Evidence map›Paper›PMID 28461572›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2017

Group B Streptococci Induce Proinflammatory Responses via a Protein Kinase D1-Dependent Pathway.

Kirtikumar Upadhyay, Jeoung-Eun Park, Tae Won Yoon, Priyanka Halder, Young-In Kim, Victoria Metcalfe, Ajay J Talati, B Keith English, Ae-Kyung Yi

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Protein kinase D mediates inflammatory responses of human placental macrophages to Group B Streptococcus.American journal of reproductive immunology (New York, N.Y. : 1989) · 2019
    Article
  10. Article
  11. Article
  12. Review
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 at 2 institutions in 1 country.

Kirtikumar UpadhyayDepartment of Pediatrics, The University of Tennessee Health Science Center, Memphis, TN 38163.ORCID 0000-0002-5951-8686
Jeoung-Eun ParkDepartment of Pediatrics, The University of Tennessee Health Science Center, Memphis, TN 38163.ORCID 0000-0002-4080-4447
Tae Won YoonDepartment of Microbiology, Immunology and Biochemistry, The University of Tennessee Health Science Center, Memphis, TN 38163; and.
Priyanka HalderDepartment of Microbiology, Immunology and Biochemistry, The University of Tennessee Health Science Center, Memphis, TN 38163; and.
Young-In KimDepartment of Pediatrics, The University of Tennessee Health Science Center, Memphis, TN 38163.ORCID 0000-0003-3215-2685
Victoria MetcalfeDepartment of Microbiology, Immunology and Biochemistry, The University of Tennessee Health Science Center, Memphis, TN 38163; and.ORCID 0000-0002-5760-3852
Ajay J TalatiDepartment of Pediatrics, The University of Tennessee Health Science Center, Memphis, TN 38163.ORCID 0000-0003-1798-9970
B Keith EnglishDepartment of Pediatrics and Human Development, Michigan State University, Lansing, MI 48912.ORCID 0000-0002-4450-0715
Ae-Kyung YiDepartment of Microbiology, Immunology and Biochemistry, The University of Tennessee Health Science Center, Memphis, TN 38163; and ayi@uthsc.edu.
University of Tennessee Health Science Center · USMichigan State University · US

Funding

TLR/IL-1R signaling intermediaries and a target-specific therapeutic for arthritiR01AR064723 · NIAMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI YI, AE-KYUNG · 2014 to 2018
$1.6M
Induction of immunological paralysis by CpG DNAR01AI053137 · NIAID · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI YI, AE-KYUNG · 2004 to 2008
$1.4M
NIAID NIH HHS R01 AI053137NIAMS NIH HHS R01 AR064723
6 · The paper itself

Abstract

Group B streptococci (GBS) are one of the leading causes of life-threatening illness in neonates. Proinflammatory responses to GBS mediated through host innate immune receptors play a critical role in the disease manifestation. However, the mechanisms involved in proinflammatory responses against GBS, as well as the contribution of signaling modulators involved in host immune defense, have not been fully elucidated. In the present study, we investigated the role of protein kinase D (PKD)1 in the proinflammatory responses to GBS. We found that both live and antibiotic-killed GBS induce activation of PKD1 through a pathway that is dependent on the TLR signaling adaptor MyD88 and its downstream kinase IL-1R-associated kinase 1, but independent of TNFR-associated factor 6. Our studies using pharmacological PKD inhibitors and PKD1-knockdown macrophages revealed that PKD1 is indispensable for GBS-mediated activation of MAPKs and NF-κB and subsequent expression of proinflammatory mediators. Furthermore, systemic administration of a PKD inhibitor protects d-galactosamine-sensitized mice from shock-mediated death caused by antibiotic-killed GBS. These findings imply that PKD1 plays a critical regulatory role in GBS-induced proinflammatory reactions and sepsis, and inhibition of PKD1 activation together with antibiotic treatment in GBS-infected neonates could be an effective way to control GBS diseases.

Indexed as

AnimalsHumansInfant, NewbornInflammationInterleukin 1 Receptor Antagonist ProteinMacrophagesMiceMyeloid Differentiation Factor 88NF-kappa BProtein Kinase CSepsisSignal TransductionStreptococcal InfectionsStreptococcus agalactiaeTumor Necrosis Factor-alphaIl1rn protein, mouseInterleukin 1 Receptor Antagonist ProteinMyeloid Differentiation Factor 88NF-kappa BProtein Kinase Cprotein kinase DTumor Necrosis Factor-alpha

Identifiers

PMID28461572
PMCPMC5509061
OpenAlexW2610409653

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.