Evidence map›Paper›PMID 35650365›Full record

ArticleBiometals : an international journal on the role of metal ions in biology, biochemistry, and medicine2023

Deficiency of Lactoferrin aggravates lipopolysaccharide-induced acute inflammation via recruitment macrophage in mice.

Can Liu, Qiu Peng, Lingyu Wei, Zhengshuo Li, Xiaoyue Zhang, Yangge Wu, Jia Wang, Xiang Zheng, Yuqing Wen, Run Zheng and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 22% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
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

13 authors at 4 institutions in 3 countries.

Can LiuHunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.
Qiu PengHunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.
Lingyu WeiDepartment of Pathology, Heping Hospital Affiliated to Changzhi Medical College, Changzhi, Shanxi, China.
Zhengshuo LiCancer Research Institute and School of Basic Medical Science, Central South University, Changsha, China.
Xiaoyue ZhangCancer Research Institute and School of Basic Medical Science, Central South University, Changsha, China.
Yangge WuCancer Research Institute and School of Basic Medical Science, Central South University, Changsha, China.
Jia WangDepartment of Immunology, Heping Hospital Affiliated to Changzhi Medical College, Changzhi, Shanxi, China.
Xiang ZhengDepartment of Pathology, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Yuqing WenCancer Research Institute and School of Basic Medical Science, Central South University, Changsha, China.
Run ZhengCancer Research Institute and School of Basic Medical Science, Central South University, Changsha, China.
Qun YanDepartment of Clinical Laboratory, Xiangya Hospital, Central South University, Changsha, China.
Qiurong YeDepartment of Pathology, People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi, China. yeqiurong1601@163.com.
Jian MaHunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China. majian@csu.edu.cn.ORCID http://orcid.org/0000-0001-9395-0416
Central South University · CNChangzhi Medical College · CNGuilin Medical University · CNThe People's Hospital of Guangxi Zhuang Autonomous Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lactoferrin (Lf), a multiple functional natural immune protein, is widely distributed in mammalian milk and glandular secretions (bile, saliva, tears and nasal mucosal secretions, etc.). In the previous study, we found that Lf plays an anti-inflammatory and anti-tumorigenesis role in AOM/DSS (azoxymethane/dextran sulfate sodium) induced mouse colitis-associated colon cancer model. Although we found that Lf has anti-inflammatory effects in chronic inflammation, its specific role and mechanisms in acute inflammation have not been clarified. Here, we reported that the expression levels of Lf were significantly increased when the organism was infected by Gram-negative bacteria. We then explored the role and potential mechanism of Lf in lipopolysaccharide (LPS)-induced acute inflammation. In the LPS-induced acute abdominal inflammation model, Lf deficiency aggravated inflammatory response and promoted macrophage chemotaxis to the inflammation site. Lf inhibited macrophage chemotaxis by suppressing the expression of macrophage-associated chemokines Ccl2 and Ccl5. Highly activated NF-κB signaling in Lf

Indexed as

InflammationLactoferrinAnimalsLipopolysaccharidesMacrophagesMiceNF-kappa BLactoferrinLipopolysaccharidesNF-kappa BAcute inflammationChemokinesLactoferrin

Identifiers

PMID35650365
PMCPMC9159647
OpenAlexW4282026756

What OpenQuestion holds

Textmetadata
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.