Evidence map›Paper›PMID 17379707›Full record

ArticleMicrobiology (Reading, England)2007

Defect in early lung defence against Pseudomonas aeruginosa in DBA/2 mice is associated with acute inflammatory lung injury and reduced bactericidal activity in naive macrophages.

Kari R Wilson, Jennifer M Napper, James Denvir, Vincent E Sollars, Hongwei D Yu

Open access · greenAbstract read
In one paragraph

Article in Microbiology (Reading, England), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  4. The impact of host genetic background in the Pseudomonas aeruginosa respiratory infections.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    Review
  5. Article
  6. Article
  7. Role of Interleukin-17 in defense against pseudomonas aeruginosa infection in lungs.International journal of clinical and experimental medicine · 2014
    Article
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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

5 authors at 1 institution in 1 country.

Kari R WilsonDepartment of Biochemistry and Microbiology, Joan C. Edwards School of Medicine at Marshall University, Huntington, WV 25755-9320, USA.
Jennifer M NapperDepartment of Biochemistry and Microbiology, Joan C. Edwards School of Medicine at Marshall University, Huntington, WV 25755-9320, USA.
James DenvirDepartment of Biochemistry and Microbiology, Joan C. Edwards School of Medicine at Marshall University, Huntington, WV 25755-9320, USA.
Vincent E SollarsDepartment of Biochemistry and Microbiology, Joan C. Edwards School of Medicine at Marshall University, Huntington, WV 25755-9320, USA.
Hongwei D YuDepartment of Pediatrics, Joan C. Edwards School of Medicine at Marshall University, Huntington, WV 25701-3655, USA.
Marshall University · US

Funding

WVU &MU NEW FACULTY GRANTSP20RR016477 · NCRR · MARSHALL UNIVERSITY · PI RANKIN, GARY O · 2001 to 2011
$35.5M
Transcription Factors in CancerP20RR020180 · NCRR · MARSHALL UNIVERSITY · PI NILES, RICHARD M. · 2004 to 2009
$9.5M
Genetic basis of P. aeruginosa lung infections in miceR15DK058128 · NIDDK · MARSHALL UNIVERSITY · PI YU, HONGWEI DAVID · 2002 to 2004
$296k
NCRR NIH HHS RR 016477NCRR NIH HHS RR 20180NIDDK NIH HHS DK 58128NIDDK NIH HHS R15 DK058128
6 · The paper itself

Abstract

Pseudomonas aeruginosa is an opportunistic pathogen that causes serious respiratory disease in the immune-compromised host. Using an aerosol infection model, 11 inbred mouse strains (129/Sv, A/J, BALB/c, C3H/HeN, C57BL/6, DBA/2, FVB, B10.D2/oSnJ, B10.D2/nSnJ, AKR/J and SWR/J) were tested for increased susceptibility to P. aeruginosa lung colonization. DBA/2 was the only mouse strain that had increased bacterial counts in the lung within 6 h post-infection. This deficiency incited a marked inflammatory response with reduced bacterial lung clearance and a mortality rate of 96.7 %. DBA/2 mice displayed progressive deterioration of lung pathology with extensive alveolar exudate and oedema formation at 48-72 h post-infection. The neutrophil-specific myeloperoxidase activity remained elevated throughout infection, suggesting that the increased leukocyte infiltration into alveoli caused acute inflammatory lung injury. DBA/2 mice lack the haemolytic complement; however, three additional mouse strains (AKR/J, SWR/J and A/J) with the same defect effectively cleared the infection, indicating that other host factors are involved in defence. Bone marrow-derived macrophages of DBA/2 showed an initial increase in phagocytosis, while their bactericidal activity was reduced compared to that of C57BL/6 macrophages. Comparison of pulmonary cytokine profiles of DBA/2 versus C57BL/6 or C3H/HeN indicated that DBA/2 had similar increases in tumour necrosis factor (TNF)-alpha, KC and interleukin (IL)-1a as C3H/HeN, but showed specific induction of IL-17, monocyte chemotactic protein (MCP)-1 and vascular endothelial growth factor (VEGF). Together, DBA/2 mice have a defect in the initial lung defence against P. aeruginosa colonization, which causes the host to produce a greater, but damaging, inflammatory response. Such a response may originate from the reduced antimicrobial activity of DBA/2 macrophages.

Indexed as

AnimalsComplement C5LungMacrophagesMiceMice, Inbred DBAMice, Inbred StrainsPseudomonas aeruginosaPseudomonas InfectionsSpecies SpecificityComplement C5

Identifiers

PMID17379707
PMCPMC2074882
OpenAlexW2006327796

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.