Evidence map›Paper›PMID 30057698›Full record

ArticleToxicological research2018

Lactobacillus Aggravate Bile Duct Ligation-Induced Liver Inflammation and Fibrosis in Mice.

Yoon Seok Roh, Ara Cho, Youn-Soo Cha, Suk-Heung Oh, Chae Woong Lim, Bumseok Kim

Open access · hybridAbstract read
In one paragraph

Article in Toxicological research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 2 pooled it
0.6field-weighted citation impact, top 29% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 2 syntheses or guidelines pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
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  10. Aryl Hydrocarbon Receptor (AhR) Activation by 2,3,7,8-Tetrachlorodibenzo-International journal of molecular sciences · 2021
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Yoon Seok RohDepartment of Pharmacy, Chungbuk National University, College of Pharmacy and Medical Research Center, Cheongju, Korea.
Ara ChoBiosafety Research Institute and College of Veterinary Medicine (BK21 Plus Program), Chonbuk National University, Iksan, Korea.
Youn-Soo ChaDepartment of Food Science and Human Nutrition, Fermented Food Research Center, Chonbuk National University, Jeonju, Korea.
Suk-Heung OhDepartment of Food & Biotechnology, Woosuk University, Jeonju, Korea.
Chae Woong LimBiosafety Research Institute and College of Veterinary Medicine (BK21 Plus Program), Chonbuk National University, Iksan, Korea.
Bumseok KimBiosafety Research Institute and College of Veterinary Medicine (BK21 Plus Program), Chonbuk National University, Iksan, Korea.
Jeonbuk National University · KRChungbuk National University · KRWoosuk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lactobacillus (LAB) have been reported to exert both harmful and beneficial effects on human and animal health. Recently, it has been reported that dysbiosis and bacterial translocation contribute to liver fibrosis. However, the role of Gram-positive LAB in the situation of chronic liver diseases has not been yet elucidated. Liver injury was induced by bile duct ligation (BDL) in LAB or control-administered mice. Liver fibrosis was enhanced in LAB-administered mice compared with control-treated mice as demonstrated by quantification of Sirius-red positive area, hydroxyproline contents and fibrosis-related genes (Col1α1, Acta2, Timp1, Tgfb1). Moreover, LAB-administered mice were more susceptible to BDL-induced liver injury as shown by increased ALT and AST level of LAB group compared with control group at 5 days post BDL. Consistent with serum level, inflammatory cytokines (TNF-α, IL-6 and IL-1β) were also significantly increased in LAB-treated mice. Of note, LAB-treated liver showed increased lipoteichoic acid (LTA) expression compared with control-treated liver, indicating that LAB-derived LTA may translocate from intestine to liver via portal vein. Indeed, responsible receptor or inflammatory factor (PAFR and iNOS) for LTA were upregulated in LAB-administered group. The present findings demonstrate that administration of LAB increases LTA translocation to liver and induces profibrogenic inflammatory milieu, leading to aggravation of liver fibrosis. The current study provides new cautious information of LAB for liver fibrosis patients to prevent the detrimental effect of LAB supplements.

Indexed as

LABLiver fibrosisLTA

Identifiers

PMID30057698
PMCPMC6057294
OpenAlexW2884852486

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.