Evidence map›Paper›PMID 28458623›Full record

ArticleImmune network2017

IL-32-induced Inflammatory Cytokines Are Selectively Suppressed by α1-antitrypsin in Mouse Bone Marrow Cells.

Siyoung Lee, Dong-Ki Choi, Areum Kwak, Sinae Kim, Tam Thanh Nguyen, Gaae Gil, Eunhye Kim, Kwang Ha Yoo, In Ae Kim, Youngmin Lee and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immune network, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. 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

16 authors.

Siyoung LeeLaboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Dong-Ki ChoiDepartment of Molecular Science and Technology, Ajou University, Suwon 16499, Korea.
Areum KwakLaboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Sinae KimLaboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Tam Thanh NguyenLaboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Gaae GilLaboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Eunhye KimLaboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Kwang Ha YooDivision of Pulmonology, Department of Internal Medicine, School of Medicine, Konkuk University, Seoul 05029, Korea.
In Ae KimDivision of Pulmonology, Department of Internal Medicine, School of Medicine, Konkuk University, Seoul 05029, Korea.
Youngmin LeeDepartment of Medicine, Pusan Paik Hospital, College of Medicine, Inje University, Busan 47392, Korea.
Hyunjhung JhunLaboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Edward D ChanDepartments of Medicine and Academic Affairs, National Jewish Health, Denver, CO 80206, USA.
Xiyuan BaiDepartments of Medicine and Academic Affairs, National Jewish Health, Denver, CO 80206, USA.
Hyunwoo KimDivision of Nephrology, Department of Internal Medicine, Jeju National University School of Medicine, Jeju 63243, Korea.
Yong-Sung KimDepartment of Molecular Science and Technology, Ajou University, Suwon 16499, Korea.
Soohyun KimLaboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The induction of interleukin (IL)-32 in bone marrow (BM) inflammation is crucial in graft versus host disease (GvHD) that is a common side effect of allogeneic BM transplantation. Clinical trials on α-1 antitrypsin (AAT) in patients with GvHD are based on the preliminary human and mouse studies on AAT reducing the severity of GvHD. Proteinase 3 (PR3) is an IL-32-binding protein that was isolated from human urine. IL-32 primarily induces inflammatory cytokines in myeloid cells, probably due to PR3 expression on the membrane of the myeloid lineage cells. The inhibitory activity of AAT on serine proteinases may explain the anti-inflammatory effect of AAT on GvHD. However, the anti-inflammatory activity of AAT on BM cells remains unclear. Mouse BM cells were treated with IL-32γ and different inflammatory stimuli to investigate the anti-inflammatory activity of AAT. Recombinant AAT-Fc fusion protein inhibited IL-32γ-induced IL-6 expression in BM cells, but failed to suppress that induced by other stimuli. In addition, the binding of IL-32γ to PR3 was abrogated by AAT-Fc. The data suggest that the specific anti-inflammatory effect of AAT in mouse BM cells is due to the blocking of IL-32 binding to membrane PR3.

Indexed as

Interleukin-32Interleukin-6Mouse bone marrow cellProteinase 3Recombinant AAT-Fc

Identifiers

PMID28458623
PMCPMC5407983

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.