccharide/D-galactosamine-induced liver injury in mice by activating the Nrf2 antioxidant pathway and subsequently inhibiting NF-κB-mediated cytokine production

Chen

et al. 2016

Molecular Medicine Reports

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Inflammation and oxidative stress serve an important role in the development of lipopolysaccharide/D-galactosamine (LPS/GalN)‑induced acute liver injury. Nobiletin, which is found in high quantities in the peel of citrus fruits, is able to modulate immune responses, including inflammatory response and oxidative stress. The present study aimed to evaluate the protective effects of nobiletin on LPS/GalN‑induced acute liver injury. Male C57BL/6 mice were intraperitoneally treated with nobiletin (50, 100 and 200 mg/kg) 2 h prior to LPS/GalN injection. Liver injury was observed in the LPS/GalN group, as demonstrated by increased levels of serum hepatic enzymes and hepatic inflammatory mediators, as well as by histopathological alterations. Treatment with nobiletin reduced serum alanine aminotransferase and aspartate aminotransferase levels, improved hepatic structure, and suppressed hepatic interleukin (IL)‑1β, IL‑6 and tumor necrosis factor‑α production 24 h after LPS/GalN exposure. Western blot analysis revealed that nobiletin treatment inhibited inducible nitric oxide synthase and cyclooxygenase‑2 liver expression. In addition, nobiletin suppressed LPS/GalN‑induced phosphorylation and degradation of inhibitor of nuclear factor (NF)‑κB (IκB)α, as well as NF‑κB p65 translocation into the nucleus. Nobiletin also upregulated the expression of nuclear NF‑E2‑related factor 2 (Nrf2) and cytoplasmic heme oxygenase‑1. In conclusion, these results indicate that nobiletin serves a protective role in LPS/GalN‑induced acute liver injury via activation of the Nrf2 antioxidant pathway and subsequent inhibition of NF‑κB‑mediated cytokine production. These findings support the potential for nobiletin as a therapeutic agent for the treatment of acute liver injury.

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Bifidobacterium pseudocatenulatum CECT7765 induces an M2 anti-inflammatory transition in macrophages from patients with cirrhosis

Cited by 34 publications

References 37 publications

Bifidobacterium animalis ssp. Lactis 420 Mitigates Autoimmune Hepatitis Through Regulating Intestinal Barrier and Liver Immune Cells

Bifidobacterium animalis ssp. Lactis 420 Mitigates Autoimmune Hepatitis Through Regulating Intestinal Barrier and Liver Immune Cells

Effect of EPEC endotoxin and bifidobacteria on intestinal barrier function through modulation of toll-like receptor 2 and toll-like receptor 4 expression in intestinal epithelial cell-18

Nobiletin attenuates lipopolysaccharide/D-galactosamine-induced liver injury in mice by activating the Nrf2 antioxidant pathway and subsequently inhibiting NF-κB-mediated cytokine production

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