Evidence map›Paper›PMID 20164426›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

CC chemokine ligand 3 overcomes the bacteriocidal and phagocytic defect of macrophages and hastens recovery from experimental otitis media in TNF-/- mice.

Anke Leichtle, Michelle Hernandez, Joerg Ebmeyer, Kenshi Yamasaki, Yuping Lai, Katherine Radek, Yun-Hoon Choung, Sara Euteneuer, Kwang Pak, Richard Gallo and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 24% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Dysregulation of immune response in otitis media.Expert reviews in molecular medicine · 2021
    Pooled it
  2. Article
  3. Article
  4. Immunomodulation as a Protective Strategy in Chronic Otitis Media.Frontiers in cellular and infection microbiology · 2022
    Article
  5. Article
  6. Leukotriene B4 Is a Major Determinant of Leukocyte Recruitment During Otitis Media.Frontiers in cellular and infection microbiology · 2021
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Panel 3: Genetics and Precision Medicine of Otitis Media.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2017
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. NOD-Like Receptor Signaling in Cholesteatoma.BioMed research international · 2015
    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

12 authors at 6 institutions in 3 countries.

Anke LeichtleDivision of Otolaryngology, Department of Surgery, University of California, San Diego, La Jolla, CA 92093, USA.
Michelle Hernandez
Joerg Ebmeyer
Kenshi Yamasaki
Yuping Lai
Katherine Radek
Yun-Hoon Choung
Sara Euteneuer
Kwang Pak
Richard Gallo
Stephen I Wasserman
Allen F Ryan
University of California San Diego · USInstitute for Integrative and Experimental Genomics · DEAjou University · KRENT and Allergy · USKlinikum Bielefeld · DEUniversity of North Carolina at Chapel Hill · US

Funding

Middle ear responses in Otitis MediaR01DC000129 · NIDCD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RYAN, ALLEN F. · 1989 to 2021
$6.8M
Cathelicidins in Skin ImmunityR01AI052453 · NIAID · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI GALLO, RICHARD L, NIZET, VICTOR · 2002 to 2017
$5.3M
Cathelicidin in Skin ImmunityR37AI052453 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Richard L Gallo, Victor Nizet · 2019 to 2026
$4.6M
Proteolysis and Skin AntimicrobialsR01AR052728 · NIAMS · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI GALLO, RICHARD L · 2006 to 2015
$3.3M
Mechanisms of Persistence and Recovery in Otitis MediaR01DC006279 · NIDCD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI WASSERMAN, STEPHEN I · 2003 to 2014
$3.1M
Loyola Alcohol Research Center (LARC)P30AA019373 · NIAAA · LOYOLA UNIVERSITY CHICAGO · PI KOVACS, ELIZABETH J. · 2009 to 2010
$832k
Basic Mechanisms on Hearing Loss of Cochlear OriginI01BX001205 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI RYAN, ALLEN F. · 2013 to 2024
–
BLRD VA I01 BX001205NIAAA NIH HHS P30 AA019373NIAID NIH HHS AI052453NIAID NIH HHS R01 AI052453NIAID NIH HHS R37 AI052453NIAMS NIH HHS AR052728NIAMS NIH HHS R01 AR052728NIDCD NIH HHS DC000129NIDCD NIH HHS DC006279NIDCD NIH HHS R01 DC000129NIDCD NIH HHS R01 DC006279
6 · The paper itself

Abstract

Innate immune mechanisms are crucial in defense against bacterial illnesses in humans, as evidenced by abnormal antibacterial responses due to defects in TLR signaling, seen in children with MyD88 or IL-1R-associated kinase 4 deficiency. Otitis media (OM) is the most common disease of childhood, and the role of innate immune molecules in this disorder remains unclear. In a murine model of OM, we show that, in the absence of TNF, a key effector of innate immunity, this disease is prolonged after middle ear infection with nontypeable Haemophilus influenzae (NTHi). In the absence of TNF, mice fail to upregulate both TLRs and downstream genes and proteins, such as CCL3, resulting in defects in both inflammatory cell recruitment and macrophage function. Peritoneal macrophages of mice lacking TNF have a diminished ability to phagocytose and kill NTHi, and this defect is partially corrected in vitro by exogenous rTNF. Addition of rCCL3 alone or in combination with rTNF restores phagocytosis and killing by TNF-deficient macrophages to that of unstimulated wild-type macrophages. In vivo administration of rCCL3 to animals deficient in TNF fully restores the ability to control OM due to NTHi, whereas a CCL3-blocking Ab impaired the ability of wild-type mice to recover from OM. Thus, CCL3 is a potent downstream effector of TNF-mediated inflammation in vitro and in vivo. Manipulation of CCL3 and/or TNF may prove to be effective therapeutic approaches in OM or other conditions associated with defective TNF generation.

Indexed as

AnimalsBlood Bactericidal ActivityChemokine CCL3Disease Models, AnimalDown-RegulationHaemophilus InfectionsHaemophilus influenzaeInflammation MediatorsMacrophages, PeritonealMiceMice, Inbred C57BLMice, KnockoutOtitis MediaPhagocytosisRecombinant ProteinsToll-Like ReceptorsCcl3 protein, mouseChemokine CCL3Inflammation MediatorsRecombinant ProteinsToll-Like ReceptorsTumor Necrosis Factor-alpha

Identifiers

PMID20164426
PMCPMC2929161
OpenAlexW2095591126

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.