Evidence map›Paper›PMID 38097561›Full record

ArticleNature communications2023

Maternal antibiotic exposure enhances ILC2 activation in neonates via downregulation of IFN1 signaling.

Haixu Xu, Xianfu Yi, Zhaohai Cui, Hui Li, Lin Zhu, Lijuan Zhang, JiaLe Chen, Xutong Fan, Pan Zhou, Mulin Jun Li and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  8. Skin-lung axis in the atopic march: The immune link from skin to lungs.Chinese medical journal pulmonary and critical care medicine · 2025
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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

15 authors at 3 institutions in 1 country.

Haixu Xu *Department of Immunology, Tianjin Institute of Immunology, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, State Key Laboratory of Experimental Hematology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Xianfu Yi *Department of Bioinformatics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.ORCID 0000-0002-8094-2676
Zhaohai Cui *Department of Immunology, Tianjin Institute of Immunology, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, State Key Laboratory of Experimental Hematology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Hui LiDepartment of Immunology, Tianjin Institute of Immunology, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, State Key Laboratory of Experimental Hematology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Lin ZhuDepartment of Immunology, Tianjin Institute of Immunology, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, State Key Laboratory of Experimental Hematology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Lijuan ZhangDepartment of Immunology, Tianjin Institute of Immunology, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, State Key Laboratory of Experimental Hematology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
JiaLe ChenDepartment of Immunology, Tianjin Institute of Immunology, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, State Key Laboratory of Experimental Hematology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Xutong FanDepartment of Bioinformatics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Pan ZhouDepartment of Immunology, Tianjin Institute of Immunology, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, State Key Laboratory of Experimental Hematology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Mulin Jun LiDepartment of Bioinformatics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Ying YuDepartment of Pharmacology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.ORCID 0000-0002-6476-1752
Qiang LiuDepartment of Neurology, Institute of Neuroimmunology, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Dandan HuangDepartment of Pharmacology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China. mikey.huang2011@gmail.com.
Zhi YaoDepartment of Immunology, Tianjin Institute of Immunology, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, State Key Laboratory of Experimental Hematology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China. yaozhi@tmu.edu.cn.ORCID 0000-0001-8472-0731
Jie ZhouDepartment of Immunology, Tianjin Institute of Immunology, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, State Key Laboratory of Experimental Hematology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China. zhoujie@tmu.edu.cn.ORCID 0000-0001-5964-1599
Tianjin Medical University · CNThird Affiliated Hospital of Guangzhou Medical University · CNTianjin Medical University General Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82130049
6 · The paper itself

Abstract

Microbiota have an important function in shaping and priming neonatal immunity, although the cellular and molecular mechanisms underlying these effects remain obscure. Here we report that prenatal antibiotic exposure causes significant elevation of group 2 innate lymphoid cells (ILC2s) in neonatal lungs, in both cell numbers and functionality. Downregulation of type 1 interferon signaling in ILC2s due to diminished production of microbiota-derived butyrate represents the underlying mechanism. Mice lacking butyrate receptor GPR41 (Gpr41

Indexed as

Anti-Bacterial AgentsImmunity, InnateInterferon Type ILymphocytesAnimalsButyratesCytokinesDown-RegulationInflammationLungMaternal ExposureMiceAnti-Bacterial AgentsButyratesCytokinesInterferon Type I

Identifiers

PMID38097561
PMCPMC10721923
OpenAlexW4389765069

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.