Evidence map›Paper›PMID 21300777›Full record

ArticleInfection and immunity2011

Preterm infants have deficient monocyte and lymphocyte cytokine responses to group B streptococcus.

Andrew J Currie, Samantha Curtis, Tobias Strunk, Karen Riley, Khemanganee Liyanage, Susan Prescott, Dorota Doherty, Karen Simmer, Peter Richmond, David Burgner

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.3field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 75 citations in OpenAlex.

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  14. Association of immune cell recruitment and BPD development.Molecular and cellular pediatrics · 2022
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  19. [Group B streptococcus colonization in pregnant women and group B streptococcus infection in their preterm infants].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2019
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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

10 authors at 3 institutions in 1 country.

Andrew J CurrieSchool of Veterinary & Biomedical Sciences, Murdoch University, Murdoch, Western Australia. a.currie@murdoch.edu.au
Samantha Curtis
Tobias Strunk
Karen Riley
Khemanganee Liyanage
Susan Prescott
Dorota Doherty
Karen Simmer
Peter Richmond
David Burgner
University of Western Australia · AUMurdoch University · AURoyal Children's Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Group B streptococcus (GBS) is an important cause of early- and late-onset sepsis in the newborn. Preterm infants have markedly increased susceptibility and worse outcomes, but their immunological responses to GBS are poorly defined. We compared mononuclear cell and whole-blood cytokine responses to heat-killed GBS (HKGBS) of preterm infants (gestational age [GA], 26 to 33 weeks), term infants, and healthy adults. We investigated the kinetics and cell source of induced cytokines and quantified HKGBS phagocytosis. HKGBS-induced tumor necrosis factor (TNF) and interleukin 6 (IL-6) secretion was significantly impaired in preterm infants compared to that in term infants and adults. These cytokines were predominantly monocytic in origin, and production was intrinsically linked to HKGBS phagocytosis. Very preterm infants (GA, <30 weeks) had fewer cytokine-producing monocytes, but nonopsonic phagocytosis ability was comparable to that for term infants and adults. Exogenous complement supplementation increased phagocytosis in all groups, as well as the proportion of preterm monocytes producing IL-6, but for very preterm infants, responses were still deficient. Similar defective preterm monocyte responses were observed in fresh whole cord blood stimulated with live GBS. Lymphocyte-associated cytokines were significantly deficient for both preterm and term infants compared to levels for adults. These findings indicate that a subset of preterm monocytes do not respond to GBS, a defect compounded by generalized weaker lymphocyte responses in newborns. Together these deficient responses may increase the susceptibility of preterm infants to GBS infection.

Indexed as

CytokinesFetal BloodHumansInfant, NewbornInfant, PrematureLymphocytesMonocytesSepsisStreptococcal InfectionsStreptococcus agalactiaeCytokines

Identifiers

PMID21300777
PMCPMC3067554
OpenAlexW2151980264

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.