Evidence map›Paper›PMID 18426877›Full record

ArticleInfection and immunity2008

Toll-like receptor 9 regulates the lung macrophage phenotype and host immunity in murine pneumonia caused by Legionella pneumophila.

Urvashi Bhan, Glenda Trujillo, Kenneth Lyn-Kew, Michael W Newstead, Xianying Zeng, Cory M Hogaboam, Arthur M Krieg, Theodore J Standiford

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

42 citing papers in PubMed, 69 citations in OpenAlex.

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  20. Fibrocytes are not an essential source of type I collagen during lung fibrosis.Journal of immunology (Baltimore, Md. : 1950) · 2014
    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

8 authors at 3 institutions in 1 country.

Urvashi BhanUniversity of Michigan Medical Center, Division of Pulmonary and Critical Care Medicine, Ann Arbor, MI 48109-2200, USA.
Glenda Trujillo
Kenneth Lyn-Kew
Michael W Newstead
Xianying Zeng
Cory M Hogaboam
Arthur M Krieg
Theodore J Standiford
Pulmonary and Critical Care Associates · USUniversity of Michigan–Ann Arbor · USWellesley College · US

Funding

Pulmonary innate immune activation for bioterror defenseU01AI057264 · NIAID · COLEY PHARMACEUTICAL GROUP, INC. · PI KRIEG, ARTHUR M. · 2003 to 2005
$6.3M
Role of TLR9 in Lung Antibacterial Host DefenseR01HL057243 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI STANDIFORD, THEODORE J. · 1997 to 2011
$3.6M
NHLBI NIH HHS HL25243NHLBI NIH HHS R01 HL057243NIAID NIH HHS U01 AI057264NIAID NIH HHS U01 AI57264
6 · The paper itself

Abstract

Experiments were performed to determine the contribution of TLR9 to the generation of protective immunity against the intracellular respiratory bacterial pathogen Legionella pneumophila. In initial studies, we found that the intratracheal (i.t.) administration of L. pneumophila to mice deficient in TLR9 (TLR9(-/-)) resulted in significantly increased mortality, which was associated with an approximately 10-fold increase in the number of lung CFU compared to that of wild-type BALB/c mice. Intrapulmonary bacterial challenge in TLR9(-/-) mice resulted in the reduced accumulation of myeloid dendritic cells (DC) and activated CD4(+) T cells. Lung macrophages isolated from Legionella-infected TLR9(-/-) mice displayed the impaired internalization of bacteria and evidence of alternative rather than classical activation, as manifested by the markedly reduced expression of nitric oxide and type 1 cytokines, whereas the expression of Fizz-1 and arginase-1 was enhanced. The adoptive transfer of bone marrow-derived DC from syngeneic wild-type, but not TLR9(-/-), mice administered i.t. reconstituted anti-legionella immunity and restored the macrophage phenotype in TLR9(-/-) mice. Finally, the i.t., but not intraperitoneal, administration of the TLR9 agonist molecule CpG oligodeoxynucleotide stimulated protective immunity in Legionella-infected mice. In total, our findings indicate that TLR9 is required for effective innate immune responses against the intracellular bacterial pathogen L. pneumophila, and approaches to maximize TLR9-mediated responses may serve as a means to augment antibacterial immunity in pneumonia.

Indexed as

AnimalsCpG IslandsCytokinesFemaleHumansLegionella pneumophilaLegionnaires' DiseaseLungMacrophages, AlveolarMiceMice, Inbred BALB CPhenotypeToll-Like Receptor 9CytokinesToll-Like Receptor 9

Identifiers

PMID18426877
PMCPMC2446723
OpenAlexW2112853487

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.