Evidence map›Paper›PMID 33042416›Full record

ArticleAmerican journal of translational research2020

Blockade of CXCR2 suppresses proinflammatory activities of neutrophils in ulcerative colitis.

Fengqin Zhu, Heng He, Li Fan, Cuimei Ma, Zhen Xu, Yuan Xue, Yibo Wang, Cuiping Zhang, Guangxi Zhou

Abstract read
In one paragraph

Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

  1. Article
  2. Article
  3. Autophagy activation by the Becn1Brain, behavior, and immunity · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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

9 authors.

Fengqin ZhuDepartment of Gastroenterology, Affiliated Hospital of Jining Medical University, Jining Medical University Jining 272000, Shandong, P. R. China.
Heng HeDepartment of Gastroenterology, Affiliated Hospital of Jining Medical University, Jining Medical University Jining 272000, Shandong, P. R. China.
Li FanDepartment of Gastroenterology, Affiliated Hospital of Jining Medical University, Jining Medical University Jining 272000, Shandong, P. R. China.
Cuimei MaDepartment of Gastroenterology, Affiliated Hospital of Jining Medical University, Jining Medical University Jining 272000, Shandong, P. R. China.
Zhen XuDepartment of Gastroenterology, Affiliated Hospital of Jining Medical University, Jining Medical University Jining 272000, Shandong, P. R. China.
Yuan XueDepartment of Gastroenterology, Affiliated Hospital of Jining Medical University, Jining Medical University Jining 272000, Shandong, P. R. China.
Yibo WangDepartment of Gastroenterology, Affiliated Hospital of Jining Medical University, Jining Medical University Jining 272000, Shandong, P. R. China.
Cuiping ZhangDepartment of Gastroenterology, The Affiliated Hospital of Qingdao University Qingdao 266003, Shandong, P. R. China.
Guangxi ZhouDepartment of Gastroenterology, Affiliated Hospital of Jining Medical University, Jining Medical University Jining 272000, Shandong, P. R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ulcerative colitis (UC) is one chronically remittent and progressive inflammatory disorder. Chemokine receptor CXCR2 is reported to be involved in the pathogenesis of several inflammatory diseases. However, how CXCR2 modulate mucosal inflammation in UC is still obscure. In this study, CXCR2 expression was determined in inflamed mucosa and peripheral blood cells from patients with UC by qRT-PCR. Neutrophils isolated from peripheral blood were pretreated with CXCR2 inhibitor (SB225002), and proinflammatory mediators were examined by qRT-PCR, ELISA and IF. The migratory capacity of neutrophils after SB225002 treatment was examined by using Transwell plate. Furthermore, SB225002 was administrated daily in DSS-induced colitis mice. We found that CXCR2 expression was significantly increased in colonic mucosal tissues and peripheral blood cells from patients with active UC. Besides, CXCR2 was highly expressed in neutrophils, and was positively correlated with disease activity. Inhibition of CXCR2 in neutrophils decreased the production of proinflammatory mediators, such as reactive oxygen species (ROS), MPO, S100a8, S100a9, TNF-α, IL-1β, IL-8 and IL-6, and the migratory capacity of neutrophils was markedly impaired after SB225002 treatment. Moreover, blockade of CXCR2 with SB225002 could markedly ameliorate DSS-induced colitis in mice. In summary, CXCR2 plays a critical role in the pathogenesis of UC through modulating immune responses of neutrophils. Blockade of CXCR2 may serve as a new therapeutic approach for treatment of UC.

Indexed as

CXCR2mucosal inflammationneutrophilulcerative colitis

Identifiers

PMID33042416
PMCPMC7540107

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.