RETRACTED ARTICLE: Bifidobacterium plays a protective role in TNF-α-induced inflammatory response in Caco-2 cell through NF-κB and p38MAPK pathways

Nie, Nana; Bai, Cui; Song, Shanai; Zhang, Yanyan; Wang, Benzhen; Li, Zipu

doi:10.1007/s11010-019-03651-3

Cited by 37 publications

(22 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As we all know, the inflammatory response is resulted from many signaling pathways, among which NF-κB pathway is the major regulator to the inflammatory genes [31]. In addition, several reports have revealed that suppression of NF-κB promoted LPS-stimulated sepsis [32].…”

Section: Discussionmentioning

confidence: 99%

Expression and role of ABIN1 in sepsis: In vitro and in vivo studies

Sun

Meng

et al. 2020

Open Medicine

View full text Add to dashboard Cite

In this research, we attempted to explain the effect and the related molecular mechanisms of ABIN1 in lipopolysaccharide (LPS)-induced septic mice or RAW264.7 macrophages. LPS was adopted to treat RAW264.7 macrophages for 4 h, and the levels of inflammatory factors were assessed by ELISA. Besides, ABIN1 expression was measured by quantitative reverse transcription polymerase chain reaction. Apparently, LPS enhanced immunoreaction, suggested by increased expression of IL-1β, tumor necrosis factor (TNF)-α, and IL-6. ABIN1 levels were obviously reduced compared to the control. Furthermore, we evaluated the roles of ABIN1-plasmid in immunoreaction and nuclear factor-κB (NF-κB) pathway. We found that ABIN1-plasmid significantly reduced the expression of IL-1β, TNF-α, and IL-6 in LPS-treated cells and inhibited NF-κB pathway activation. Meanwhile, a septic mouse mode was conducted to validate the role of ABIN1 in inflammatory response and organ damage in vivo. These data suggested that ABIN1-plasmid significantly inhibited the secretion of inflammatory cytokines and Cr, BUN, AST, and ALT levels in the serum of LPS-stimulated mice compared to LPS + control-plasmid group, reflecting the relieved inflammation and organ injury. In summary, the present findings indicated that ABIN1 alleviated sepsis by repressing inflammatory response through NF-κB signaling pathway, emphasizing the potential value of ABIN1 as therapeutic strategy for sepsis.

show abstract

Section: Discussionmentioning

confidence: 99%

Expression and role of ABIN1 in sepsis: In vitro and in vivo studies

Sun

Meng

et al. 2020

Open Medicine

View full text Add to dashboard Cite

show abstract

“…Sodium propionate was reported to induce apoptosis in H1299 and H1703 lung cancer cells, as evidenced by increased protein expression of p21, Bad, and Bax as well as apoptosis markers, including cleaved PARP and cleaved caspase 3 [ 47 ]. According to Nie et al, Bifidobacterium (BIF) ameliorates TNF- α -induced cell apoptosis in Caco-2 cells [ 48 ]. Likewise, butyrate causes apoptosis and cell cycle arrest in kidney epithelial cells [ 49 ].…”

Section: Mechanisms Underlying the Interaction Between Gut Microbimentioning

confidence: 99%

“…Nie et al discovered that BIF ameliorates TNF- α -induced autophagy in Caco-2 cells by suppressing the level of p62 and inhibiting the expression of autophagy-related markers such as Beclin1 and LC3II [ 48 ]. According to their research, BIF may provide a therapeutic target aimed at the Kawasaki disease, which is highly related to acquired heart disease in children.…”

Section: Mechanisms Underlying the Interaction Between Gut Microbimentioning

confidence: 99%

Implication of Gut Microbiota in Cardiovascular Diseases

Zhou

Cheng

Zhu

et al. 2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Emerging evidence has identified the association between gut microbiota and various diseases, including cardiovascular diseases (CVDs). Altered intestinal flora composition has been described in detail in CVDs, such as hypertension, atherosclerosis, myocardial infarction, heart failure, and arrhythmia. In contrast, the importance of fermentation metabolites, such as trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), and secondary bile acid (BA), has also been implicated in CVD development, prevention, treatment, and prognosis. The potential mechanisms are conventionally thought to involve immune regulation, host energy metabolism, and oxidative stress. However, numerous types of programmed cell death, including apoptosis, autophagy, pyroptosis, ferroptosis, and clockophagy, also serve as a key link in microbiome-host cross talk. In this review, we introduced and summarized the results from recent studies dealing with the relationship between gut microbiota and cardiac disorders, highlighting the role of programmed cell death. We hope to shed light on microbiota-targeted therapeutic strategies in CVD management.

show abstract

“…To support this hypothesis, we should examine whether BBG9-1 treatment ameliorates the disruption of the epithelial cell barrier induced by cytokine stimulation in vitro but this issue remains a limitation to be addressed in a future study. In this context, Nie et al have shown that Bifidobacterium strains suppressed TNF-α-induced overexpression of IL-6 and its associated barrier disruption of Caco2 cells monolayer [41]. Furthermore, Ling et al demonstrated that Bifidobacterium strains enhance the expression of tight junction proteins in Caco2 cells [34].…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2021

View full text Add to dashboard Cite

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.

show abstract

RETRACTED ARTICLE: Bifidobacterium plays a protective role in TNF-α-induced inflammatory response in Caco-2 cell through NF-κB and p38MAPK pathways

Cited by 37 publications

References 34 publications

Expression and role of ABIN1 in sepsis: In vitro and in vivo studies

Expression and role of ABIN1 in sepsis: In vitro and in vivo studies

Implication of Gut Microbiota in Cardiovascular Diseases

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

Contact Info

Product

Resources

About