Evidence map›Paper›PMID 27328412›Full record

ArticleIslets2016

Reparixin, a CXCR1/2 inhibitor in islet allotransplantation.

Rena L Pawlick, John Wink, Andrew R Pepper, Antonio Bruni, Nasser Abualhassen, Yasmin Rafiei, Boris Gala-Lopez, Mariusz Bral, A M James Shapiro

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Islets, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Trial
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  11. Neutrophils as emerging therapeutic targets.Nature reviews. Drug discovery · 2020
    Review
  12. Porcine CXCR1/2 antagonist CXCL8Scientific reports · 2020
    Article
  13. Article
  14. Review
  15. Review
  16. 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 at 1 institution in 1 country.

Rena L Pawlicka Alberta Diabetes Institute, University of Alberta , Edmonton , AB , Canada.
John Winka Alberta Diabetes Institute, University of Alberta , Edmonton , AB , Canada.
Andrew R Peppera Alberta Diabetes Institute, University of Alberta , Edmonton , AB , Canada.
Antonio Brunia Alberta Diabetes Institute, University of Alberta , Edmonton , AB , Canada.
Nasser Abualhassena Alberta Diabetes Institute, University of Alberta , Edmonton , AB , Canada.
Yasmin Rafieia Alberta Diabetes Institute, University of Alberta , Edmonton , AB , Canada.
Boris Gala-Lopeza Alberta Diabetes Institute, University of Alberta , Edmonton , AB , Canada.
Mariusz Brala Alberta Diabetes Institute, University of Alberta , Edmonton , AB , Canada.
A M James Shapiroa Alberta Diabetes Institute, University of Alberta , Edmonton , AB , Canada.
University of Alberta · CA

Funding

CIHR
6 · The paper itself

Abstract

Quality of life in Type 1 diabetic patients may be improved with islet transplantation, but lifelong immunosuppression is required to prevent rejection. Allo-immune response is a key player in graft dysfunction and although the adaptive immune response is well characterized, the effect of the innate immune reaction after transplantation is only recently becoming appreciated. In this study, we address how the innate response affects long-term outcomes in a murine islet allotransplant model. CTLA-4 Ig treatment is known to significantly prolong kidney subcapsular islet allograft survival and enhance glucose tolerance. The combination of CTLA-4 Ig with reparixin, which blocks against inflammatory neutrophil infiltration, yielded no long-term graft survival in an intrahepatic allotransplant model but had similar long-term graft survival in the kidney subcapsular model. Seven days after transplant, serum blood IFN-γ levels were significantly lower in the CTLA-4 Ig with reparixin treatment group compared to controls. IL-12p70 cytokine levels were increased with combination treatment, a positive modulation of the inflammatory response to the allograft. Furthermore, KC GRO, also known as CXCL1, was decreased in serum 7 d after transplant. Histologically, we found that immune cell infiltrate, CD4+ and CD8+ T cell populations along with both CXCR1+ and CXCR2+ cell populations were decreased within the CTLA-4 Ig and reparixin islet transplant graft. Overall these data provide insight into the down regulation of T-cell recruitment by CTLA-4 Ig and decreased neutrophil activation and recruitment with reparixin after long-term islet graft survival.

Indexed as

AnimalsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Glucose Tolerance TestGraft RejectionGraft SurvivalIslets of Langerhans TransplantationMaleMiceMice, Inbred BALB CSulfonamidesreparixinSulfonamidesAllo rejectionCTLA-4 Igdiabetesisletreparixintransplant

Identifiers

PMID27328412
PMCPMC5029202
OpenAlexW2474025349

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.