Evidence map›Paper›PMID 42839034›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026

IL-18-associated basophil and mast cell activation in sepsis.

Junling Wang, Bingyu Qin, Xueyan Zhang, Mengmeng Zhan, Chao Chen, Junfen Li, Shihao Liu, Fangqiu Gu, Huanzhang Shao

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Junling WangDepartment of Critical Care Medicine, Henan Key Laboratory for Critical Care Medicine, Zhengzhou Key Laboratory for Critical Care Medicine, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, No. 7, Weiwu Street, Jinshui District, Zhengzhou, 450003, Henan, China.
Bingyu QinDepartment of Critical Care Medicine, Henan Key Laboratory for Critical Care Medicine, Zhengzhou Key Laboratory for Critical Care Medicine, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, No. 7, Weiwu Street, Jinshui District, Zhengzhou, 450003, Henan, China.
Xueyan ZhangDepartment of Critical Care Medicine, Henan Key Laboratory for Critical Care Medicine, Zhengzhou Key Laboratory for Critical Care Medicine, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, No. 7, Weiwu Street, Jinshui District, Zhengzhou, 450003, Henan, China.
Mengmeng ZhanAllergy and Clinical Immunology Research Centre, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, 121001, Liaoning, China.
Chao ChenDepartment of Critical Care Medicine, Henan Key Laboratory for Critical Care Medicine, Zhengzhou Key Laboratory for Critical Care Medicine, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, No. 7, Weiwu Street, Jinshui District, Zhengzhou, 450003, Henan, China.
Junfen LiDepartment of Critical Care Medicine, Henan Key Laboratory for Critical Care Medicine, Zhengzhou Key Laboratory for Critical Care Medicine, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, No. 7, Weiwu Street, Jinshui District, Zhengzhou, 450003, Henan, China.
Shihao LiuDepartment of Critical Care Medicine, Henan Key Laboratory for Critical Care Medicine, Zhengzhou Key Laboratory for Critical Care Medicine, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, No. 7, Weiwu Street, Jinshui District, Zhengzhou, 450003, Henan, China.
Fangqiu GuAllergy and Clinical Immunology Research Centre, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, 121001, Liaoning, China.
Huanzhang ShaoDepartment of Critical Care Medicine, Henan Key Laboratory for Critical Care Medicine, Zhengzhou Key Laboratory for Critical Care Medicine, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, No. 7, Weiwu Street, Jinshui District, Zhengzhou, 450003, Henan, China. shaohuanzhang001@126.com.

Funding

Doctoral Scientific Research of Henan Provincial People's Hospital KK20260049Key Research and Development and Promotion Special Foundation of Henan Province 232102311022the Foundation for Postdoctoral Scientific Research of Henan Province HN2022097the Natural Science Foundation of Henan Province 202300410458the Youth Cultivation Project of Henan Provincial People's Hospital ZC20260015
6 · The paper itself

Abstract

backgroundThe contributions of basophils and mast cells to sepsis immunopathology remains poorly understood. Interleukin-18 (IL-18) has established roles in innate immune activation, but its relationships with basophil and mast cell activation during sepsis have not been fully defined.

methodsWe investigated expression of IL-18Rα and activation marker CD63 on blood basophils of patients with sepsis using flow cytometry and RNA-sequencing. Sepsis mouse model and human cell lines were used to assess the effect of IL-18 on basophil and mast cell activation.

resultsClose correlations between elevated plasma IL-18 level and increased CD63, IL-18Rα and IL-18Rβ protein expression on basophils of patients with sepsis were observed. Transcriptomic analysis revealed extensive reprogramming of septic basophils, including upregulation of CD63 and IL18RAP, together with enrichment of pathways related to ribosome biogenesis, mitochondrial translation, oxidative phosphorylation, proteasome, DNA replication and cell cycle. Furthermore, we observed increased expression of CD63 and IL-18Rα on basophils and mast cells in septic mice, and IL-18 upregulated their expression and mast cell accumulation in both healthy and septic mice. Additionally, elevated plasma and peritoneal levels of IL-18, IL-5, CCL2 and tryptase were observed in septic mice. In vitro experiments demonstrated that both IL-18 and plasma from patients with sepsis induced upregulation of CD63 and IL-18Rα on KU812 and HMC-1 cell lines.

conclusionsCollectively, our findings suggest that IL-18-associated basophil and mast cell activation may participate in sepsis-related inflammation.

Indexed as

BasophilsInterleukin-18Mast CellsSepsisAnimalsCell LineFemaleHumansInterleukin-18 Receptor alpha SubunitMaleMiceMice, Inbred C57BLMiddle AgedTetraspanin 30CD63 protein, humanInterleukin-18Interleukin-18 Receptor alpha SubunitTetraspanin 30ActivationBasophilCD63IL-18IL-18RαMast cellSepsis

Identifiers

PMID42839034

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.