Evidence map›Paper›PMID 18554706›Full record

ArticleThe Journal of allergy and clinical immunology2008

Surfactant protein D inhibits TNF-alpha production by macrophages and dendritic cells in mice.

László Hortobágyi, Sonja Kierstein, Kateryna Krytska, Xiaoping Zhu, Anuk M Das, Francis Poulain, Angela Haczku

Abstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.3field-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

20 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Innate Immunity and Influenza A Virus Pathogenesis: Lessons for COVID-19.Frontiers in cellular and infection microbiology · 2020
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Paradigms in chronic obstructive pulmonary disease: phenotypes, immunobiology, and therapy with a focus on vascular disease.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2017
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. SP-D and regulation of the pulmonary innate immune system in allergic airway changes.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2010
    Review
  18. Social stress and asthma: the role of corticosteroid insensitivity.The Journal of allergy and clinical immunology · 2010
    Review
  19. Therapeutic use of surfactant components in allergic asthma.Naunyn-Schmiedeberg's archives of pharmacology · 2009
    Review
  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

7 authors at 2 institutions in 1 country.

László Hortobágyi *Department of Medicine, University of Pennsylvania, Philadelphia.
Sonja Kierstein *Department of Medicine, University of Pennsylvania, Philadelphia.
Kateryna KrytskaDepartment of Medicine, University of Pennsylvania, Philadelphia.
Xiaoping ZhuDepartment of Medicine, University of Pennsylvania, Philadelphia.
Anuk M DasCentocor, King of Prussia.
Francis PoulainDepartment of Pediatrics, University of California at Davis.
Angela HaczkuDepartment of Medicine, University of Pennsylvania, Philadelphia.
University of Pennsylvania · USUniversity of California, Davis · US

Funding

Regulation of Inflammation in Asthma by Fas LigandR01HL076646 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI HACZKU, ANGELA · 2005 to 2009
$1.8M
Surfactant-Protein Innate Immunity in an Asthma ModelR01AI055593 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI HACZKU, ANGELA · 2004 to 2008
$1.6M
NHLBI NIH HHS R01 HL076646NIAID NIH HHS R01 AI055593NIAID NIH HHS R01-AI055593-01
6 · The paper itself

Abstract

backgroundSurfactant protein (SP) D shares target cells with the proinflammatory cytokine TNF-alpha, an important autocrine stimulator of dendritic cells and macrophages in the airways.

objectiveWe sought to study the mechanisms by which TNF-alpha and SP-D can affect cellular components of the pulmonary innate immune system.

methodsCytokine and SP-D protein and mRNA expression was assessed by means of ELISA, Western blotting, and real-time PCR, respectively, by using in vivo models of allergic airway sensitization. Macrophage and dendritic cell phenotypes were analyzed by means of FACS analysis. Maturation of bone marrow-derived dendritic cells was investigated in vitro.

resultsTNF-alpha, elicited either by allergen exposure or pulmonary overexpression, induced SP-D, IL-13, and mononuclear cell influx in the lung. Recombinant IL-13 by itself was also capable of enhancing SP-D in vivo and in vitro, and the SP-D response to allergen challenge was impaired in IL-13-deficient mice. Allergen-induced increase of SP-D in the airways coincided with resolution of TNF-alpha release and cell influx. SP-D-deficient mice had constitutively high numbers of alveolar mononuclear cells expressing TNF-alpha, MHC class II, CD86, and CD11b, characteristics of proinflammatory, myeloid dendritic cells. Recombinant SP-D significantly suppressed all of these molecules in bone marrow-derived dendritic cell cultures.

conclusionsTNF-alpha can contribute to enhanced SP-D production in the lung indirectly through inducing IL-13. SP-D, on the other hand, can antagonize the proinflammatory effects of TNF-alpha on macrophages and dendritic cells, at least partly, by inhibiting production of this cytokine.

Indexed as

AnimalsDendritic CellsInterleukin-13LungMacrophagesMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, TransgenicPulmonary Surfactant-Associated Protein DTumor Necrosis Factor-alphaInterleukin-13Pulmonary Surfactant-Associated Protein DTumor Necrosis Factor-alpha

Identifiers

PMID18554706
PMCPMC4024109
OpenAlexW2066361433

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.