Evidence map›Paper›PMID 15501762›Full record

ArticleInfection and immunity2004

The infecting dose of Chlamydia muridarum modulates the innate immune response and ascending infection.

Heather K Maxion, Wei Liu, Mi-Hyang Chang, Kathleen A Kelly

Abstract read
In one paragraph

Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

37 citing papers in PubMed, 64 citations in OpenAlex.

  1. Infectivity of a pathogenicity-attenuatedInfection and immunity · 2025
    Article
  2. Chlamydiosis in Animals.Animals : an open access journal from MDPI · 2024
    Review
  3. Advances inMicroorganisms · 2024
    Review
  4. Microbiology spectrum · 2023
    Article
  5. Article
  6. Modulation of Immune Response toFrontiers in cellular and infection microbiology · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Frontiers in cellular and infection microbiology · 2020
    Article
  11. Genital Infiltrations of CD4Frontiers in microbiology · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

4 authors at 1 institution in 1 country.

Heather K MaxionDavid Geffen School of Medicine at UCLA, Department of Pathology & Laboratory Medicine, Los Angeles, CA 90095-1732, USA.
Wei Liu
Mi-Hyang Chang
Kathleen A Kelly
University of California, Los Angeles · US

Funding

MULTIDISCIPLINARY TRAINING IN MICROBIAL PATHOGENESIST32AI007323 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Peter John Bradley · 1988 to 2026
$8.6M
T-CELL MEDIATED IMMUNITY IN CHLAMYDIAL GENITAL INFECTIONR01AI026328 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KELLY, KATHLEEN A. · 1988 to 2012
$3.6M
NIAID NIH HHS 5-T32-AI-07323-16NIAID NIH HHS R01 AI026328NIAID NIH HHS R01 AI26328-13NIAID NIH HHS T32 AI007323
6 · The paper itself

Abstract

Murine vaginal infection with the obligate intracellular bacterium Chlamydia muridarum is commonly used as a model for ascending Chlamydia infections of the human female genital tract. Gamma interferon-producing Th1 cells, in concert with other mononuclear infiltrates, primarily mediate antichlamydial immunity. However, many factors modify this response, including the bacterial load. To investigate the manner in which the inoculating dose of C. muridarum modulates a genital infection, we measured innate and adaptive cell numbers, CD4+ lymphocyte cytokine profile, chemokine expression, course of infection, and pathological sequelae in genital tracts of BALB/c mice infected with doses of C. muridarum ranging from 10(4) to 10(7) inclusion-forming units. We found that the influx of both innate and adaptive immune cells responded similarly in the lower genital tract (cervical-vaginal tissues) and upper genital tract (oviduct tissues) to increasing inoculating doses. However, cells expressing the innate markers Gr-1 and CD11c were affected to a greater degree by increasing dose than lymphocytes of the adaptive immune response (Th1, CD4+, CD8+, CD19+), resulting in a change in the balance of innate and adaptive cell numbers to favor innate cells at higher infecting doses. Surprisingly, we detected greater numbers of viable chlamydiae in the oviducts at lower inoculating doses, and the number of organisms appeared to directly correlate with hydrosalpinx formation after both primary infection and repeat infection. Taken together, these data suggest that innate immune cells contribute to control of ascending infection.

Indexed as

Immunity, InnateAnimalsCD4-Positive T-LymphocytesCervix UteriChlamydia InfectionsChlamydia muridarumColony Count, MicrobialCytokinesFallopian TubesFemaleGenital Diseases, FemaleHumansInterferon-gammaMiceMice, Inbred BALB CTh1 CellsCytokinesInterferon-gamma

Identifiers

PMID15501762
PMCPMC523032
OpenAlexW1970212132

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.