Evidence map›Paper›PMID 24643536›Full record

ArticleInfection and immunity2014

Helminth-induced interleukin-4 abrogates invariant natural killer T cell activation-associated clearance of bacterial infection.

Yi-Ju Hsieh, Chi-Ling Fu, Michael H Hsieh

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
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  10. Metabolism at the centre of the host-microbe relationship.Clinical and experimental immunology · 2019
    Review
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  14. Therapeutic exploitation of IPSE, a urogenital parasite-derived host modulatory protein, for chemotherapy-induced hemorrhagic cystitis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
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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

3 authors at 1 institution in 1 country.

Yi-Ju HsiehDepartment of Urology, Stanford University School of Medicine, Stanford University, Stanford, California, USA.
Chi-Ling Fu
Michael H Hsieh
Stanford University · US

Funding

Estrogenic Modulation of Genitourinary Epithelial-Probiotic Cross-TalkK08DK087895 · NIDDK · STANFORD UNIVERSITY · PI HSIEH, MICHAEL HARRISON · 2010 to 2014
$902k
NIDDK NIH HHS DK087895NIDDK NIH HHS K08 DK087895
6 · The paper itself

Abstract

Helminth infections affect 1 billion people worldwide and render these individuals susceptible to bacterial coinfection through incompletely understood mechanisms. This includes urinary tract coinfection by bacteria and Schistosoma haematobium worms, the etiologic agent of urogenital schistosomiasis. To study the mechanisms of S. haematobium-bacterial urinary tract coinfections, we combined the first tractable model of urogenital schistosomiasis with an established mouse model of bacterial urinary tract infection (UTI). A single bladder exposure to S. haematobium eggs triggers interleukin-4 (IL-4) production and makes BALB/c mice susceptible to bacterial UTI when they are otherwise resistant. Ablation of IL-4 receptor alpha (IL-4Rα) signaling restored the baseline resistance of BALB/c mice to bacterial UTI despite prior exposure to S. haematobium eggs. Interestingly, numbers of NKT cells were decreased in coexposed versus bacterially monoinfected bladders. Given that schistosome-induced, non-natural killer T (NKT) cell leukocyte infiltration may dilute NKT cell numbers in the bladders of coexposed mice without exerting a specific functional effect on these cells, we next examined NKT cell biology on a per-cell basis. Invariant NKT (iNKT) cells from coexposed mice expressed less gamma interferon (IFN-γ) per cell than did those from mice with UTI alone. Moreover, coexposure resulted in lower CD1d expression in bladder antigen-presenting cells (APC) than did bacterial UTI alone in an IL-4Rα-dependent fashion. Finally, coexposed mice were protected from prolonged bacterial infection by administration of α-galactosylceramide, an iNKT cell agonist. Our findings point to a previously unappreciated role for helminth-induced IL-4 in impairment of iNKT cell-mediated clearance of bacterial coexposure.

Indexed as

AnimalsEscherichia coli InfectionsFemaleInterleukin-4Interleukin-4 Receptor alpha SubunitMiceMice, Inbred BALB CMice, KnockoutNatural Killer T-CellsOvumReceptors, Cell SurfaceSchistosomiasis haematobiaUrinary Tract InfectionsUropathogenic Escherichia coliIl4ra protein, mouseInterleukin-4Interleukin-4 Receptor alpha SubunitReceptors, Cell Surface

Identifiers

PMID24643536
PMCPMC3993428
OpenAlexW2148632341

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.