Evidence map›Paper›PMID 21149587›Full record

ArticleInfection and immunity2011

Interleukin-17 contributes to generation of Th1 immunity and neutrophil recruitment during Chlamydia muridarum genital tract infection but is not required for macrophage influx or normal resolution of infection.

Amy M Scurlock, Lauren C Frazer, Charles W Andrews, Catherine M O'Connell, Isaac P Foote, Sarabeth L Bailey, Kumar Chandra-Kuntal, Jay K Kolls, Toni Darville

Abstract 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 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
7.4field-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

73 citing papers in PubMed, 123 citations in OpenAlex.

  1. Review
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  12. Article
  13. Article
  14. Th17/Treg Imbalance: Implications in Lung Inflammatory Diseases.International journal of molecular sciences · 2023
    Review
  15. The role of infected epithelial cells inFrontiers in cellular and infection microbiology · 2023
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

13 more citing papers are in PubMed but not listed here.

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 4 institutions in 1 country.

Amy M ScurlockDepartment of Pediatrics, University of Arkansas for Medical Sciences, Arkansas Children's Hospital Research Institute, 13 Children's Way, Slot 512-13, Little Rock, AR 72202, USA. scurlockamym@uams.edu
Lauren C Frazer
Charles W Andrews
Catherine M O'Connell
Isaac P Foote
Sarabeth L Bailey
Kumar Chandra-Kuntal
Jay K Kolls
Toni Darville
University of Pittsburgh Medical Center · USUniversity of Arkansas for Medical Sciences · USArkansas Children's Hospital · USLouisiana State University Health Sciences Center New Orleans · US

Funding

The UPMC Sexually Transmitted Infections Cooperative Research CenterU19AI084024 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CHERPES, THOMAS L. · 2009 to 2013
$12.9M
Cell Death and Innate Immunity in Chlamydial InfectionR01AI054624 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DARVILLE, TONI · 2003 to 2014
$3.2M
Immunoregulatory Networks in Chlamydia Genital Tract InfectionK08AI077932 · NIAID · ARKANSAS CHILDREN'S HOSPITAL RES INST · PI SCURLOCK, AMY M. · 2009 to 2013
$662k
NIAID NIH HHS 1K08AI077932NIAID NIH HHS AI054624NIAID NIH HHS AI084024NIAID NIH HHS K08 AI077932NIAID NIH HHS R01 AI054624NIAID NIH HHS U19 AI084024
6 · The paper itself

Abstract

Interleukin 17 (IL-17) contributes to development of Th1 immunity and neutrophil influx during Chlamydia muridarum pulmonary infection, but its role during C. muridarum genital tract infection has not been described. We detected similar numbers of Chlamydia-specific Th17 and Th1 cells in iliac nodes of wild-type mice early during genital C. muridarum infection, while Th1 cells predominated later. il17ra(-/-) mice exhibited a reduced chlamydia-specific Th1 response in draining iliac nodes and decreased local IFN-γ production. Neutrophil influx into the genital tract was also decreased. However, il17ra(-/-) mice resolved infection normally, and no difference in pathology was observed compared to the wild type. Macrophage influx and tumor necrosis factor alpha (TNF-α) production were increased in il17ra(-/-) mice, providing a compensatory mechanism to effectively control chlamydial genital tract infection despite a reduced Th1 response. In ifnγ(-/-) mice, a marked increase in cellular infiltrates and chronic pathology was associated with an increased Th17 response. Although neutralization of IL-17 in ifnγ(-/-) mice decreased neutrophil influx, macrophage infiltration remained intact and the bacterial burden was not increased. Collectively, these results indicate that IL-17 contributes to the generation of Th1 immunity and neutrophil recruitment but is not required for macrophage influx or normal resolution of C. muridarum genital infection. These data highlight the redundant immune mechanisms operative at this mucosal site and the importance of examining site-specific responses to mucosal pathogens.

Indexed as

AnimalsCervix UteriChlamydia InfectionsChlamydia muridarumFemaleFlow CytometryInterleukin-17MacrophagesMiceMice, Inbred C57BLMice, KnockoutNeutrophil InfiltrationOviductsReverse Transcriptase Polymerase Chain ReactionTh17 CellsTh1 CellsInterleukin-17

Identifiers

PMID21149587
PMCPMC3067500
OpenAlexW2113463914

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.