Evidence map›Paper›PMID 24913976›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

The peritrophic matrix mediates differential infection outcomes in the tsetse fly gut following challenge with commensal, pathogenic, and parasitic microbes.

Brian L Weiss, Amy F Savage, Bridget C Griffith, Yineng Wu, Serap Aksoy

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
8.9field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 80 citations in OpenAlex.

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  7. bioRxiv : the preprint server for biology · 2024
    Article
  8. Tethering of soluble immune effectors to mucin and chitin reflects a convergent and dynamic role in gut immunity.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Review
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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

5 authors at 1 institution in 1 country.

Brian L WeissDepartment of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, CT 06520 brian.weiss@yale.edu.
Amy F SavageDepartment of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, CT 06520.
Bridget C GriffithDepartment of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, CT 06520.
Yineng WuDepartment of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, CT 06520.
Serap AksoyDepartment of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, CT 06520.
Yale University · US

Funding

Molecular Aspects of Tsetse and Trypanosome TransmissionR01AI051584 · NIAID · YALE UNIVERSITY · PI AKSOY, SERAP · 2003 to 2013
$4.3M
Adaptive evolution of pathogenesis towards symbiosisR01GM069449 · NIGMS · YALE UNIVERSITY · PI AKSOY, SERAP · 2004 to 2009
$1.2M
Symbiosis and Immunity in the Tsetse FlyR21AI101456 · NIAID · YALE UNIVERSITY · PI WEISS, BRIAN L · 2012 to 2013
$427k
NIAID NIH HHS AI051584NIAID NIH HHS AI101456NIAID NIH HHS R01 AI051584NIGMS NIH HHS GM069449
6 · The paper itself

Abstract

The insect gut is lined by a protective, chitinous peritrophic matrix (PM) that separates immunoreactive epithelial cells from microbes present within the luminal contents. Tsetse flies (Glossina spp.) imbibe vertebrate blood exclusively and can be exposed to foreign microorganisms during the feeding process. We used RNA interference-based reverse genetics to inhibit the production of a structurally robust PM and then observed how this procedure impacted infection outcomes after per os challenge with exogenous bacteria (Enterobacter sp. and Serratia marcescens strain Db11) and parasitic African trypanosomes. Enterobacter and Serratia proliferation was impeded in tsetse that lacked an intact PM because these flies expressed the antimicrobial peptide gene, attacin, earlier in the infection process than did their counterparts that housed a fully developed PM. After challenge with trypanosomes, attacin expression was latent in tsetse that lacked an intact PM, and these flies were thus highly susceptible to parasite infection. Our results suggest that immunodeficiency signaling pathway effectors, as opposed to reactive oxygen intermediates, serve as the first line of defense in tsetse's gut after the ingestion of exogenous microorganisms. Furthermore, tsetse's PM is not a physical impediment to infection establishment, but instead serves as a barrier that regulates the fly's ability to immunologically detect and respond to the presence of these microbes. Collectively, our findings indicate that effective insect antimicrobial responses depend largely upon the coordination of multiple host and microbe-specific developmental factors.

Indexed as

AnimalsChitinEnterobacterEpithelial CellsGastrointestinal TractGene ExpressionGreen Fluorescent ProteinsHost-Pathogen InteractionsInsect ProteinsMicroscopy, FluorescenceRatsReverse Transcriptase Polymerase Chain ReactionRNA InterferenceSerratia marcescensSignal TransductionTrypanosoma brucei bruceiattacin antibacterial protein, insectChitinGreen Fluorescent ProteinsInsect Proteins

Identifiers

PMID24913976
PMCPMC4107339
OpenAlexW2116890693

What OpenQuestion holds

Textmetadata
LicenceTDM
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.